Rhabdomyolysis part 2.

[my hounds 307]

Exertional rhabdomyolysis is caused when a dog runs beyond its capabilities.

 

 

In simple terms muscles breakdown when they run out of oxygen/energy, muscles need more when they get hot, dogs running to the point of collapse may get so much muscle destruction that it can threaten life or damage the kidneys.

More heavily muscled dogs create more heat when running.

 

non exertional Rhabdomyolysis can also be caused by medication, poisons, electrolyte imbalances or a genetic predisposition. The latter are uncommon as working sighthound types are rarely on the medications that are risky, they have few inherited problems and are unlikely to have an electrolyte imbalance as their bodies are very good at maintaining the right balance.

I mean no disrespect but thanks for describing the symptoms/causes in laymans terms

[budgie123 163]

The bulk of the information you post sandymere has no relavance in this debate as it is relating to humans and not dogs.

Systems which regulate a dogs system an instance of this is how they regulate temperature are totaly different to humans.

 

You say from your postings that you correspond regularily with vets on various subjects what are they telling you about the condition?

 

Thankfully this conditin is rare when you think about the amount of work some dogs get and possibly we will possibly never know why it comes on.It is testament to a dog resiliance to undertake the work they do without succombing to the condition when you think about some of the repeat runs on hares some dogs undertake.

 

By lost the will to live reading rubbish about human conitions.

[skycat 6,173]

There is always a problem trying to correlate information about a similar condition in two completely different species: I hear what you are saying Budgie, and agree to a great extent, but in defence of Sandy (who I don't know at all) I think he is just trying to give us more information on the problem as he sees it. At the very least, its giving us all something to think about, whether or not we agree with him. I'll try and dig out the information my own vet gave to me a few years ago, but even he compared it to the human condition of the same name to a certain extent.

[sandymere 8,263]

Budgie I had an idea that you were posting 'copy and past' fashion because you didn't understand the subject, this post confirms it! When considering such basic biological functions we need to bare in mind that their basic biochemistry pre dates either species, so is very similar due to the shared nature. Basically a straw man .

Now if I'm wrong then here's a paper http://www.ncbi.nlm....?tool=pmcentrez

Please tell us where it goes wrong re dogs?

 

And for the less sciencey types wiki

 

http://en.wikipedia....ise_and_lactate

 

The cooling systems are later and vary, this is why I brought over heating up and I've looked at this in other posts re cramping etc.

 

Thank you Skycat,

The information is cross species in this instance due to the shared nature but I do take into consideration that variances exist and certainly don't just base posts on humans science. An example of such shared nature could be the heart, a dog, a human or a cat, they all have very similar hearts because all inherited from a common ancestor, basically the heart predates the species. There are some differences, size etc, but the cells, the electrical impulses, energy use etc are the same. So we can say a clot in the artery of a cats heart, a dogs heart or a human is heart is a heart attack, or that raised potassium levels in the blood will upset the electrical activity which could lead to irregular rhythm and cardiac arrest in all three.

On the other hand if i was to do a post on say diabetes i would look at the differences as much as the similarities between dogs and humans s there are relevant variances that would need discussing.

Edited June 21, 2012 by sandymere

[paulus 26]

these are extracts from darren morris`s book `training and racing the greyhound` in a nutshell there are 3 causes for acidosis to occur,

1) in dogs that are out of condition or have had a long lay off,and which are then subjected to a workload they can not cope with,This may also include dogs that are physically fit,but which are then worked beyond there capabilitys to recover, for example a coursing dog that has had an exceptionally long course or courses.,

2)a dog that gets excited or stressed before a race, this is because when a dog becomes stressed and pants excessively large amounts of the critical buffer agents are used up before the race, thus leaving the dog in short supply when eventually it runs.

3) dogs that are overworked with excessive running and trialing. a very stressfull racing programme can effect the chemical ballance within the dogs body.

 

he goes on to say

prevention is far better than cure, a sound excercise regiem and a good nutritional diet, vitamin E plays an important role in how efficiently the muscles utilize the oxygen within the muscles, this is usefull in that shortage of oxygen within the performance muscles can directly increase the likelyhood of acidosis, the use of creatine can also be of benifit as it helps in combating the onset of lactic acid.A mild kidney tonic such as Neutradex can also be used when a greyhound is in hard work, to help flush the natural build up of muscle waste from the system.

[sandymere 8,263]

these are extracts from darren morris`s book `training and racing the greyhound` in a nutshell there are 3 causes for acidosis to occur,

1) in dogs that are out of condition or have had a long lay off,and which are then subjected to a workload they can not cope with,This may also include dogs that are physically fit,but which are then worked beyond there capabilitys to recover, for example a coursing dog that has had an exceptionally long course or courses.,

2)a dog that gets excited or stressed before a race, this is because when a dog becomes stressed and pants excessively large amounts of the critical buffer agents are used up before the race, thus leaving the dog in short supply when eventually it runs.

3) dogs that are overworked with excessive running and trialing. a very stressfull racing programme can effect the chemical ballance within the dogs body.

 

he goes on to say

prevention is far better than cure, a sound excercise regiem and a good nutritional diet, vitamin E plays an important role in how efficiently the muscles utilize the oxygen within the muscles, this is usefull in that shortage of oxygen within the performance muscles can directly increase the likelyhood of acidosis, the use of creatine can also be of benifit as it helps in combating the onset of lactic acid.A mild kidney tonic such as Neutradex can also be used when a greyhound is in hard work, to help flush the natural build up of muscle waste from the system.

Pretty much what I already said other than perhaps some dodgy biochemistry such as example one is likely based on the old theories of lactic acid but as its out of context I can't say if it's mentioned but I would guess it is. The end result is the same rhabdomyolysis due to the body's inability to cope with the stresses being placed on it just not because of lactate.

 

The second example is backwards as when a dog pants it becomes more alkolotic due to blowing off excessive carbon dioxide rather than more acidotic, I discussed this in a topic on cramping, so it may well unbalance the base line biochemistry but away from rather than into acidosis. In a post above I allude to heating of the muscles through excessive breathing along with the increased heart rate may well increase the likelihood of rhabdomyolysis.

 

The 3rd example is a greyhound special in that the use of diuretics are the most likely cause of electrolyte imbalance in a healthy dog. Lurchers carrying out multiple runs often run 2 or 3 nights a week don't suffer electrolyte depletion so it would be odd that a greyhound doing 3 runs a fortnight suffers with this complaint. Potassium etc is readily available in the diet well in excess of requirements and little is lost other than that excreted as excess by the kidneys. So without the unnecessary diuretics there should be no shortfall. If a dog had a problem maintaining electrolyte balance in normal circumstances it would be unsuitable as a working dog and need investigation by a vet.

 

Lastly vitamin E, well it slows greyhound's race times and may well slow healing and muscle repair so all in all not a good idea. I would agree prevention is better than cure but think I've already said that a few times. It may be that the author was trying to put the biochemistry in simple terms but in doing so left it open to be interpreted wrongly.Lastly I would add that the world of greyhounds is rife with dodgy medicinal practice such as diuretics, thyroxin use etc not an example that the lurcher world needs to follow!

Edited June 21, 2012 by sandymere

[paulus 26]

forgetting body chemistry ect for a minute, the bit i carnt understand is wht it only effects certain muscles namely the latissimus dorsi and gluteal and not the main biceps and gracalis. is there a reason for this?

[martnmagik 68]

[sandymere 8,263]

forgetting body chemistry ect for a minute, the bit i carnt understand is wht it only effects certain muscles namely the latissimus dorsi and gluteal and not the main biceps and gracalis. is there a reason for this?

 

It would be interesting to look at a study of muscle impulses in greyhounds whilst they run to see exactly how the muscles are being used. My theory would be that we base our basic understanding on our own bio mechanics and so as we use our legs as the main muscles of locomotion we expect dogs to as well. The reality is perhaps that dogs use the bodies in a different way, ie the back muscles are the main muscles of locomotion and the legs are more about transferring that energy.

 

On the subject in general

 

The main point of this posting this topic was to high light the change away from lactic acidosis and towards rhabdomyolysis. If people know what's broken then it's more likely that they will look for the right method to fix it.

To put it another way, when we have pneumonia we increase our rate of breathing but increased breathing isn't pneumonia it's just a possible symptom of pneumonia. We all breathe all of the time, when we exercise we increase our breathing rate to blow off more carbon dioxide and take in more oxygen, again this is not pneumonia rather a normal symptom of running. It's the same with lactic acid, we produce it all the time that's normal, when we exercise we increase the rate of production as part of the energy cycle, lactic is energy. So it is not an illness or poison but rather a symptom of exercise. We can't run without increasing our breathing rate or our lactate use. In normal healthy dogs increased breathing or lactic acid will not cause a direct problem, after all its necessary to the process.

Lastly when it does happen we need to be very clear that we are treating rhabdomyolysis.

Edited June 22, 2012 by sandymere

[paulus 26]

so to sum up what we know about rhabdomyolysis so far then, unless someone can tell me any different the myth that this only happens to unfit dogs had been busted. everyone ive spoken to who has has a dog suffer from rhabdomyolysis has said their dogs were fit, including my own. we do know what chemical reactions take place within the dogs body when rhabdomyolysis occurs but we dont know why it occurs or when it is likely to occur. we know the symptoms can take up to 72 hrs after physical exertion. The dog looking and acting perfectly normal up to this point. The key identifying feature of rhabdomyolysis is the pain the dog is suffering in its back muscles and its unwillingness to move from a set position, be that standing of laying down. treatment will vary from vet to vet, normally fluids, anti inflammatories and painkillers, although i have herd of some promoting full blood transfusions. the pain period lasted three and a half days in my dog. The resulting muscle and consequential weight loss was astounding. without any futher heart,kidney complications the dog should make a full recovery and run again as normal given time for the skeletal muscle to grow back and fitness once again be obtained. As to wether a dog will suffer again with this condition, well who knows as i said we dont fully understand what the trigger is in the first place, all we have is theories.

[sandymere 8,263]

An umbrella description I like is "When oxygen delivery can no longer keep up with increasing requirements, cellular hypoxia ensues" and the link to heat "every 1 degrees C increase in body temperature increases metabolic demand by approximately 10% " (quoted from the critical care article link I've posted earlier). So when reaching it maximum ability to supply the muscles with their requirements the extra demand placed on them by the added heat pushes the muscles over the edge. The result is that the cells control of electrolytes fails and the cells contents are released into the blood stream.

 

 

I'd go with the theory that it is more common in unfit dogs just because they are less well adapted to cope with the extremes, as with pulled muscles or any other injury, training adapts the body to reduce the risk.

I'd also say that very many lurcher owners over estimate how fit their dogs are; I've noticed time and again people coming over to work fat slack muscled dogs that I would hesitate to slip on a rabbit.

The other extreme is heavily muscled dogs, you see them on here "look at my dog" posts and there follows a pic of an animal that would not look out of place in Muscle weekly! They are ok for one or two runs but are far to muscled to keep going, fine if they are only slipped once or twice but for multiple runs or that really long course they risk overheating to a dangerous degree.

Based on personal experience the more a dog works the lighter it gets, heavy muscles get honed till the best compromise of strength versus weight is achieved. I found that the greyhounds I worked after their racing careers finished changed from muscled up powerhouses to slimmer honed down versions, in human terms from a hundred metre sprinter to a eight hundred metre runner.

[paulus 26]

An umbrella description I like is "When oxygen delivery can no longer keep up with increasing requirements, cellular hypoxia ensues" and the link to heat "every 1 degrees C increase in body temperature increases metabolic demand by approximately 10% " (quoted from the critical care article link I've posted earlier). So when reaching it maximum ability to supply the muscles with their requirements the extra demand placed on them by the added heat pushes the muscles over the edge. The result is that the cells control of electrolytes fails and the cells contents are released into the blood stream.

 

 

I'd go with the theory that it is more common in unfit dogs just because they are less well adapted to cope with the extremes, as with pulled muscles or any other injury, training adapts the body to reduce the risk.

I'd also say that very many lurcher owners over estimate how fit their dogs are; I've noticed time and again people coming over to work fat slack muscled dogs that I would hesitate to slip on a rabbit.

The other extreme is heavily muscled dogs, you see them on here "look at my dog" posts and there follows a pic of an animal that would not look out of place in Muscle weekly! They are ok for one or two runs but are far to muscled to keep going, fine if they are only slipped once or twice but for multiple runs or that really long course they risk overheating to a dangerous degree.

Based on personal experience the more a dog works the lighter it gets, heavy muscles get honed till the best compromise of strength versus weight is achieved. I found that the greyhounds I worked after their racing careers finished changed from muscled up powerhouses to slimmer honed down versions, in human terms from a hundred metre sprinter to a eight hundred metre runner.

have to disagree mate, lack of fitness is always blamed for anything that carnt be rationally explained, as you said in an earlier post, some of our forces personel also suffer from this, aswell as greyhounds. i believe from expeirence its one of two things that make the difference, excitability (prey drive) and or over worked. the dog i have here that suffered from it would die before he gave up on something its just in his nature, ive seen it with more heavily saturated bull crosses to, were they get so worked up they pass out or fit whilst chasing/holding prey.

[budgie123 163]

Please find below information from greyhound vet on the subject.

 

 

It has been a while since I had a poke about in the literature about this

subject and I can remember that it was quite frustrating as the most recent

research like a lot of things in dog racing was in the 90 `s at the

earliest. Much subsequent work has been reviews of the former or academic

papers which have not used dogs in the fields. You will have to forgive me

as I do not have the references to hand.

 

I think the biggest problem is that true acidosis that is acidosis which

occurs spontaneously is not the only explanation and often dogs which

succumb to acidosis have other underlying causes e.g. sub clinical urinary

tract infections. Overtraining, undertraining, electrolytes, being in false

pregnancy, water diabetes (if you believe that actually exists) probably all

have a part to play

 

The other problem is that acidosis or lactic acidosis is often mis/self

diagnosed, you need a blood test to diagnose, blood in the urine on a

dipstick is not enough as this can be normal in working dogs and a sore back

is not always acidosis, I know this because I have done blood and urine on

quite a few dogs which have shown this after a run and they have been

negative for acidosis. Once diagnosed dogs also have to be monitored and the

problem is people rarely wish to pay for this hence the many threads that

start "I phoned my vet but what do you think" rather than "I have been to

the vet and had these tests" so unfortunately much of the information is

anecdotal and unreliable. This is not helped by the complete ignorance of

the condition by many vets and subsequently they do not test for CK(creatine kinase) and AST(asparlate aminotransferase)

and have not way of interpreting the results.

 

Also there is a lot spoken about electrolytes and the belief is that if you

fill them up with recharge they don`t get it. Personally I reckon that

potassium is probably the main mineral which counts and sugar for a bit of

energy (most electrolyte solutions are basically salt nacl and kcl).

 

As for care of the racing greyhound it was reviewed recently (Care of racing

and retired greyhound) so is not hopelessly out of date and although it does

contain so inaccuracies it is still a good resource. The obvious problem is

in the greyhound title, the advice does not always fit lurchers and whippets

because the way they are worked is different, greys doing a single 30 second

run cannot be compared to 3-6 2-6 minute runs, the physiology of longer runs

and the dogs themselves is different.

 

I have certainly followed Care Of Racing Greyhound when treating severely

ill greys and the advice was good.

 

It may be worth you contacting Paul Evans at Oldham as he is much more

academically gifted than me and was involved in bits of research relating to

dogs especially season suppression.

 

There has been talk of University of Liverpool doing some research into

cramping which will likely touch on acidosis but I am not in the loop on

that, I suspect that budget constraints may have slowed this research

 

There is an International Greyhound database produced under the supervision of Linda L Blyth at the college of vetetinary medicine at oregon state university.

The directory is a comprehensive list of all research relating to the care of the greyhound.

I have emailed Mrs Blyth about the subject underdiscussion and will post any information if she replies.

[budgie123 163]

The information below is from web address shady-acres.com/susan/tying-up.shtml.

 

It is relating to horses but the information about carbohydrates is the first time i have seen this mentioned relating to his condition.

Exertional rhabdomyolysis---excruciatingly specific details of what's happening at the cellular level.

 

The complete pathophysiology (Why It Happens) of exertional rhabdomyolysis (most commonly called "tying up") is still not completely understood. Currently, the conditions that are known to be factors in causing tying up are

1. resting a conditioned horse on a full-grain diet, followed by exercise ("Monday morning disease");
    
   
2. whole-body potassium depletion;
    
   
3. selenium deficiency;
    
   
4. an unaccustomed level of exercise;
    
   
5. postviral infections, particularly rhino;
    
   
6. intoxications with ionophores (a substance which increases cellular permeability to a specific ion, which would in turn disrupt the electrical potential of the cell), blister beetle, mercury, coffee bean (cassia) or gossypol from raw cottonseed.
   

Other factors which have been suggested as being contributory are hypothyroidism, some high-performance lines of horses, nervous horses, fillies, shock, laminitis, tetanus, neural injury, estrus, hyperestrogenism (resulting from possibly a granulosa cell tumor), cold damp weather, heavy muscling, and low-sodium rations. Electrolyte depletion, especially calcium, magnesium and chloride may also cause muscle cramps, which are sometimes referred to as slow-onset rhabdomyolysis; or synchronous diaphragmatic flutter, commonly called "thumps". These are related syndromes, but not exactly the same as the syndrome described here, which is most accurately described as acute rhabdomyolysis.

One of the current hypotheses is that when a conditioned horse is not worked and kept on full feed high in soluble carbohydrates (such as grain), the horse will accumulate carbohydrates in the muscles. If there is a sudden demand for work, the body cannot adequately remove the rapidly accumulating lactic acid in the muscles. This in turn causes vasospasms and ischemia---which means essentially that the surrounding blood vessels "clamp down" so that the lactic acid waste product cannot be removed. As a result, intracellular pH drops, the muscle cell is disrupted and you get the hard, crampy muscles you see when a horse ties up.

Other theories of the biochemical mechanism is that there is a deficiency of the high-energy phosphates in muscle cells following maximal, anaerobic exertion, and/or a depletion of muscle glycogen after prolonged, slow (endurance-type) exercise. High body temperatures and electrolyte imbalances/depletions are also probably contributing causes, and certainly major factors in endurance horses that tie up during competitions.

Unless you're a biochemist, all of these different theories essentially boil down to the same net effect---the ion pumps (ie, sodium/potassium, calcium/magnesium and calcium/ATPase) in the membrane surrounding the muscle cell which move substrates in and out of the cell are disrupted, and so the interior environment of the muscle cells either cannot get rid of waste products of metabolism, OR has too much of a metabolic substrate to be able to function, OR can't get enough of a metabolic substrate to be able to function. And so the muscle cell simply shuts down. When muscle cells shut down, they don't do so in the relaxed position, they freeze up in the contracted position, which is why you get those rock-hard muscles. Biochemically, it's not all that different from rigor mortis.

The effect on kidneys comes in when the connective tissue (the sarcolemma) surrounding and enclosing the muscle cell is disrupted, releasing the contents of the muscle cell into the bloodstream. There are lots of different proteins and substrates and whatnot in a muscle cell, but the important one for this particular discussion is myoglobin. Myoglobin is a protein pigment which is responsible for oxygen transport in the muscle cell. Hemoglobin transports oxygen in the bloodstream, myoglobin transports oxygen in the muscle cell. When myoglobin is released from a disrupted muscle cell into the bloodstream, it travels to the kidneys and is filtered out. In being filtered out of the bloodstream (and keep in mind, there's probably a lot of it from the kidney's point of view), it causes (or CAN cause) kidney damage or even total renal failure by overwhelming and clogging up the kidney tubules and restricting the blood (and therefore oxygen) supply to the kidney tissue. This effect will be worsened if the animal is hypovolemic, meaning he's dehydrated and therefore has a decreased total plasma volume. A decreased plasma volume means that in turn the blood is thicker and that the heart must work harder to circulate. And this in turn means that less oxygen to delivered to the muscles and organs, fewer substrates, less waste product removed, and so on. A vicious cycle sort of thing.

So while myoglobin does not directly damage the kidneys, in great enough concentration it will cause damage indirectly by clogging them up and creating what is called myoglobinuric nephrosis and possibly renal failure. It's also the myoglobin being filtered out that shows up as very dark urine. The dark urine itself is not what you have to worry about---what you DO have to worry about is the fact that myoglobin in the urine means that significant muscle disruption and damage has occurred in the system, and that the kidneys are being overwhelmed with a whole lot of waste product to try and get rid of. Needless to say, this is serious s**t from the physiological point of view. However, dark urine doesn't always mean myoglobinuria. Dark urine can be caused by other things as well. But if your horse is dehydrated, won't move and is standing there hunched up and miserable and the urine looks a lot like coffee---you've got problems.

Some of the other things a veterinarian will look for in a suspected tying-up horse are elevated enzymes in the blood plasma, specifically CK (creatinine kinase) and AST (aspartate aminotransferase). AST is also referred to as SGOT, but both refer to the same enzyme. There are other things the vet will look for as well, like creatinine, urea, electrolytes and so on, but enzyme levels are at the top of the list. CK and AST are both enzymes contained in the muscle cell (as well as other types of cells) which are released into the blood when the muscle cell is disrupted. Therefore, if the enzyme levels are elevated in the blood panel, it must mean that tissue cells somewhere are being (or were being) damaged. The tricky part in diagnosis is figuring out where tissue damage is occurring---AST occurs in both muscle and liver cells, so elevated levels could mean problems in either muscle OR liver (and for that matter, AST levels can also be elevated by certain drugs or toxins). CK levels will indicate muscle damage, while other elevated enzymes in the blood panel will indicate liver damage. And to make things even more confusing, there are various isoforms of yet another enzyme, LDH (lactate dehydrogenase) which will indicate whether muscle damage occurring is from skeletal or cardiac (heart) muscle.

The elevation in CK will be detectable within a few hours of the onset of clinical symptoms, peak within 24 hours and decline fairly quickly. CK's half-life is six hours, meaning that half of the amount remaining is removed within six hours. Hence, 50% is gone within 6 hours, 75% isgone within 12 hrs, 87.5% is gone within 18 hrs, 93.75% is removed within 24 hrs, and so on. The concept of "half-lifes" doesn't refer only to enzymes, by the way, the same general idea applies to drug half-lifes, isotope half-life, etc etc (just a little extra trivia for you)(I know, riveting.)

The rise in levels of AST will peak approximately 24 hours after the onset of the clinical signs of tying up, and decline much more slowly---AST has a half-life of about 14 days, so with significant muscle damage, it'll be awhile before levels are really back to normal. The relative levels of these two enzymes, among other things, are what a DVM will look at in determining the extent of damage, whether damage is still occurring and how long ago the initial damage occurred. For example, if a horse transport company delivers a horse doing a good impersonation of a piece of granite, and swears the horse must have injured himself last week before they ever laid eyes on him...but the blood analysis shows screaming CK levels (indicating recent muscle damage) and relatively low AST levels (also indicating recent damage), then the transport companies arguments can be classified under the heading of I Don't Think So Chuckles.

[sandymere 8,263]

Firstly most of the relevant bits from your post has already been covered, in parts in layman's terms, and that which hasn't, the horse stuff, seem a little odd, after all weren't you the one who decried my use of other species science?

Now if there is one problem with using other species science you need to make sure it is shared biochemistry! The carbohydrate references???? Consider do horse carb load? To what extent? Did you consider the relevance in relation to dogs reduced capacity ands its impact to this issue??

 

Secondly the idea that there is no new knowledge on this subject shows your stuff is dated, after all I’ve linked to recent studies in relation to lactic acid etc,. You really need to move foreword although I note you are using the term less now and using just acidosis which is very different indeed.

 

Third, I've already explained that there are many reason for rhabdomyolysis these can include things like electrolyte imbalances etc but as already been stated they are rare and would mean that a dog has some underlying genetic or disease process that would exclude it from work in the first place.

 

Cramping is another subject, likely some similarities but also differences, and one I've covered in specific posts so I'll not get into that here but feel free to check my earlier stuff.

.

Ps as your using info from other species I take it you now except the relevance of my earlier posts and now feel a little silly re your rather childish I'm bored type remarks?

 

edit for spelling

Edited June 26, 2012 by sandymere