Capture Myopathy
This condition has many names: exertional, transport, stress, degenerative myopathy and
white muscle disease.
It affects all species - and is most widely
recognized in hoofed animals such as deer.
All ages and sexes are susceptible .
HOW DOES IT HAPPEN?
When the muscle is exerted (used) its metabolism changes from aerobic (uses oxygen) to
anaerobic (uses stored energy in the muscles). This leads to the build up of lactic acid causes
acidosis. Lactic acid in the bloodstream drops the pH in the body, affecting heart output. If
the heart does not pump oxygen to the muscle it starts to die. When the muscle dies over the
next 7 days, it releases a product called myoglobin (breakdown product of muscle).
Myoglobin damages the excretion part of the kidney (the renal tubule). Other organs are
affected: the lungs become congested and bleed. The liver becomes swollen and pale.
CLINICAL SIGNSWe need to appreciate that we are seeing a disease in a spectrum of severity, over a number
of days. It may occur in any muscle group in front and back legs or heart. It has been
classified into four appearances that can help to understand what carers can see:
1. hyperacute - very sudden onset with death often noted.
2. acute - from heart muscle necrosis and occurs over 2- 4 days.
3. subacute - kidney failure from the release of myoglobin.
4. chronic - die over 2-4 weeks due to heart failure and paralysis
The range of clinical signs begin in the early stages as hyperthermia (body temperature is
above normal - animal is hot - sweats, pants), trouble breathing, fast heart rate. The animal
may become weak or have a stiff gait. Muscle tremors - either involving a few muscles or an
entire muscle group may be seen. The animal may collapse and die.
WHAT CAUSES CAPTURE MYOPATHY?
There are several situations that can cause capture myopathy. These include trapping,
capture, transport and even simple restraint. In other words - we humans cause this condition!
However, it is also used successfully as a hunting tool by large carnivores such as dogs.
IS WHITE MUSCLE DISEASE RELATED TO CAPTURE MYOPATHY?Muscle is a pretty simple organ. All it can do when it is sick is to die! So white muscle
disease, which is seen in fawns due to a lack of vitamin E and selenium deficiency has the
same appearance as myopathy when you slice the muscle and look at it under a microscope.
HOW IS CAPTURE MYOPATHY TREATED?The bad news is that if you have an deer with clinical signs, its prognosis is poor. In other
words - it is probably not going to get better.
In other words - treatment is not very effective and continuing to let the animal suffer becomes a
welfare issue.
The muscle has died. It cannot re-grow. This has an implication with the welfare of the
animal then being treated, only to suffer horrible cramping, pain from failing kidneys, inability
to breathe from congested lungs and then to die up to 1 month later. It also has an
implication for release - if the muscles are destroyed - then how is it ever going to be 100% fit
for release? Field treatment in the hands of many experienced veterinarians has not been
successful. Please remember, that humans are sometimes not saved in similar situations
(ecstasy overdose, malignant hyperthermia in susceptible people).
However, in situations where it is recognized at the hyperthermia stage, it is believed to be
possible to treat it. Treatment is quite intensive and expensive.
1. The first step is to sedate the animal. Although from a prevention perspective, this
should have already been performed. Sedation with valium may reduce anxiety
and assist in muscle relaxation.
2. The most important treatment for this condition is intravenous fluids eg: with
Hartmans solution or 0.9% saline. Essentially, what you are treating is acute
kidney failure.
The goal of giving fluids is to:
• Improve the blood supply to the kidney
• Dilute the damage that myoglobin does to the kidney
• Dilute the lactic acid in the blood stream, thus improving heart function
• Expand the blood volume and address the mechanisms of shock
• Reverse the hyperthermia
3. Another muscle relaxant that is used by zoos is Dantrolene. This is used in
humans for a similar condition - malignant hyperthermia. The drug is given
intravenously within 6 hours of reconstitution. It can damage the liver and kidney.
It is a human prescription only drug - few vets stock this and I do not recommend its use in deer.
4. Cortisone can be used for its anti-inflammatory properties. It may also help to
reverse hyperthermia.
5. Vitamin E and selenium can be used. This comes as Selvite-E. The dose rate is
1ml per 50 kg. It is given every 7 days under the skin. More frequently will harm
the animal. Selenium works in the cell membrane as an antioxidant, and similarly,
Vitamin E out of the cell.
PREVENTION
This is the key to this condition as you cannot undo the damage, you want prevent it from
occurring in the first instance. The deer's life is in your hands.
The goal is planning: plan the capture, plan to use sedation, plan what to do if something
goes wrong.
1. The method of capture needs to be well-planned, with sufficient people-power to
quickly trap the animal. And that is the key - we do not chase deer, we
encourage them into a trap. Time spent observing the animal and the escape route
it wants to follow, and then coordinating your movements is invaluable.
• Minimize the pursuit time - ideal is less than 3 minutes! After this, muscle
enzymes are beginning to climb and the damage begins.
• Reduce struggling by covering eyes and placing the captured animal into a bag.
• Keep the human noise down. ABSOLUTELY, No dogs should be present.
• Reduce the amount of handling time and then release to a less stressful place as
soon as possible.
2. Sedation. Consider the use of valium, azaperone , or
haldol
3. Do not catch animals when the ambient temperature is over 80°F. Do not leave
a sedated animal in direct sunlight.
4. Ensure that you keep the animal's temperature down: good ventilation, damp
cloths if required.