use in Miniature Horses
BUTE vs BANAMINE use in Minis
By "Dr. Pam" - Pam Ripperda D.V.M.
Bute is incredibly toxic to minis, and for some reason a lot of vets out there
don't realize this. Not only is there a very narrow safety margin, i.e. you have
to be very accurate at dosing them, but there are minis who will have problems
even at the correct dose. It should be given at 1mg per pound body weight, which
means most minis will get 150 mg to 250 mg--1/4 tablet or less. A lot of vets
seem to think the average mini weighs 500 pounds and have owners give 1/2 tablet
twice daily. ARGGGG!!!
Bute toxicity can cause severe gastric and intestinal ulceration, to the point
of perforation and death (in as little as 5-7 days), kidney and liver damage,
bone marrow suppression, and lowered blood protein levels.
That said, I have used bute on selected minis for laminitis, but at a low dose
and for short periods of time. For almost everything else I use Banamine (which
can also cause problems if dosed too high or too long, but has a much wider safety
From Plumb's Veterinary Drug Handbook:
Adverse effects: Horses: oral and GI erosions and ulcers, hypoalbuminemia,
diarrhea, anorexia, and renal (KIDNEY) effects.
Cautious use in both foals and ponies is recommended because of increased
incidences of hypoproteinemia (LOW BLOOD PROTEIN LEVELS)and GI ulceration. Foals
with a heavy parasite burden or that are undernourished may be more susceptible
to development of adverse effects.
Phenylbutazone may cause decreased renal blood flow and sodium and water
retention, and should be used cautiously in animals with preexisting renal
disease or CHF (CONGESTIVE HEART FAILURE).
The primary concerns with phenylbutazone therapy in humans include its bone
marrow effects (agranulocytosis, aplastic anemia), renal and cardiovascular
effects (fluid retention to acute renal failure), and GI effects (perforated
ulcers). Other serious concerns with phenylbutazone include, hypersensitivity
reactions, neurologic, dermatologic (SKIN), and hepatic toxicities.
While phenylbutazone is apparently a safer drug to use in horses and dogs than
in people, serious adverse reactions can still occur. Toxic effects that have
been reported in horses include oral and GI erosions and ulcers, hypoalbuminemia
(LOW BLOOD PROTEIN LEVELS), diarrhea, anorexia (LOSS OF APPETITE), and renal
effects (azotemia (HIGH LEVELS OF UREA/AMMONIA IN THE BLOOD)). Unlike humans, it
does not appear that phenylbutazone causes much sodium and water retention in
horses at usual doses, but edema has been reported. In dogs however,
phenylbutazone may cause sodium and water retention, and diminished renal blood
...acute overdosage with phenylbutazone include, a prompt respiratory or
metabolic acidosis with compensatory hyperventilation, seizures, coma, and acute
hypotensive crisis. In an acute overdose, symptoms of renal failure (oliguric,
with proteinuria and hematuria), liver injury (hepatomegaly and jaundice), bone
marrow depression, and ulceration (and perforation) of the GI tract may develop.
More Than a
Pain in the Neck
by: Tracy Norman, VMD
January 2006 Article # 6466
If you have horses, you've probably at one time
or another found yourself in the following
situation. You arrive at the barn to feed for
the evening and your gelding, who is usually a
chow-hound, doesn't come up for dinner. After
you bring him up to the barn, you notice that
he's been rolling, and he paws and looks at his
sides. Concerned by these signs of colic, you
call your veterinarian, but she's on another
call and won’t arrive for at least an hour. His
continued signs of pain worry you, and you
remember that there is a bottle of Banamine in
the tack room medicine cabinet. You want to give
this effective pain reliever to your horse, but
don't feel confident about giving intravenous
injections, and know that missing the vein can
have very serious side effects. You remember
hearing that Banamine can be given by the
intramuscular (IM) route, and the label on the
bottle indicates that this is an approved route.
Moreover, you feel comfortable giving an IM
injection, as you have seen hundreds of these
shots given, and you and your veterinarian have
discussed how best to administer IM injections.
You wipe the top if the bottle with an alcohol
swab, draw up 10 mL of Banamine using a sterile
syringe and needle, and head for your horse’s
neck, ready to give the injection.
* Now it is time to STOP: DON'T GIVE THAT
BANAMINE SHOT IM!
Why Not Inject?
IM injections in horses are fairly easy to
administer, and many horse owners find this
route convenient, especially when a veterinarian
is not available to give an intravenous shot.
Vaccines, hyaluronic acid products, some
antibiotics, sedatives, vitamins,
antihistamines, and some anti-inflammatory drugs
are labeled for IM use in the horse.
Product labeling is not a guarantee of safety,
however, and it is important to remember that
any invasive procedure carries with it some
degree of risk.
Specific to IM injections is the risk of a
disease known as clostridial myonecrosis (also
known as "gas gangrene"). This is an uncommon
condition that can be associated with any
penetrating soft tissue injury in the horse,
including a needle puncture. When it occurs as a
complication of an IM injection, it is usually
associated with the injection of a relatively
large volume (greater than 5 mL) of an
Injectable ivermectin, antihistamines, and
flunixin meglumine (Banamine) are the drugs most
commonly associated with the disease (1,2,3). In
the case of flunixin, this risk is probably
associated with its very high frequency of use,
rather than the product itself. Although
flunixin is only available through a
veterinarian, many barns have bottles sitting on
the shelves, sometimes for long periods of time.
Owners and trainers, either while awaiting the
veterinarian or as a first line of treatment,
often give horses with fever or mild signs of
discomfort IM flunixin meglumine. Although this
practice is very common and usually uneventful,
the potential consequences can be devastating.
What Is It?
Clostridial myonecrosis is a rapidly
progressive, often fatal infection caused by a
number of clostridial organisms, most commonly
Clostridium perfringens and C. septicum. These
bacteria can be found everywhere in the
environment, and they are in especially high
concentrations in soil and manure. They exist in
the environment in an inactive, or spore, form
that is very resistant to environmental
conditions and antiseptics. In order to grow,
they require an anaerobic (oxygen-free)
It is unclear whether the organisms enter the
skin at the time of puncture, or if the spores
already exist within the horses' muscles. There
is some evidence that sterile preparation of
injection sites does not reduce the risk of
developing clostridial myonecrosis (4) and that
clostridial spores can be in the muscle tissues
of horses that do not have myonecrosis (2).
However they arrive at the puncture site, the
bacteria germinate in the anaerobic environment
that is created when the tissue is damaged and
the blood supply is interrupted, either by
trauma or by the introduction of an irritating
substance. Once the bacteria begin to germinate
and release toxins, there is often a very rapid
onset and progression of clinical illness.
Identifying a case of clostridial myonecrosis
early in the course of disease is important to
increase the likelihood of a successful outcome.
Signs might appear as soon as several hours
following an injection, or might not appear for
two to three days. Horses might have a fever or
be off of feed, and there is usually painful
swelling at the site of injection or injury.
There can be crepitus (audible and/or crackling)
palpable in the skin if the gas produced by the
bacteria is trapped under the skin. Swelling
might be extensive and extend down a leg, and
there could be associated lameness (Figure 1).
An affected horse will usually suffer a rapid
deterioration of health and might show signs of
colic, poor circulation, and toxemia; many
untreated horses die within 48 hours of the
onset of clinical signs.
Usually, a history including a soft tissue
puncture or injection and physical examination
findings are enough to raise a veterinarian's
suspicion. Other diagnostic tests that are
helpful in confirming the diagnosis are
ultrasound, complete blood count, blood
chemistry, and clotting profile.
Ultrasound can show gas deep within the tissues
and the loss of normal muscle architecture as it
becomes necrotic (Figure 2). Complete blood
counts are useful to assess the state of the
horse's immune response and can help in
evaluating for other potential effects of the
clostridial infection, such as low platelet
counts and hemolysis (red blood cell
destruction). Blood chemistries can guide
treatment by giving information about the
horse's body systems and hydration status. The
degree of muscle damage is often not accurately
reflected in increased muscle enzymes in the
bloodstream, as blood flow to the affected area
is often very poor. Clotting profiles can help
to determine the stage and severity of disease
and will help guide treatment by prompting
intervention before clinical signs of clotting
Horses with clostridial disease can have
exaggerated clotting responses, forming clots
inappropriately in vessels. This can lead to
organ failure by disrupting the blood supply to
different parts of the body. If systemic
clotting factors become depleted, the horse's
blood will not clot properly, resulting in
Clostridial organisms cause disease by producing
damaging enzymes and toxins known as exotoxins.
The type of toxins a given bacterium produces
determines its classification. The various
toxins serve to destroy cell membranes, dissolve
collagen, destroy DNA, and inactivate the immune
response of the host.
Swelling with edema fluid can be dramatic and
exert pressure on surrounding tissues, further
impairing blood flow.
The result is a perpetuation of the disease
process with extensive tissue destruction and
expansion of the anaerobic environment. Large
areas of tissue can become affected rapidly,
with extensive sloughing of skin and muscle
(Figure 3). Toxins released into the horse's
bloodstream affect the ability of the heart to
circulate blood effectively. Poor blood flow
damages the body's organs, and shock and
septicemia might ensue. Cardiovascular
compromise can rapidly lead to death, even with
aggressive supportive treatment by a
It appears that C. perfringens might be more
successfully treated than some of the other
clostridial species, but the approach to
treatment is the same regardless of the
causative agent (2). An aggressive approach to
treatment, including both medical and surgical
therapy, is warranted in all cases.
The cornerstones of treatment are the use of
antibiotics that are effective against anaerobic
bacteria and surgical removal of devitalized
tissue. There is some controversy and debate
among veterinary researchers about which
antibiotic regimen is best, but regardless of
the drug selected, early intervention is
Many horses will require intravenous fluids to
correct dehydration and provide cardiovascular
support, and all will require pain management.
The affected area should be surgically opened to
allow exposure of the tissues to oxygen, reduce
swelling, remove dead tissue, and allow drainage
(Figure 4). In some cases, removal of large
amounts of tissue might be necessary. Following
these procedures, careful wound care and
monitoring are indicated, and the procedures
might need to be repeated in several days. Some
horses will require other treatments if
complications such as clotting disorders,
endotoxemia, laminitis, pericarditis
(inflammation of the membrane surrounding the
heart), or diarrhea develop.
Horses that develop clostridial myonecrosis
often face long, expensive hospital stays, and
even with appropriate care, approximately 40%
will die as a result of their disease (2). Those
that survive often face intensive care,
prolonged wound management, and high treatment
"Daisy," a 2-year-old Thoroughbred race filly,
was given 10 mL of Banamine in the muscle to
treat signs of mild colic. Her colic resolved
uneventfully, but two days later she developed a
large, painful swelling at the injection site,
edema that extended down her neck, and signs of
severe systemic illness. She was admitted to the
hospital, and the injection site was
ultrasounded. On ultrasound, it was clear that
the underlying muscle was being destroyed, and
gas in the tissues clinched the diagnosis of
clostridial myonecrosis. Bloodwork revealed that
Daisy was indeed quite ill. Surgery on the
necrotic muscle was performed immediately, and
Daisy was placed on IV fluids, antibiotics,
anti-inflammatory drugs, and local oxygen
therapy. Daisy made a full recovery with minimal
scarring (Figure 5), but sustained a hospital
bill of several thousand dollars.
"Lucy," a 6-year-old Thoroughbred mare, was
given 10 mL of Banamine in the muscles at the
top of her right rump to relieve signs of muscle
soreness after work. Her right hind leg was so
swollen at presentation that she was unable to
bear weight on it. She had a fever and was
showing signs of toxemia. She was treated in a
very similar fashion to Daisy, but developed
fevers that were not responsive to medication.
After a week of intensive treatment, costing
several thousand dollars, she died without
Prevention is much simpler and more economical
than treatment, and boils down to avoiding
unnecessary IM shots. Flunixin meglumine is
available in a granule for top dressing on feed,
and an oral paste. If these products are not
available, the injectable formulation can be
given orally, and it has been shown in research
to be well absorbed, reaching active
concentrations in the blood in 15 minutes (5).
If possible, trained personnel should give
injections intravenously rather than relying on
the IM route as an alternative. Some injections,
such as vaccinations and other drugs, can only
be given in the muscle, but they are usually of
relatively low volume and probably pose a lower
risk. Shots in the muscle should always be given
in areas that can drain easily, such as the
neck, the pectoral muscles at the bottom of the
chest, and the back of the hindquarters. The
results of one study suggest that the neck
region might be an at-risk location, and that
the superior blood supply of the hindquarters
makes it a better location1. Shots should never
be given to horses in the top of the rump.
Before giving any shots, check with a
veterinarian to review the appropriate
Again, in the case of Banamine, the
injectable product can be effectively
administered by mouth. Contaminated or
expired medication should never be used via any
rate. Careful monitoring of injection sites and
prompt intervention by a veterinarian are key to
catching problems early and increasing the
chance of treating complications successfully,
should they arise. Most importantly, the
consequences of clostridial myonecrosis,
although rare, far outweigh the perceived
convenience of giving IM injections that could
The author would like to extend special thanks
to Drs. Noah Cohen and Joanne Hardy for their
insight and support with this piece.
1. Peek, S.F.; Semrad, S.D.; Perkins, G.A.
Clostridial myonecrosis in horses (37 cases
1985-2000). Equine Veterinary Journal 2003;
2. Peek, S.F.; Semrad, S.D. Tutorial Article:
Clostridial mynecrosis in horses. Equine
Veterinary Education 2002; 4:207-215.
3. Rebhun, W.C.; Shin, S.J.;King, J.M.; Baum,
K.H.; Patten, V. Malignant edema in horses.
Journal of the Veterinary Medical Association
4. Brown, M.B.; Kaneene, J.B.; Walker, R.D.
Intramuscular injection techniques and the
development of clostridial myositis or
cellulitis in horses. Journal of the American
Veterinary Medical Association 1988; 6:668-670.
5. Pellegini-Masini, A.; Poppenga, R.H.;
Sweeney, R.W. Disposition of flunixin meglumine
injectable preparation administered orally to
healthy horses. Journal of Veterinary
Pharmacologic Therapy 2004; 27:183-186.
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