~ Bute (Phenylbutazone) 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 margin)

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 flow.

...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.

Banamine Injections

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.


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 irritating substance.

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) environment.

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.

Clinical Signs

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 disorders appear.

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 excessive bleeding.

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 veterinarian.


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 crucial.

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 costs.

Case Examples

"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 warning.

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 technique.

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 be avoided.

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; 35:86-92.
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 1985; 7:732-736.
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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