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Colic is a general term used to signify abdominal pain. It is a sign of a problem, not a diagnosis. Colic can be the result of a number of gastrointestinal or abdominal problems. Most often the problem originates in the colon, the large intestine, of the horse. However, colic can also be the result of a tumor, peritonitis, a variety of plant poisons, uterine tears, torsion of the uterus, renal problems, and others.

Some of the causes of colic respond to medical treatment, others can become fatal without surgical intervention. In domestic horses, colic is the leading cause of premature death. An estimated 4-10% of the horse population will die from complications of colic. A much larger percentage will suffer from colic at some time during their lifetime.

Many different types or causes of abdominal pain in horses are commonly described. They include; gas and spasmodic colic, impaction colic, displacement in the form of torsion and volvulus colic, intussusception colic, entrapment colic, inflammatory colic, ulcerative disease colic, foal colic, herniation colic, colic the result of uterine tears or torsions, as well as other possibilities.

Perhaps the most important signs of colic that should result in a call to your veterinarian are; anorexia (won’t eat), looking around at the abdomen, depression, sometimes grunting with pain, kicking at the abdomen with a hind hoof, sinking or falling to the ground and moderate to violent rolling on the ground. Because of the manner in which the gastrointestinal tract is suspended in the equine abdomen, and its weight, a horse rolling in pain on the ground is susceptible to a tear or twisting of the mesentery (the tissue from which the intestinal tract is suspended within the abdomen) through which the intestine can twist on itself resulting in torsion (twisting of the bowel on itself longitudinally through a tear in the mesentery) or volvulus (when a loop of intestine twists around itself vertically with the mesentery that supports it resulting in bowel obstruction). When this happens the blood supply to the affected intestine is blocked or cut off entirely leading to death of the tissue, gangrene and death without successful surgical intervention.

Because of the danger of a twisted intestine from rolling the first instruction your veterinarian will provide when contacted is to keep the horse up and walking. You need to do everything possible to not allow the horse to go down and roll.

To treat uncomplicated colic your veterinarian will generally start treatment with analgesia (pain relief), if the animal is very anxious perhaps sedation, then the insertion of a nasogastric tube. The nasogastric tube will relieve any gas accumulation in the stomach and possibly from the first portion of the small intestine and will be used to pump in intestinal lubricants, laxatives and sometimes surfactants to prevent further gas accumulation. If the colic is severe and the animal doesn’t respond to the initial treatments within a reasonable amount of time it may be necessary to support the horse with intravenous fluids and possibly with nutritional support. In severe cases treatment for endotoxemia (toxins produced in the gut) may be necessary.

We generally recognize the following major types of colic; excessive e gas accumulation in the intestine (gas colic), simple obstruction (impaction colic), strangulation (volvulus or torsion colic’s), non-strangulation or infarction colic (blockage of a blood vessel to the gut), inflammation of the gastrointestinal tract (enteritis or colitis), colic from peritonitis (inflammation of the peritonium, the lining of the abdomen), and ulceration of the gastrointestinal lining or mucosa (ulcerative colic).  I will describe each of the various types of colic in future articles.

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Official Apex Reviews Rating:

Animals Don’t Blush takes the reader on an enjoyable, eye-opening journey through the ups and downs of a first-year veterinarian in Montana. In accessible, often hilarious language, author David Gross shares a variety of different anecdotes highlighting his rather entertaining experiences as the primary caregiver for a wide cross section of four-legged patients. Throughout the pages of Animals Don’t Blush, Gross’ considerable expertise shines through, as well as the deep-rooted compassion he has for both animals and their owners. Informative without being pedantic, and amusing without being pandering, this page-turning tome is sure to please more than just the animal lovers amongst us.

A highly satisfying literary treat from a truly gifted storyteller.

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The Animal Poison Control Center was started prior to my arrival as Head of the then named Veterinary Biosciences department in the College of veterinary medicine at the University of Illinois, Champaign-Urbana. After I took office the Center was taken over by the ASPCA and has grown and become more effective as a result. The service answered more than 167,000 calls in 2014 all involving exposure of animals to possible toxicants. Nearly 16% of those calls were about pets getting into medicines intended for human use, the seventh year in a row that this type of exposure was the most common.

Here are the most common pet toxins of 2014 as reported by the ASPCA:

  1. Human prescription medications. Especially dangerous are ADD/ADHD drugs.
  2. Over-the-counter medications including herbal and natural supplements as well as cough, cold and allergy medications. Many of these contain acetaminophen and/or pseudoephedrine or phenylephrine. All are highly toxic to pets. Glucosamine joint supplements are often flavored and will appeal to some animals, particularly dogs. Overdose can result in diarrhea and occasionally in liver failure.
  3. Insecticides particularly insect bait stations can result in bowel obstructions from ingesting the plastic shell containing the bait.
  4. Household items including paints and cleaning products.
  5. Human foods. Dogs were usually the culprits getting into serious trouble by ingesting large quantities of onions, garlic, grapes, raisins and particularly a sugar substitute xylitol found in sugar-free gum and other products.
  6. Veterinary medications, particularly chewable medications are particularly attractive to some pets.
  7. Chocolate, discussed in a previous blog.
  8. Plants, a long list of plant poisons have been covered in this blog.
  9. Rodenticides, haven’t discussed these but toxicity is obvious.
  10. Lawn and garden products, these include fertilizers as well as weed killers, etc.

Other potential hazards include:

  1. Oxygen absorbers and silica gel packs often found in packages of pet treats, jerky and other edibles. These can result in iron poisoning.
  2. Toxic lily plants including the Tiger, Asiatic, Stargazer, Casablanca, Rubrum, Day, Japanese Show and Easter lilies. Some cats are attracted to these plants and a small amount can result in kidney failure. The Calla, Peace and Peruvian lilies are relatively non-toxic but can result in GI inflammation and upset. These were also described in a previous blog.
  3. For reasons unknown some cats are attracted to antidepressants such as Cymbalta and Effexor. Ingestion can result in severe neurological and cardiac toxicities.
  4. Cats are also more sensitive to non-steroidal anti-inflammatory drugs like ibuprofen and naproxen. Don’t be tempted to treat your cat or dog with these agents.
  5. Glow sticks and glow jewelry contain dibutyl phthalate. If your cat’s mouth and/or skin are exposed from chewing on these objects it can result in a chemical burn.
  6. The leaves, fruit, seeds and bark of avocado trees, particularly those from Guatemala, commonly found in our supermarkets, can be toxic to birds, rabbits and horses resulting in respiratory distress, pulmonary congestion, pericarditis (inflammation of the sac surrounding the heart) and death from large doses. Dogs and cats seem to be much less sensitive to avocado toxicity.
  7. Raw bread dough made with live yeast when ingested, usually by dogs, can expand in the stomach resulting in gastric dilatation that can be life threatening.
  8. Ethanol poisoning, inebriation, was recently discussed along with hops poisoning.
  9. Grape and raisin poisoning has also been covered previously.
  10. Macadamia nuts are attractive to some dogs but are not usually fatal. After ingesting a sufficient quantity dogs may show weakness of the hind legs, demonstrate pain behavior, may show muscle tremors and/or develop a low-grade fever.
  11. Moldy foods can produce tremor genic mycotoxins. Since it’s not possible to determine whether a particular mold is producing these toxins the safest thing is not to empty that container from the back of the refrigerator into your dog’s dish. Cats will just turn up their nose and walk away. Also be on the lookout for garbage, road-kill, fallen fruit or nuts that could be moldy. Don’t let your dog get to them.

As always if your pet is showing any kind of suspected toxicosis get it to your veterinarian as soon as possible.

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Ingesting hops can be highly toxic to susceptible dogs. Hops can act as an inciting cause or trigger for malignant hyperthermia but it seems the animal must have a genetic pre-disposition for this to occur.

Hops%20photo-2

Scientific Name: Humulus lupulus, Family: Cannabidaceae

Malignant hyperthermia, an uncontrolled increase in body temperature, is a rare life-threatening condition usually triggered by exposure to general anesthetic agents, most commonly volatile anesthetics, in certain genetically susceptible humans, pigs and horses. Caffeine can also act as a “trigger”. Hops have been shown to trigger the reaction in susceptible dogs and cats. The triggers can induce a drastic and uncontrolled increase in oxidative metabolism, the utilization of oxygen, in skeletal muscle. This overwhelms the body’s ability to regulate body temperature. The result is high fever leading to circulatory collapse and death if not immediately treated.

The susceptibility to malignant hyperthermia is often inherited as an autosomal dominant disorder, for which there are at least 6 genetic sites of interest. In 50–70% of cases, the propensity for malignant hyperthermia is due to a mutation of the ryanodine receptor located on the sarcoplasmic reticulum of skeletal muscle cells where calcium ions are stored. The ryanodine receptor acts to open calcium ion channels that allows the ion to enter the skeletal muscle cells and initiate contraction. Malignant hyperthermia results when the normal processes of entry and subsequent removal of calcium ions from the muscle cells are interfered with. The process of sequestering excess calcium ion within the cell consumes large amounts of adenosine triphosphate (ATP), the main cellular energy carrier, and results in the generation of the excessive heat (hyperthermia) that is the hallmark of the disease. The muscle cell is damaged by the depletion of ATP and possibly the high temperatures and cellular constituents “leak” into the circulation.

The other major known causative gene for malignant hyperthermia is the protein encoding a different type of calcium channel. There are two known mutations in this protein. When these mutant channels are expressed in human embryonic kidney cells, the resulting channels are five times more sensitive to activation by caffeine (and presumably volatile anesthetic agents and hops). Other mutations causing malignant hyperthermia have been discovered but. in most cases. the relevant genes remain to be identified.

Research into malignant hyperthermia was limited until the discovery of “porcine stress syndrome” in Danish Landrace and other breeds of pigs. This “awake triggering” was not observed in humans and cast doubt on the value of the animal model. However susceptible humans were discovered to develop malignant hyperthermia the “awake trigger” in stressful situations. This supported the use of the pig model for research.

Pig farmers began to expose piglets to halothane. Those that died were malignant hyperthermia-susceptible, thus saving the farmer the expense of raising a pig whose meat was not marketable. This also reduced the use of breeding stock with the genes. The condition in swine was also found to be due to a defect in ryanodine receptors. The causative mutation in humans was only discovered after similar mutations had been described in pigs. Another argument for the use of animal models in research. Sorry, that was my career for thirty-six years and I still have to climb onto the soap box from time to time.

A causative mutated ryanodine receptor gene has been identified in Quarter Horses and other breeds and is inherited as an autosomal dominant. It can be triggered by overwork, anesthesia, or stress. In dogs the susceptibility seems to be autosomal recessive.

A malignant hyperthermia mouse model has been developed using molecular biology techniques. These mice display signs similar to those in susceptible animals when exposed to halothane as a trigger. This model was used to demonstrate that the injection of dantrolene, a muscle relaxant, reversed the response to the halothane in these mice and in humans. The current treatment of choice is the intravenous administration of dantrolene, discontinuation of triggering agents, and supportive therapy directed at correcting hyperthermia, acidosis, and organ dysfunction. Treatment must be instituted rapidly on clinical suspicion of the onset of malignant hyperthermia. After the widespread introduction of treatment with dantrolene, the mortality of malignant hyperthermia fell from 80% in the 1960s to less than 5%. However, the clinical use of dantrolene has been limited by its low solubility in water. This means it must be dissolved in large volumes of fluids complicating clinical management. Azumolene is 30 times more water-soluble than dantrolene and also works to decrease the release of intracellular calcium by its action on the ryanodine receptor. In susceptible pigs it was just as potent as dantrolene. However it has not yet been approved for use in humans. Hopefully those clinical trials are in progress. Research in mouse models continues in efforts to more completely describe the genetic mechanisms that trigger this condition.

So we know that hops can be poisonous to at least some breeds of dogs and also sometimes to cats. The cones are the culprit when enough of them are eaten. The initial symptoms are restlessness, panting, abdominal pain and vomiting. In serious cases, symptoms progress into seizures, rapid heart rate and life-threatening high body temperature. Greyhounds seem to be the most susceptible breed but also susceptible are golden retrievers, St. Bernards, Dobermans, border collies and English springer spaniels. Hops grown by aficionados pose a threat when the mature cones are low enough for the animal to reach or drop to the ground. With home-brewing becoming more popular we could see an increase in hops poisoning. A potentially bigger threat than hops plants is dogs getting into bags of stored hops or spent, dumped hops sediment.

Dogs are far more sensitive to ethanol than humans. Even ingesting a small amount of a product containing alcohol can cause significant intoxication. No matter how popular beer drinking dogs are on U-Tube hops poisoning is probably not a threat but intoxication from the alcohol is. Alcohol intoxication results in vomiting, loss of coordination, disorientation and stupor. Sound familiar? In severe cases, coma, seizures and death may occur. Dogs showing mild signs of alcohol intoxication should be closely monitored, and dogs that are so inebriated that they can’t stand up must be taken to your veterinarian.

 

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The story continues. Just a reminder, the toxicity of any substance is dependent upon the dose, the greater exposure the greater the toxicity. If you suspect your pet has ingested any of these plants get him or her to your veterinarian as soon as possible.

Plants belonging to the family Amaryllidaceae, the Kaffir Lily (Clivia Lily, Clivies, Caffre Lily, Cape Clivia, Kilvia), Daffodils (Narcissus, Jonquil, Paper White) the Barbados Lily (Amaryllis, Fire Lily, Lily of the Palace, Ridderstjerne) and the Hyacinth (Garden Hyacinth) all contain lycorine and other alkaloids. Ingestion of these plants results in gastric distress with hyper salivation (drooling), vomiting and diarrhea. Ingestion of large quantities of the plant, particularly of the bulbs, can cause convulsions, low blood pressure (hypotension) tremors and cardiac arrhythmias (irregular heartbeats).

The Autumn Crocus (Meadow Saffron) contains colchicines and other alkaloids. Ingestion of this plant can result in irritation of the oral mucous membranes (everything in the mouth and throat) bloody vomiting, diarrhea, shock, multi-organ damage and bone marrow suppression. This one is nasty!

The Yarrow plant (Milfoil) contains glycoalkaloids, monoterpenes and sesquiterpene lactones, all alkaloids and all toxic. Ingestion can result in vomiting, diarrhea, depression, loss of appetite (anorexia) and drooling. The Morning Glory contains at least four different indole alkaloids. After eating this plant your pet can show signs of GI upset, agitation, tremors, disorientation, ataxia (trouble with balance while moving) anorexia. The seeds of Yarrow can cause hallucinations.

The Burning Bush (Wahoo, Spindle Tree) contains both alkaloids and cardenolides. Ingestion can result in GI distress, abdominal pain and weakness. Large doses can result in cardiac (heart) arrhythmias. Bittersweet (Limbing Bittersweet, Waxwork, Shrubby Bittersweet, False Bittersweet, Climbing Bittersweet and American Bittersweet) contains euonymin and sesquiterpene alkaloids. Ingestion of Bittersweet can result in weakness, convulsions and severe gastroenteritis (inflammation of the stomach and intestines).

Over eighty species of Larkspur can be found in North America, most west of the Mississippi River, but are cultivated as an ornamental almost everywhere. In nature the dwarf or low Larkspurs live on lowland slopes and grasslands and are generally less than three feet tall. Tall Larkspurs can grow to four to six feet and are usually found on upper slopes of mountain locations. These plants contain diterpene alkaloids and are more toxic to horses than other species. However horses will no usually consume these plants unless drought conditions exist and there is little else to eat. Dogs and cats have been poisoned from these plants but it is a rare occurrence. As the plant matures it is usually less toxic. Ingestion can result in neuromuscular paralysis along with gastroenteritis, muscle tremors, stiffness, weakness, and convulsions. Animals can die from either cardiac or respiratory arrest.

Ragwort (Golden Ragwort) contains pyrrolizidine alkaloids. It is not palatable but again can be a problem for animals that graze during drought conditions. Dogs and cats will usually not bother this plant, but there are some strange pets out there and poisonings have been reported. Ingestion causes liver failure, and many neurological problems associated with liver failure.

Periwinkle (Running Myrtle, Vinca) contain vinca alkaloids. Ingestion of this plant results in gastroenteritis and depression with moderate intake, tremors, seizures, coma and death if large quantities are consumed. The Lobelia (Cardinal Flower, Indian Pink) contains the alkaloid lobeline. Animals that ingest this plant can develop gastroenteritis, depression and abdominal pain. Large quantities can result in cardiac arrhythmias.

Ambrosia Mexicana (Jerusalem Oak, Feather Geranium) and Bittersweet (American Bittersweet, Waxwork, Shrubby Bittersweet, False Bittersweet, Climbing Bittersweet) may contain euonymin and sesquiterpene alkaloids. Animals ingesting these plants can show signs of gastroenteritis, depression, weakness and convulsions.

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I found my kitten chewing on a houseplant, is this dangerous?

Maybe, the most important aspect of potential poisoning, from any source, is dose. How much was the animal exposed to per pound of body weight? Kittens and puppies will chew on almost anything. Mainly because of their size, young animals are more susceptible to toxic substances. Fortunately, most animals, especially dogs and cats, after a small taste, will avoid eating most dangerous plants. However, we animal lovers know that some dogs will eat anything and even some cats are less than discerning.

Many plants contain toxic substances. On their website, the ASPCA Animal Poison Control Center lists well over 300 potentially toxic plants. I was very surprised to find the names of plants that I recognized and didn’t know were potentially dangerous, others I knew to advise animal owners to avoid.

There are so many potentially poisonous plants I cannot possibly mention all of them in one column, so I have decided to do a series. First, let’s talk about those plants that contain insoluble calcium oxalates. Most of the plants that accumulate calcium oxalate accumulate the insoluble form of the compound. Ingestion of these plants results in irritation of the mucous membranes of the mouth, tongue and lips accompanied by an intense burning sensation. Animals afflicted usually drool excessively and may vomit and have difficulty swallowing.

Most of the Philodendrons accumulate these oxalate crystals including; the Saddle Leaf Philodendron, also known as Horsehead, Cordatum, Heartleaf, Panda Plant, Split Leaf, Fruit Salad Plant, Red Emerald, Red Princess and Fiddle Leaf and the Cut leaf Philodendron also called the Hurricane Plant, Swiss Cheese Plant, Ceriman, Mexican Breadfruit and Window Leaf Plant.

Various Dieffenbachia, contain insoluble calcium oxalates. These include; the Charming Dieffenbachia, Dumb Cane, Giant Dumb Cane, Spotted Dumb Cane, Tropic Snow, Exotica, Exotica Perfection, and the Gold Dieffenbachia.

Many of us have Schefflera growing in our homes. My wife has been nurturing one, and it’s offspring, for more than thirty years. The Schefflera (Umbrella Tree, Australian Ivy Palm), the Octopus Tree and the Star Leaf all contain insoluble calcium oxalates.

A host of plants, all classified in the Araceae family, harbor these substances. These include; the Flamingo flower also known as; Devil’s Ivy, Pothos, Golden Pothos, Taro Vine, Ivy Arum, Marble Queen. Other Araceae are the Caladium, also known as; Elephant Ears, Malanga, Stoplight, Seagull, Mother-in-law Plant, Pink Cloud, Texas Wonder, Angel-Wings, Exposition, Candidum, Fancy-leaved Caladium, and Alocasia. The Flamingo Lily (Tail Flower, Oilcloth Flower, Pigtail Plant, Painter’s Pallet) and various species of Calla including; Calla Lily, Pig Lily, White Arum, Trumpet Lily, Arum Lily, Garden Calla, Black Calla, Solomon’s Lily, Wild Calla, Wild Arum, and the Mauna Loa Peace Lily. This family also includes the Nephthytis (Arrow-Head Vine, Green Gold Nephthytis, African Evergreen and Trileaf Wonder). Arums including; Lord-and-Ladies, Wake Robin, Starch Root, Bobbins and Cuckoo Plant accumulate oxalates.

On some of our area hikes, my now ten-year old granddaughter has shown me Skunk Cabbage (also known as Skunk Weed, Polecat Weed, Meadow Cabbage, Swamp Cabbage). The Chinese Evergreen has insoluble oxalate crystals as do the Greater Ammi (Bishop’s Weed, False Queen Anne’s Lace). Finally, there are over a thousand species and ten thousand hybrid Begonias that can accumulate these crystals, ouch!

It doesn’t end there. Some plants contain soluble rather than insoluble calcium oxalates. Ingestion of these plants can result in excessive salivation, tremors and even kidney failure. Plants with the soluble calcium oxalates found in their leaves include; Rhubarb (Pie Plant), Sorrel (Dock) and Moss Rose (Wild Portulaca, Rock Moss, Purslane, Pigweed, Pusley). Don’t let your pet munch on the leaves of these plants.

If you believe your pet has been grazing on any of the plants described please take the animal to your veterinarian and bring along a sample of the plant for identification.

I’m far from done. In follow-up columns, I will let you know about plants that contain saponins, alkaloids, glycosides, volatile oils, deadly ricin, and at least thirty other toxic substances. It’s a scary world we live in and it’s not just the politicians.

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