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Posts Tagged ‘Cats’

First let’s talk about the thyroid gland. Dogs and cats have a divided thyroid gland located on either side of the trachea just below the larynx. Humans usually have just one gland more or less the shape of a butterfly. Some individual humans, dogs and cats can have ancillary thyroid tissue, usually small amounts, located along the trachea and airways. These are termed ectopic thyroid tissue and in some cases can maintain thyroid function if it is necessary to remove the thyroid gland surgically.

 

The thyroid gland is responsible for, or plays an important role in, many normal body functions. These include the regulation of body temperature, metabolism of fats and carbohydrates, weight control (both loss and gain), heart rate and cardiac output, normal function of the nervous system, growth and brain development in young animals, reproduction, muscle tone, and the condition of the skin and hair. So if the thyroid gland is not functioning normally we can expect changes in these functions and those changes result in symptoms or signs of the disease.

 

Thyroid disease is manifest as either low or absent thyroid activity (hypothyroidism) or excess thyroid activity (hyperthyroidism).

 

Signs of hypothyroidism include; weight gain, lethargy, generalized weakness, mental dullness, alopecia (loss of hair that can be generalized or in spots), excessive shedding, poor new hair growth, dry and/or dull hair coat, excessive scaling of the skin, recurring skin infections, and the inability to tolerate cold. In rare cases the animal may have seizures, a head tilt and infertility.

 

Signs of hyperthyroidism are, as one might expect, the opposite. There is a generalized increase in metabolism resulting in loss of weight despite an increased appetite. There is a general unkempt appearance and poor body condition. The animal may vomit and have diarrhea and frequently will be seen drinking water. This results in increased urine production. Some animals will have difficulty breathing and compensate with rapid shallow breathing. There is usually a rapid heart rate sometimes accompanied by so-called “gallop rhythm” a type of abnormal beat. The animals are usually hyperactive, and often the thyroid gland is enlarged.

 

Hypothyroidism is most common in middle-aged medium to large breeds of dogs. The condition is rare in cats. It is more commonly found in middle-aged dogs four to ten years of age. Anecdotal evidence seems to indicate that neutered males and females are at higher risk than intact animals. This condition is most commonly the result of inflammation of the thyroid gland or a decrease in active thyroid tissue from unknown cause(s). The condition can also occur as a result of treatment with the sulfa drug trimethoprim-sulfamethoxazole. In very rare cases iodine deficiency in dogs can result in hypothyroidism but commercially prepared dog and cat foods all contain adequate levels of iodine. The treatment for this condition is replacement therapy with levothyroxine or another type of thyroid replacement.

 

The diagnosis of hypothyroidism usually requires laboratory testing that includes a complete blood count, biochemistry profile, and urinalysis. Your veterinarian may be able to make an initial diagnosis based on the results of these tests, but it might be necessary to measure the levels of T3 and T4 and other endocrine lab tests. Your veterinarian may also recommend X-ray studies to check for other associated abnormalities.

 

Hyperthyroidism is the result of overproduction of thyroxin by the thyroid gland usually the result of a thyroid gland tumor. It can also be an aftermath of inappropriate overmedication for hypothyroidism. It is rare in dogs but can occur. It is most commonly diagnosed in older cats usually about thirteen years old or older. Less than five percent of cats with hyperthyroidism are under ten years of age. In addition to a thyroid tumor hyperthyroidism can also be the result of congenital disease, iodine deficiency or the result of inappropriate therapy. Sometimes it is impossible to identify the cause.

 

The diagnosis of hyperthyroidism is often initiated by palpation of an enlarge thyroid gland during a physical exam and documentation of clinical signs suggesting this disease. This will usually lead your veterinarian to measure a thyroid profile that includes T3, T4, Free T4 and TSH in the blood. If the T4 is higher than normal the diagnosis is confirmed however some early cases demonstrate T4 and the other hormone levels in the normal range. The performance of a T3 suppression test might be indicated and can produce a diagnosis. If the T3 suppression test results are still equivocal and if hyperthyroidism is still suspected further tests including nuclear isotope imaging may be necessary to arrive at a diagnosis.

 

There are three types of treatment for hyperthyroidism; life long oral anti-thyroid medications, surgical removal of affected thyroid glands and treatment with radioactive iodine. Tapazole (methimazole) is a specific anti-thyroid medication. This is a treatment that must be continued for the rest of the life of the animal unless surgical removal or radioactive iodine removal are indicated. Sometimes Tapazole treatment is used prior to surgery or radioactive iodine therapy to reduce thyroid hormone levels into the normal range to reduce the risk of surgery or radioactive isotope therapy. It is also indicated when the animal has congestive heart failure resulting from the hyperactive thyroid. Side effects from Tapazole include depression, vomiting, appetite loss and more seriously blood abnormalities. If surgical removal is the choice of therapy the surgeon must be very careful to avoid damage to the parathyroid glands. Removal or injury to these glands will result in significant problems.

 

As always if you suspect your animal has thyroid disease consult your veterinarian.

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Patent Ductus Arteriosus, also known as PDA, is a congenital heart defect that can be found in any breed or species of animal including humans. When I graduated from veterinary school in 1960 we were taught about this condition but very few, if any, veterinarians were prepared to do thoracic surgery to attempt a correction.

One of the most helpful things I learned, after graduating from veterinary school, was that most clients wouldn’t talk to me when I had a stethoscope in my ears. It was a perfect time to think about what I had observed and how to communicate with the client.

While I was in school Dr. Smith lectured to our class about heart murmurs, including the continuous murmur associated with a PDA. I remember him standing at the lectern making a very particular noise, mimicking this murmur. The sound was “whoosh, whoosh, whoosh, whoosh.” I never heard the murmur in an animal while still in school but the first time I did hear the murmur it sounded exactly like the noise Dr. Smith made while leaning into the microphone in the lecture hall. The condition can also be detected by feeling the animal’s pulse detecting what is described as a water -hammer or continuous pulse.

When trying to explain this condition to a client, or to students while I’m teaching, I resort to a sketch where I draw a rough outline of the heart with the aorta coming off the left ventricle and supplying the body with arterialized blood and the pulmonary artery coming off the right ventricle going to the lungs so carbon dioxide can be expelled from the blood and oxygen taken on.

Before any mammal is born the lungs haven’t inflated yet, the fetus doesn’t need blood to go the lungs. There’s an opening between the pulmonary artery and the aorta so the blood can cross over into the aorta because until the lungs are inflated the pressure in the pulmonary artery is higher than the pressure in the aorta. The blood crosses over through a structure called the ductus arteriosus.

As soon as the newborn takes a couple of breaths the alveoli, the little air sacs in the lungs, open and the blood vessels that surround each alveolus also open. The resistance to blood flow into the lungs is reduced and the blood pressure in the pulmonary artery drops below the blood pressure in the aorta. This causes the aortic side of the ductus arteriosus to close since the ductus is more of a slit than a tube. So normally the ductus closes shortly after the animal starts breathing. Unfortunately sometimes, for reasons not yet completely understood, the ductus stays open. When that happens, it’s called a patent ductus arteriosus. Since the pressure in the aorta is higher than the pressure in the pulmonary artery, the blood leaks continuously through the opening. With each heartbeat, the pressure increases in the aorta and that causes the leak to be greater.

When we listen to the heart of a normal animal it makes a noise that sounds like; lub dub . . . lub dub . . . lub dub.” A continuous murmur makes the whoosh, whoosh, whoosh sound as the pressure and blood flow into the pulmonary artery increase with each beat while the blood flows continuously surging with the beating heart.

The defect causes both the left and right sides of the heart to work harder and harder. The heart enlarges and finally it fails. Since my time in practice veterinary medicine has made enormous advances. We now have board certified veterinary surgeons capable of performing the relatively simple surgery to tie off the patent ductus. We also have board certified veterinary cardiologists who, if they make the diagnosis early enough, can use a catheter system to deliver a plug to the ductus and correct the problem without surgery. The key to a successful outcome is early diagnosis before the animal goes into heart failure and that means a thorough physical examination by your veterinarian for your new pet while it is still young.

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I am running this post again because too many people seem to be searching for a way to kill their neighbor’s dog or cat. Since it was originally posted on Jan. 31, 2012 this post receives the most hits almost every day and many reach it by searching, “how to kill an animal with antifreeze” or similar queries. Find information here about how to save your pet if it drinks antifreeze.

This is one of the most common forms of poisoning seen in dogs and cats. It usually happens when the antifreeze drips from your vehicle’s radiator forming a puddle on the garage floor or driveway. The active ingredient in antifreeze is ethylene glycol a syrupy liquid that seems almost addictive to some pets. You must take special care if you change your antifreeze yourself, since pets can get into containers left open or spilled. It is possible for a cat to poison itself by walking through a puddle then licking its paws. As little as five tablespoons of commercial antifreeze is enough to kill a medium sized dog. If you see or suspect your pet has ingested antifreeze you should make it vomit, by giving it a teaspoonful of hydrogen peroxide per five pounds of body weight, but not more than three teaspoonfuls at a time. If it vomits or not, take it to your veterinarian as quickly as possible and explain what you think has happened. If your pet has already vomited, do not try to make it vomit more. Do not try to induce vomiting if the pet is showing signs of distress, shock, difficult breathing or is unconscious.

Ethylene glycol is also an ingredient in some liquid rust-inhibitors, incorporated in solar collectors, used in many chemical manufacturing processes and can be found in a variety of household products. Check the labels! To be most effective, your veterinarian must administer treatment within three to eight hours. Ethylene glycol is actually an alcohol converted, by enzymes in the liver, particularly alcohol dehydrogenase, into oxalic acid. The oxalic acid combines with calcium in the blood to form calcium oxalate crystals that block the nephrons in the kidneys and result in kidney failure.

Since ethylene glycol is an alcohol, the early signs of poisoning resemble drunkenness; euphoria and/or delirium, wobbly gait, uncoordinated movements, nausea as evidenced by excessive salivation, lip smacking, dry heaving, and vomiting. This phase can persist for about six hours and the animal may appear to be better, not so! If untreated the signs progress to excessive urination, diarrhea, rapid heart rate, depression, weakness and eventually into fainting, tremors, convulsive seizures, and coma, all signs of kidney failure.

If you arrive at the animal hospital in time and give a history of your pet ingesting antifreeze, or your veterinarian runs appropriate tests and makes the diagnosis, before signs of kidney failure occur, there is a good chance your pet will be saved. Treatment involves the induction of vomiting. Using activated charcoal to bind any ethylene glycol still in the digestive tract is not effective, but may be indicated when other toxins are suspected. Since 1996, your veterinarian has had access to fomepizole (Antizol-Vet). This drug is an effective antidote, if administered intravenously before kidney damage occurs. Back in the olden days, we used grain alcohol as an antidote, significantly less expensive than fomepizole. Alcohol dehydrogenase has about 100 times the affinity for grain alcohol than it does for ethylene glycol. When used as an antidote the liver metabolizes less ethylene glycol and fewer oxalate crystals form. Depending upon the severity of kidney damage it still might be possible to save your pet with aggressive fluid therapy to flush the kidneys, and other supportive treatment. Some specialty practices may be equipped to provide kidney (renal) dialysis. You do not want to know how much a kidney transplant will cost, but it is possible, in both dogs and cats, in specialized centers with the necessary equipment and experience.

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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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Sidney, Montana, the summer of 1960. Ike Williams and Jon Wilkins were partners, the owners of Williams & Wilkins Blacksmiths and Mechanics. Their shop was large, chaotic and dirty. It occupied the entire frontage of their property hiding their small, immaculate, frame house. The shop and their considerable skills shielded them from the necessity of acknowledging their relationship, something the community had no real need or desire to hear or talk about. The partners were able to repair and, if necessary, fabricate parts for any type of motorized or pulled agricultural implement. That was what the community considered important. They had lived and worked together in Sidney for twenty-five years before my new bride and I arrived. I was a recent graduate and new associate veterinarian in the only veterinary practice within a fifty-mile radius.

Like an old married couple Ike and Jon finished each other’s thoughts, knew how to avoid conflict, were comfortable in their own skins, and with each other. All necessary accommodations had been made.

They both loved cats. I was never able to determine exactly, or even approximately, how many cats they had. There were shop cats, outside cats and house cats, all well cared for.

From time to time one or both of them would bring in a house or shop male for castration or a female to be spayed. All received annual vaccinations. I guess they had a method for deciding which cats would occupy which spaces. The outside cats were free to reproduce but each new litter of kittens was brought in for vaccinations and caring homes were found for them.

They were both sitting in the waiting room when I returned from doing rectal exams on twenty-five head of half-wild range cattle to check for pregnancy. I rubbed my sore left arm as I greeted them.

“Mr. Williams, Mr. Wilkins, what have you got for me today?”

They stood up as if joined at the hip. Wilkins held a huge tabby in his arms. The cat was whimpering obviously hurting.

“This is Wilma, she’s a house cat. Old Doc spayed her for us several years ago and she’s had all her shots every year. Today when we came in for lunch we found her, crying in pain. She’s paralyzed.”

As he talked tears welled up in Wilkins’ eyes. Ike put his arm over his partner’s shoulders.

“It will be OK Jon. Young Doc is good everyone says so. He’ll take care of Wilma for us, won’t you Doc?”

I held out my hands.

“Here, let me take her. Let’s go into the exam room and see what we can figure out.”

Wilma was too soft, too fat, and too lazy. Both hind limbs were flaccid. She meowed louder with Jon no longer holding her. She was also hyperventilating. I examined her carefully, noting that the white nails on her hind paws were tinged blue and the paws were cold to the touch. I was unable to palpate a pulse in either femoral artery.

“This is not good,” I told them. “I’m pretty certain she has what we call a saddle thrombus. It’s a blood clot blocking the two main arteries to her legs. I’ve never seen a case but I remember the description from vet school. All the signs are there. She is paralyzed in the hind legs, in obvious pain and there is no blood circulating to her hind legs.”

“Is there something you can do to fix her?” asked Ike.

“Well, theoretically I could operate and remove the clot. However, I’ve never done anything even remotely like that before, never actually opened an artery on purpose then tried to suture it closed afterwards. I don’t think we even have any suture material small enough to do that kind of thing. Also we have no idea what causes this and it could come right back. I’m sorry. I hate to say this. My job is to help animals not kill them. In this case I think the best thing I can do to help Wilma is to put her out of her misery.”

They were devastated.

“Are you sure you don’t want to even try?” pleaded Jon. “Cost is not a problem you know. We’ll pay whatever it costs,” he looked to his partner for confirmation. Ike nodded his agreement.

“OK, I’m willing to try anything, but I have to make certain you know this could be a disaster. I’ve never even seen anything like this done. First let me look to see if we have any suture material small enough to close an artery.”

I was apprehensive as I searched through the cabinet of surgical supplies. I found one packet of 4-0 silk, with needle attached. It looked to be several years old. I had no idea where it came from or for what my boss intended for it when he bought it. I came back into the exam room and held up the packet.

“This might work, but it’s old and I’ll need to sterilize it again, I have no idea how long it’s been around, the package says it expired two years ago. You guys are certain you want me to try this? I don’t really know what I’m doing. I’ll have to dissect down to the end of the aorta, that’s the main artery coming from the heart, where it branches to supply blood to both hind legs and the tail. Then I have to find the blockage, try to put a tourniquet around the artery above the obstruction, open the artery, remove the clot and suture the artery closed. Chances are very good Wilma will bleed to death while I’m fumbling around.”

“But she’ll be anesthetized, right Doc? She won’t feel anything? Ike asked.

“That’s correct,” I said. “As soon as I anesthetize her she’ll feel no more pain, until and unless we remove the clot and get everything repaired and let her wake up again. She could still be in a lot of pain after I’m done with the surgery, I don’t know.”

“But you can give her something for post-operative pain, right?” Jon pleaded.

“Sure, sure, we can treat post-op pain.”

“OK Doc. Go for it. Is it OK if we wait here? We already put a sign on the shop door saying we wouldn’t be back until tomorrow.”

“Sure, you’re welcome to wait here. It will take me some time to put a surgical pack together to sterilize with the suture material. I have to think about what I might need by way of instruments. I know we don’t have any specialized vascular surgical instruments or suction so I’ll have to improvise. I’ll let you know before I get started. Let me give her just a touch of tranquilizer to see if we can make her more comfortable. I’m afraid to give her anything like a full dose because her heart rate is so fast. The tranquilizer will slow her heart rate and the high heart rate may be the only thing keeping her alive.”

I got Wilma anesthetized, hooked up an intravenous drip, opened up her abdomen, packed off her abdominal organs and found the distal aorta. When I tried to dissect around the aorta I managed to break off some small branches and the abdomen quickly filled with arterial blood. The turkey baster I added to the pack was not an adequate suction device and Wilma bled out in short order. It was the unmitigated disaster I had feared.

Today we know that saddle thrombus is almost always associated with a disease called dilated cardiomyopathy. This is a condition, probably with genetic predisposition, that is uncommon but not rare in cats. The heart is enlarged and dilated and it doesn’t function properly. Normally blood is always moving inside the heart. This constant motion of the blood, even when the heart is resting between beats, helps prevent clots from forming. Because the heart is dilated and unable to beat strong enough areas of flow stasis develop within the heart chambers. Areas of flow stasis allow clots to develop. When the clot becomes large enough it is eventually washed out of the heart. It flows downstream until it lodges at a location too small for the size of the clot, usually at the terminal trifurcation of the aorta. Modern veterinary surgeons can deal with this, providing the underlying heart disease is treatable. Today, if diagnosed early enough and if the underlying heart disease is controlled, many of these animals can be saved and will go on to live a reasonably normal life. In 1960 my saving Wilma would have been a miracle.

Ike and Jon understood and were even appreciative that I tried.

I felt guilty and depressed, never acclimated to losing an animal, especially through my own clumsiness.

Excerpt from “Animals Don’t Blush”

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