When you get blood work back on a pet (Cat), it’s about nine years old and it shows kidney failure it’s not always clear what’s going on. There’s another test or two that you’d run on a dog and there are some tests you could run on a cat. Actually, there are ways to spend thousands. Or, treat the treatable? Give this a listen.
The above does not constitute advice or replace the necessary input of your regular veterinarian within the confines of a VCPR. The above is as much a ‘document’ for the benefit of a particular client I sent to this, as it is to others who may face the same situation.
Overweight cats chew the air, or anything in reach, when you scratch the top of their tail.
Heavy cats will sometimes chew the air or anything they can reach when they can’t get to it themselves. Heavy cats can’t bend around far enough to really sink their teeth into the itchiness of their own rump – so the ‘tail-scritch-air-biting-thing’ appears to be a reflex, a ‘release’ of pent-up chewing that they’d RATHER be doing to their own tailhead (top-base-of-tail) but simply, mechanically can’t.
It can be a BIG liability if someone is petting the head-end of the cat while someone else scritches the tailhead.
Further, some people worry that the cat is in PAIN – clients mention “We thought she had arthritis and it was tender” as the reason she bites when touched there.
The cat’s not angry, or in pain when it does this. It’s supposedly part-pleasure, part frustration.
Is there some kind of treatment?
Well, kind of. Weight loss can help a cat “get around to its own butt” and that’s nice. But weight loss in cats MUST BE SLOW because their liver can be ruined (fatty infiltration) with rapid weight loss. So you kind of get stuck limiting AMOUNTS of food but never really letting the cat “not eat”. I don’t even recommend changing foods in case the cat ‘goes off feed’ and contracts “hepatic lipidosis”.
Usually cutting back a tablespoon or two a day will exert some slow weight loss.
If the cat is pruritic, (itchy) then correcting the causes and condition of “itchiness” will reduce the impact of the rump-scratch. I sometimes like cortisones for this, but since those may trigger diabetes in a vast minority of cats, it should be weighed against the risks.
The use of glargine for the control of diabetes in cats
A lot of the following is irrelevant at this point, because Lantus has become quite expensive. I recall a day recently when it was as little as $100 – $110 a bottle. Manufacturers now are leveraging the absolute necessity of insulin and raising prices drastically. I am using very little if any Lantus with my patients, even though it is a superior insulin.
Here are some Lantus / Glargine notes from practice:
Firstly, I would not use Lantus and a cat that is being regulated from a condition of some instability. When they’re freshly diagnosed and only then being reigned in. It is not going to drastically or quickly lower the glucose levels and if the pet is a diabetic keto acidosis case, you probably should be using a faster insulin.
I have had good success mixing a regular and NPH insulin together for fast andslow effect during the initial phase of stabilizing the patient.
In pets that are not decompensated, their hydration status is decent and their blood sugars are under 400, I don’t feel an urgent need for instant control and I will happily use Lantus in those cats. Twice a day dosing.
What I like about Glargine, or Lantus and cats is that it’s onset of action is mild and it seems to stay up a bit longer than other insulins, in other words the blood sugars have a tendency to be more stable for a longer period of time.
It is interesting to note that almost 30% of cats being given Lantus will convert to non-diabetic status if only temporarily, requiring less and less insulin until they are in no need of insulin at all.
In practice, I have seen that to be extremely rare in cats that are getting a Humulin or NPH insulin.
It is not enough of a “selling point“ to recommend Lantus at its considerable expense. I mean the “outside chance“ that the cat will convert to non-diabetic status.
I have seen approximately the same incidence of insulin resistance develop against Lantus as I have the other available insulins.
I am prone to a deviation from the normal recommendation as far as insulin: It is commonly recommended that you would give your insulin shot and then feed. That way the insulin is in the system as the blood glucose comes up postprandially. I’m not crazy about this because if the cat decides not to eat after you’ve given the shot, you’ve made quite a commitment haven’t you?
So my advice to owners is to give the cat it’s food and almost as soon as it is done eating to go ahead and give the insulin shot. Under those circumstances there is always insulin on board for the food it has just eaten, but there is never insulin on board if the cat has not eaten. Problem solved.
If a cat does not eat, it gets half dose insulin. If the cat does not eat yet again (it’s evening meal for example), then it would get no insulin and the office should be consulted.
What you should know about lesions on the feet of dogs, especially surgical lesions. This is a post operative letter.
You’re getting this document because your dog has some sort of lesion on its foot. That could be a tumor, laceration or any kind of surgery.
Canine Foot Lesions: The Bandaged Dog
There are certain things, that just happen, every single time there are stitches in a dogs foot.
It doesn’t matter who your veterinarian is or what you do, it’s just the way it goes:
Number one: Stitches fall out
Face it, the dog is basically walking on it suture line and that kind of stretching and tearing is going to put a lot of pressure on the stitches and sooner or later, one or two of the stitches will pop. When that happens, a little bit of scar tissue fills in the gap which represents decent healing, but it does extend healing time past the normal seven or eight days it normally would take to heal.
Consider that every step the dog takes is pulling on the stitches, so the fewer steps it can take the longer the stitches will hold. But, some will pop. It is unavoidable.
Number two: Inflammation and Discharge Always Occur.
Again, the dog is walking on a surgery site and every step pushes and pulls on the line and keeps healing from occurring as quickly as other places. Discharges accumulate and at first, that requires frequent bandage changes to keep those secretions from setting up infections.
Number three: Bandages are pretty important.
At first, postoperatively, you will probably be coming to the office every day or every other day for bandage changes. That is dependent upon the estimated amount of discharges in the bandage that need to be removed. It is imperative that you keep the bandages changed according to plan, I appreciate that it is labor and time intensive, but that is the nature of lesions on the foot.
Number four: Abnormal tissues heal abnormally.
One of my reviews on Google hold that I did a poor surgery on the dogs foot because the surgery did not heal normally.
I would say that is a failure on my part to explain to the client when you remove cancer from tissues and you expect cancerous tissues to heal back normally, that is often a fail.
Of course when you go in you don’t know that you’re necessarily removing the cancer until later. So, when you are dealing with abnormal tissues, healing will often occur abnormally, whether that is delayed, weird looking, or painfully slow. A cut made by some glass in normal tissue heals a lot faster than a cut made surgically in cancerous tissue. That’s all I’m trying to get across.
Canine Foot Lesions: The Bandaged Dog
The summary of this article occurs in five points
Number one. Stitches always pop.
Number two. Discharges always occur.
Number three. Bandages require changes; sometimes frequently.
Number four. Abnormal tissues heal abnormally.
Number five. Every step the dog takes compromises the foot lesion, the fewer steps it takes, the longer the bandage and the stitches will last.
Metronidazole may be recommended along with dietary modification as the first medical therapy. Metronidazole has antibiotic, anti-inflammatory, and antiprotozoal properties, and is usually fairly well tolerated, although some cats may lose their appetite when given this drug.
If dietary modification or metronidazole are not effective, corticosteroids, which are potent anti-inflammatory and immune-suppressing agents, may be recommended, either alone or in combination with metronidazole. Cats should be monitored closely while they are on corticosteroids, as diabetes and immune suppression are among their potential side effects. Nonetheless, cats tend to tolerate these drugs well as long as they receive them at an appropriate dose.
Cats usually take corticosteroids orally, starting with a higher dose that is gradually reduced over several weeks. In cats that won’t take medication orally, or in cases in which vomiting is severe, your veterinarian may give the medications as an injection.
If none of these medications successfully controls the symptoms of IBD, more potent immunosuppressive drugs, such as chlorambucil or azathioprine, may be necessary. These drugs can suppress production of white blood cells, red blood cells, and, less commonly, platelets, in the bone marrow. A veterinarian must carefully monitor cats taking these drugs.
Inflammatory Bowel Disease ( IBD ) – Feline
As GI bacteria may play a role in the development of IBD, newer therapies include prebiotics, which are substances that promote certain bacterial populations, and probiotics, which are bacterial strains that promote GI health. The addition of soluble fiber, such as psyllium, to the diets of cats with inflammatory colitis may be helpful, and supplementation with folate or vitamin B12 should be provided if an affected cat is deficient in these B vitamins.
I’ve always liked Sulfasalazine for IBD in the past, wondered about its use in cats: Found this quality literature.
You have to scroll past the cut and paste Bull that the online pharmacies trot out as “fact” – which is often paraphrased by non-English speakers.
Sulfasalazine is considered by many veterinarians to be the preferred drug in dogs for treatment of colitis. The recommended oral dosage in dogs is 12.5 mg/kg q8h up to a maximum of one gram q8h in refractory dogs or those having severe IBD. It is important to continue initial therapy with sulfasalazine for a minimum of four weeks before modifying drug dosage. With resolution of signs, sulfasalazine dosage is gradually decreased by 25 percent at two-week intervals and eventually discontinued while maintaining the dietary management. Caution is advised in using sulfasalazine in cats because of their sensitivity to salicylates. Other oral medications of potential use in dogs include olsalazine and mesa-lamine. Olsalazine (Dipentum) consists of two molecules of mesalamine linked by an azo bond. The enteric-coated products of mesalamine (Pentasa and Asacol) release the active drug in the distal small intestine and colon, respectively. The use of olsalazine or mesalamine for treatment of IBD in dogs and cats has not been critically evaluated, but there are substantial anecdotal reports of their efficacy. The proposed dosage is about one-half that of sulfasalazine.
25 – 50 mg every 12 hours = Cat dose up to 12-14 pounds.
Interesting information has shown up (a little ‘fringe-y) that suggests that altering (spay, neuter) pets robs them of sex-hormones (testosterone, estrogens) that maintain their vitality into later years. Without those hormones, and after they pass the age of 9+ years, the odds of contracting cancer can increase up to four times. (Specific cancer, specific age range, specific gender, but still…)
Simplified: If you don’t spay or neuter your dog or cat, there’s a 8-12% chance of cancer in the reproductive / mammary tissues later in life. If you *DO* spay or neuter your dog or cat, there’s an 8-12% chance of cancer in the spleen or other organs. Sort of sounds like a dog has an 8-12% chance of cancer when they get old, right? Well, it’s just interesting that intact dogs don’t usually get spleen cancers.
Another study suggests that intact dogs are more ‘confident’ and less prone to anxiety*. This work was done as a Masters-thesis paper at Hunter College which is a decent college in New York, but the students were pretty much just dry-labbing a ‘paper’. No dogs were met, no exams were done. No experience was brought to bear, or gained. So I don’t hold a TON of stock in that paper. The statistical work was good, but they didn’t qualify what “Aggression” or “Anxiety” were, or how that was elicited. The paper was accepted but not professionally reviewed.
*The down side to ‘intact-ness’ is that there’s a flip-side anxiety and prevailing ‘distractedness’ about ‘finding a mate’ that drives owners crazy so it’s a “no win” situation, right?
Following up on the belief that spay and neuter may potentiate cancer in older altered dogs, I dug up almost-ten studies that DO SHOW that spay or neuter increases the odds of the dogs getting cancer.
Other studies confound this. A study done in Michigan at a Veterinary College. (The influence of castration on the development of prostatic carcinoma in the dog. 43 cases (1978-1985). Obradovich J1, Walshaw R, Goullaud E.)
Avoid The Spay or Neuter to Avoid Cancer?
No study showed that de-sexing CAUSES cancer in any form – but, (perhaps by weakening part of the immune system) some dogs (legitimately) were up to 4x more likely to get certain kinds of cancer than intact ones. (Spayed females and Hemangiosarcoma, for example)
Taking it “to the next level” I skimmed the abstracts and conclusions of about a hundred papers. While the statistics don’t speak to a national emergency or even a ‘prevalent’ problem, the papers are incontrovertible that even if you wanted to discount the research from one paper, you can’t discredit all of the data.
So, in some cases the results could be tabulated in “how you look at it.” and it depends on what you’re trying to convince people of.
HOWEVER, (and this is a BIG HOWEVER) the @ tenstudies that DID relate to spay, neuter and cancer, and ACTUALLY showed increased risk of cancer in the de-sexed dogs!!
So what I’m saying is, that Snowflake Vets incriminating de-sexing surgery for cancer in later life, have a valid point.
But here’s the thing: Let’s say the odds of cancer ARE increased in de-sexed dogs?
What then? Does ANYONE actually think a person would keep a male dog around that was peeing everywhere and squaring off with people and other dogs? Running off every time the neighbor dog went into heat?*
Does anyone actually believe an owner would keep a female around going through false pregnancies and bleeding on the furniture, struggling to get out the door when she’s in heat, and drawing dogs into the yard for blocks, and waxing all possessive-aggressive about bowls, closets and beds?*
*All of the above still happens, even with hormone-sparing sterilization procedures like vasectomy, hysterectomy and tubal ligations.
I don’t believe EVEN FOR ONE SECOND that aggression and anxiety are higher in de-sexed dogs. Thatpart of the Hunter College study was done by inexperienced non-vets and didn’t even discuss what aggression and anxiety looked like. Nothing in that part of the study coincided with the realitywe see in the exam room. And to me, that’s a BIG problem. I have to dismiss those findings out-of-hand because the common realityis wholly unmatched by their paper.
I am legitimately concerned that there are credible papers that support that spay and neuter are actually and palpably associated with an increase in vulnerability to cancer, and that seems to be borne out in the work done by Jeffrey Nyce, whom I hold in high regard. He is the researcher I talk about all the time, who suggests that hyper-supplementation of DHEA will replace the lost “anti-cancer” impacts of de-sexing dogs.
The Only Three Things I Know Absolutely, Without Exception:
Intact male dogs are usually oppositional-defiant, prone to roam, and urine-markers.
Intact male dogs smell unpleasant
Intact female dogs are bi-annually messy, prone to roam and attract males, and many do eventually get malignant breast cancer.
I know from a TON of experience that when any “intact” male dog comes in, he’s 95% sure to tense up, and ‘square off’ with everyone in the waiting room, pee in 5-6 places around said waiting room, and get his hackles up, and get ‘stink-eye’ when I walk into the room. VERY rarely seen an exception to that one. Keep in mind, as a professional, I can deal with that. But on the ‘day-to-day’, can the owner?
I know for a fact that ALL intact male dogs I have ever seen have consequential amounts of ‘smegma‘ (mild, persistent balanoposthitis) and smell metallic, and ‘male’.
And I know that when someone comes in with an older female dog with lumps in the breast line, and it’s intact, those are going to be malignancies with a poor prognosis without exception. And that spayed female dogs have never come in, not ever since 1991 with breastline malignancies (But they often have hyperplasia).
It’s true that pyometra can only happen in intact female dogs but that doesn’t make it COMMON. Fact is, I’ve often thought that pyometra wasn’t a compelling reason for spay. Breast cancer is, though. Regardless of the “studies”.
So, I said all of the above to say this:
I think that 99% of clients won’t avoid spay or neuter, because it will leave their pets ‘difficult’ and ‘smelly’ and bleeding on their furniture so that they can avoid a less-than-13% chance of certain cancers after the age of 9 or 10.
I think that TONS of dogs are anxious and aggressive now, NOT because of de-sexing, but because our culture has abandoned ‘dominance’ as an owner quality and has adopted emotional ‘negotiation’ and ‘counseling’ and ‘therapy’ to accommodate dangerous or defiant pets.
Finally, to the concept of hysterectomy and vasectomy of the dogs in order to spare their hormonal integrity, which is increasingly popular among a variety of Veterinary “Snowflake” – – again, identically to Raw Diet – which is another thing I endorse and have seen the merits of:
Clients don’t like BLOOD and mess. They’re not going to have dogs peeing and bleeding in their houses!
The fact that normal clients don’t want to deal with raw chicken, or bloody diapers isn’t surprising. That America is still spaying and neutering despite these percentages is not even substantially a reflection on the veterinary profession, but instead a realistic expectation on the part of a prospective pet owner.
PS: To close this document, let me say that I’ve vasectomized companion animals before and it’s not hard at all. Same with tubal ligation and or hysterectomy. No worse than a regular spay or neuter. A bit more time consuming, but whatever. No big deal.
So if, after consideration of the above, a client is okay with intact-ness in a male or female dog around the house, I acknowledge the myriad minor but undeniable health advantages of NOT desexing the dogs and cats. And I’d be glad to perform those alternative, hormone-sparing procedures as long as the clients ‘get it’ that the pets will still act like distracted, overwrought teenagers, and pee and bleed on stuff.
I’ll take it a step further: So far, (My position is subject to change) I’ve decided NOTto Spay Luna Boona. And the only reason is, that I’ve seen too many elderly dogs “live too long” and get all crippled, blind and deaf.
That just doesn’t happen to un-spayed females. Un-spayed females tend to live healthier, but shorter lives.
I know from experience that if I don’t spay Luna, then (about three years before she’s crippled, blind and deaf), she’ll show up with malignant breast cancer, a pyometra or a blood dyscrasia, and I’ll be within my ethical rights to put her down. I think to myself: What will she (and her humans) have actually missed by her so-called “early” demise at 12 instead of 15?
So you can see that all of the above is uhhhhh…. sticky. I maintain that there is no need for anti-spay-neuter proponents to demonize the veterinary community for doing what’s been expected of them, asked of them by owners, and traditional for them to do for overpopulation-control advocates. And the fact that more owners aren’t suspending spay or neuter is LESS about ‘evil’ ‘ignorant’ or ‘money-grubbing’ veterinarians*, than it is about what kind of mess-and-drama an owner is (understandably) UNWILLING to put up with at home!
*There are retired human dentists who say so.
The following are a smattering of references which require no ‘imagination’ to see that when we neuter male and female dogs we weaken them a little. We make them a little more vulnerable to cancer, we make their bones a little weaker, their joints a little weaker, their hormonal axes (balances) a little less stable.
In a nutshell, altered male and female dogs are a little LESS VIBRANT in most measurable parameters. It’s (metabolically) like we’ve aged them 3 to 4 years all at once. Interestingly, my clinical experience supports that 95+% of spayed and neutered dogs live JUST AS LONG as the intact ones. Only, they spend that time just “A Little Not-As-Strong” as intact ones.
I believe 100% that we don’t have to replace bio-identical hormones to conserve a dog’s health into later years. Affordable dosing with DHEA from Amazon is sufficient according to some of the most advanced thinkers in that area. (Dr Jeffrey Nyce)
One GOOD thing from the studies that show spay and neuter may have a weakening effect on dogs against various aging factors – is the rate of later-age surrender of dogs drops DRAMATICALLY in altered pets. In other words, people aren’t euthanizing or giving away altered pets, but they dump plenty of the intact ones.And that makes sense. Intact pets are eventually intolerable, just speaking for myself.
Ajax required neuter at 6 months, to remain a viable companion. But my former Labrador “Bailey” went to TWO YEARS of age before masculine behaviors mandated neuter or ‘giving him away’.
Here are some of the studies that support an increase in vulnerability to cancer in older, de-sexed dogs.
Teske E, Naan EC, van Dijk EM, van Garderen E, Schalken JA. Canine prostate carcinoma: epidemiological evidence of an increased risk in castrated dogs. Mol Cell Endocrinol. 2002 Nov 29;197(1-2)251-5.
Sorenmo KU, Goldschmidt M, Shofer F, Ferrocone J. Immunohistochemical characterization of canine prostatic carcinoma and correlation with castration status and ca
Ru G, Terracini B, Glickman LT. (1998) Host-related risk factors for canine osteosarcoma. Vet J 1998 Jul;156(1):31-9
Cooley DM, Beranek BC, Schlittler DL, Glickman NW, Glickman LT, Waters DJ. Endogenous gonadal hormone exposure and bone sarcoma risk. Cancer Epidemiol Biomarkers Prev. 2002 Nov;11(11):1434-40
Prymak C, McKee LJ, Goldschmidt MH, Glickman LT. Epidemiologic, clinical, pathologic, and prognostic characteristics of splenic hemangiosarcoma and splenic hematoma in dogs: 217 cases (1985). J Am Vet Med Assoc 1988 Sep; 193(6):706-12
Ware WA, Hopper, DL. Cardiac Tumors in Dogs: 1982-1995. J Vet Intern Med 1999;13:95–103.
Torres de la Riva G, Hart BL, Farver TB, Oberbauer AM, Messam LLM, Willits N, et al. (2013) Neutering Dogs: Effects on Joint Disorders and Cancers in Golden Retrievers. PLoS ONE 8(2): e55937. doi:10.1371/journal.pone.0055937
J. Armando Villamil, Carolyn J. Henry, Allen W. Hahn, Jeffrey N. Bryan, Jeff W. Tyler, and Charles W. Caldwell. Hormonal and Sex Impact on the Epidemiology of Canine Lymphoma Journal of Cancer Epidemiology. Volume 2009 (2009), Article ID 591753, 7 pages.
So there was a question on NextDoor about someone who wanted to cultivate a ‘cat colony’ of ferals to control rodent populations. The idea was that ferals and other cats that wouldn’t ‘fit’ in residential homes could at LEAST subsist with basic shots and veterinary care as outdoor cats feeding on rodents, and then whatever the colony volunteers would put out.
Concerns about coyotes and other predators, as well as the difficulties in managing disease and injuries came up in the conversation. Cats running around leaving foot prints on everything and sacking trash cans and groceries in garages as well as predation on bird feeding stations all started fires on the board.
Then the following comprehensive response from a reader which was so good I asked if I could put it up on the website.
So here it is: About Cat Colonies For Rodent Control.
When I lived in Atlanta, years ago, I assisted a group that maintained a naturally occurring feral cat colony. It was A LOT of work and expense.
Feral cats live an average of 8 years in an urban/suburban environment. To keep the colony healthy, the cats had to be captured humanely each year, vaccinated/vetted and returned to their colony. They also have to be fed, and suitable shelter must be provided during adverse weather or they will take up residence under the first available safe, heated structure.
These are not pets. They are coyote food, and will attract predators that feed on them and other targets.
They do not want to be petted or handled.
Food is expensive but without it, there is no means of keeping them healthy as cat does not live by mouse alone and without feeding, they begin to seek other food sources such as trash cans and other opportunities.
I strongly urge you to interview some “colony keepers” before launching this idea.
Are you really willing to invest so much time and money into maintaining a colony for it’s lifetime? 8 – 12 years is a huge commitment.
Believe me, you don’t want to go out in freezing weather to feed this dependent every day. Who cares them when you decide to move, or have other life circumstances that take you away from the area?
You will have, early on, lotsof volunteers but that will fade over time. Then what?
Like too many intentionally placed colonies, the volunteers stop with the time and money, and then you have a colony of sick and malnourished cats that are YOUR RESPONSIBILITY. A lower grade cat food such as Cat Chow is $20 for a 15lb bag that will last about a week for 5 cats.
Theoretically, yes. In a laboratory? That’s the only place actual Lyme’s disease has been documented in felines. I’m not the expert on Lyme’s in cats. I was asked by a customer and I stammered. So I decided to look it up and Cornell has an EXCELLENT cat unit and they had my answer.
Often, the best combination of treatments I have found for Snuffles is short or long acting cortisone, Cypraheptadine, and Clavamox. The main thing is to keep the cats eating, because when their sinuses don’t allow air passage, their appetite fails for lack of smell. Worse, breaking a fever may become critical. Cats will not eat when feverish. Many respiratory cases improve ‘faster’ with Lyseine as a dietary supplement. It’s not a cure but it will head off the severity and duration of ‘colds’.
The most common manifestation of “Feline respiratory disease” is an infection of the upper respiratory tract (nasal cavity, sinuses, and upper airways). Involvement of the lungs (pneumonia) is much less common but represents a more serious infection.
The most common signs of Feline Viral Respiratory Disease are mild to severe sneezing accompanied by a nasal discharge, discharge and redness of the eyes, and occasionally coughing. Other signs include: Lack of appetite (due to blocked nasal passages inhibiting the sense of smell), depression, and fever. Occasionally, this disease can progress to pneumonia, dehydration, and even death.
Viral respiratory disease in cats is extremely contagious.
All discharges (oral, nasal, and ocular) are infective. Contaminated feeding bowls and bedding are capable of transmitting the disease from infected cats to susceptible individuals. HUMAN “COLD” VIRUSES ARE NOT TRANSMISSIBLE TO CATS AND VICE VERSA. Often humans and cats get “colds” at the same time of year, which causes us to wonder if transmission has occurred. Humans can, however, transmit the disease from one cat to another if they are contaminated with infected discharges so it is best to wash your hands after treating your pet.
Treatment usually involves broad spectrum antibiotics to prevent or treat secondary bacterial infections, nasal decongestants, and occasionally, vitamins. For more severe cases, hospitalization may be indicated. The duration of the disease depends on the individual health of the infected cat (ie. concurrent malnutrition, stress, parasitisms, and other infections that may contribute to a more severe infection), the strength or virulence of the virus, and vaccination status of the infected cat.
Humidity is VERY soothing to cats with FVR signs.
The goals of vaccination are to try and prevent this disease complex. The “FVRCP-C” vaccine is aimed at stimulating a protective immune response against four of the major causes of upper respiratory disease in cats. Cats should be tested for feline Leukemia as early in life as possible (generally at 6-10 weeks of age when they come into a new home). New kittens and cats should be separated from existing household cats until they are tested for feline Leukemia, and are vaccinated for feline Leukemia and FVRCP-C. This may help prevent the spread of infection in a new household.
However, vaccinated kittens and adult cats can still occasionally become infected but usually their disease is much less severe.
INFORMATION ON USE OF GLARGINE IN DIABETIC CATS
Using Glargine In Diabetic Cats (June 2006)
Rhett Marshall BVSc MACVSc1,2,
Jacquie Rand BVSc DVSc Dip ACVIM1
1Centre for Companion Animal Health, School of Veterinary Science,
The University of Queensland and
2Creek Road Cat Clinic, Brisbane, Australia.
These instructions for using glargine are based on a relatively small number of cats, and caution should be exercised with the insulin until it has been used in an extensive number of cats. Because glargine is very long-acting, there is the potential for prolonged hypoglycemia if overdosed.
Glargine (Lantus) is readily available from most pharmacies with a script, is not licensed for use in cats.
Glargine must not be diluted or mixed with anything because the prolonged action is dependent on its pH.
Insulin glargine should be kept refrigerated to prolong its life.
Insulin glargine has a shelf-life of 4 weeks once opened and kept at room temperature. Opened vials stored in the refrigerator can be used for up to 6 months.
Discard vial immediately if there is any discolouration. Bacterial contamination and precipitation associated with pH change can cause cloudiness.
If using an insulin pen, the manufacturer recommends that the pen and cartridge be kept at room temperature and not refrigerated. This is to reduce the changes in volume of insulin dispensed associated with changes in temperature.
When performing a blood glucose curve, samples probably only need to be taken every 4 hrs over 12 hrs in many cats (ie. 0h [before morning insulin], 4h, 8h and 12h after morning insulin).
Dose changes should be made based on pre-insulin glucose concentration, nadir (lowest) glucose concentration, daily water drunk, and urine glucose concentration.
Better glycemic control is achieved with twice daily dosing rather than once daily.
Some pharmacies stock insulin syringes (Wal-Mart) with gradations in ¼ U, which are ideal for cats.
Some cats that have been treated with other insulin will go into remission, usually within 1-4 months after instituting Glargine. Remission in cats that have been treated for more than 2 years is extremely rare.
Remission is likely to occur if the nadir glucose is in the normal range and pre-insulin blood glucose is less than 216 mg/dL (12 mmol/l). However, for some cats to achieve remission, the dose needs to be very gradually reduced, tapering off to ½ U SID before being withdrawn. Too rapid withdrawal often requires restabilizing at a higher dose for some weeks.
INDICATIONS FOR USING GLARGINE
All newly diagnosed diabetic cats (to increase chance of remission).
Poor controlled or unstable diabetic cats (glargine’s long duration of action is likely to benefit these cats).
When SID dosing is desired or demanded (it is important to note that better glycemic control and higher remission rates will be obtained with BID dosing. SID dosing only provides similar control and remission rates to lente BID).
Ketoacidosis – combined with regular insulin IM or IV.
When corticosteroid administration is required in cats in remission. Similarly in cats at high risk of developing clinical signs of diabetes with corticosteroid administration.
STARTING CATS ON GLARINE
If blood glucose conc. > 360mg/dL (20mmol/L) begin glargine at an initial dose of 0.5U/kg ideal body weight twice daily (BID)
If blood glucose conc < 360mg/dL (20mmol/L) begin at 0.25U/kg ideal body weight BID
Perform a 12hr glucose curve with samples taken every 4hrs
DO NOT increase dose for the first week
Decrease dose if biochemical or clinical hypoglycemia occurs
It is suggested that cats stay in hospital for 3 days to check the initial response to insulin, or home glucose curves are obtained for the first 3 days
Recheck at 1, 2, 3 and 4 weeks after the cat is sent home, and then as required
Many cats have negligible glucose lowering effect in the first 3 days (do not increase dose), although by day 10 after beginning insulin, most cats have good glycemic control
Ketoacidotic cats may be treated with glargine s/c at the above dose rates in combination with regular insulin IM or IV (we have found IU regular insulin IM every 2-4 hours based on glucose conc works best). This regime is continued until hydration restored and appetite reteurns, which usually occurs in 1-3 days.
ADJUSTING TO INSULIN DOSE
1. Indications for increasing dose of glargine
If pre-insulin glucose conc. is >216mg/dL (12mmol/L), then increase dose by 0.25-1 U/injection depending on the degree of hyperglycemia.
AND / OR
If nadir (lowest) glucose conc. is >180mg/dL (>10mmol/L) then increase dose by 0.5-1 U/injection.
For well controlled cats after several weeks of therapy, increase dose if nadir is more than or equal to 8 mmol/L (145 mg/dl).
2. Indications for maintaining the same dose
If pre-insulin glucose conc. >180 – <216 mg/dL (>10 – <12mmol/L)
AND / OR
If nadir glucose conc. 90-160mg/dL (5-9mol/L).
For well controlled cats after several weeks of therapy, aim for a nadir of 72 -145 mg/dL (4-8 mmol/L)
3. Indications for decreasing dose of glargine
If pre-insulin glucose conc <180mg/dL (<10 mmol/l) decrease 0.5 – 1U
If nadir glucose conc < 54mg/dL (<3 mmol/l) decrease 1U
If clinical signs of hypoglycemia develop, administer 50% glucose IV bolus followed by 2.5% glucose infusion, then reduce dose by 50% and check for remission.
If clinical hypoglycemia develops and is not severe, it can often be managed by feeding the cat, preferably a higher carbohydrate containing food, such as a some dry foods. However, it must be palatable enough to eat. Most weight reducing and renal diets are high carbohydrate diets, as are many grocery lines of dry food.
For cats with unexpected biochemical hypoglycemia (not clinical signs), some owners find that they can manage the hypoglycemia by delaying the insulin injection until blood glucose increases to 10 mmol/l (180 mg/dL) and then give the same dose (the following dose of insulin may need to be reduced), while others find it best to reduce the dose once glucose is 10 mmol/l (180 mg/dL), although this may result in subsequent hyperglycemia.
4. Insulin dose may be maintained, increased or decreased depending on the water intake, urine glucose, clinical signs and length of time the cat has been treated with insulin
If pre-insulin glucose conc. 198 – 252 mg/dL (11 – 14 mmol/L), or if nadir 54 – 72 mg/dL (3 – 4 mmol/l), clinical parameters are essential for adjustment of insulin dose.
DETERMINING IF THE CATS IS IN REMISSION
Insulin dose should be gradually reduced by ¼-1 U/cat/injection if nadir blood glucose is in the normal range of (72 -126 mg/dL; 4-7 mmol/L) or either pre-insulin glucose concentration is < 10 mmol/L. Slow withdrawal of insulin is advocated until dose is ½ – 1 U once daily (SID).
After a minimum of 2 weeks of insulin therapy, if the pre-insulin blood glucose is < <180mg/dL (<10mmol/L) and insulin dose is ½-1 U SID, insulin should be withheld and a 12hr glucose curve performed. If at the next due dosing time the blood glucose is >200mg/dL (12mmol/L), then insulin can be administered at 1U BID and then gradually reduced as indicated. If blood glucose is <200mg/dL then continue to withhold insulin and discharge with a follow-up visit in 1 week. Water intake and urine glucose should be closely monitored and insulin reinstituted if glycosuria returns or water intake increases.
Some cats may have a pre-insulin glucose concentration below 10mmol/L (180 mg/dL) within 2 weeks, but insulin therapy should be maintained for a total of 2 weeks to give beta cells a better chance at recovery from glucose toxicity. Use 0.5-1U BID or once daily until insulin is withdrawn
With the long duration of action of glargine, there should be minimal periods when blood glucose is >14mmol/L (240mg/dL) for cats treated for more than 2 to 3 weeks, and hence well controlled cats should almost always be 0 or 1+ for urine glucose. A value 2+ or greater likely indicates that an increase in dose is required.
OTHER OBSERVATIONS FROM USING GLARGINE
For some cats, the dose needs to be increased to 5 or 6 U/cat BID, but can then usually be reduced as insulin sensitivity returns. Cats on these high doses need to be carefully monitored for hypoglycemia.
Some cats require only small doses of insulin (<1 U/cat BID) and only go into remission if the dose is reduced very slowly giving few remaining beta cells a chance to recover.
For many cats, the time at which the nadir (lowest) glucose concentration occurs is often not consistent from day to day, or between cats. Sometimes it occurs somewhere between the two doses, but sometimes the nadir occurs around the time of the next dose.
Most commonly the highest glucose concentrations occur in the morning and the lowest in the evening.
Some cats consistently have their nadir glucose concentration in the evening just before the next insulin injection, and less commonly, it occurs around the time of their morning injection.
To increase the chance of remission, we suggest aiming for perfect control or possibly slightly overdosing during the first 2 months, provided the veterinarian and owner can carefully monitor the cat. There is the potential risk of hypoglycemia, but we believe this is outweighed by the benefit of diabetic remission to the cat and owner.
Cats requiring intermittent or chronic corticosteriod administration that are either in remission or at risk of developing diabetes can usually safely be placed on IU SID or BID.
It is a very common observation by owners that when long-term stable diabetic cats are changed over to glargine, usually they do better clinically, even if blood glucose results do not support the clinical improvement.
More information on glargine and general information
Dental Scaling and Prophylaxis Will Preserve Longevity and Health in Dogs
I hate telling people that the reason their dog has a heart murmur is because of infection and rot in the poor dog’s mouth, so often, (if it’s after-the-fact) I won’t. What’s the point, the horse is out of the barn at that point so what I say is “If we clean the teeth it’s likely not to get worse.” Which is mostly true. But the fact of it, is that if they were on top of the teeth and kept the germs to a minimum the dog probably would actually never get a heart murmur.
In this document, I explain how that works, why the dogs get heart murmurs, what that means to the dog and what a “dental” is all about.