feemandvm

What you are looking for isn't what you should be looking for IMHO. If you take a hard list of numbers you will very likely misinterpret the information for your own dog. Different labs have different normal ranges for various blood tests. You need to know that Greyhounds have mildly higher creatinine concentrations than other dogs... not that normal is between X-Y for a greyhound. To prove that point... Dr. Stack wrote a wonderful article on Greyhound bloodwork referenced above. The only problem I have seen with it is that it is often misused. People will take her range of creatinine values that are normal for a Greyhound of 0.8-1.6 and say their Greyhound must have kidney failure b/c the value of their hound was 1.8 and that is outside of the Greyhound range. At Dr. Stack's lab that may well be true but the normal range at Marshfield labs for ANY dog is 0.8-2.0. Therefore at Marshfield a Greyhound with a creatinine of 2.3 is still quite possibly normal for a Greyhound. A normal value at Dr. Stack's lab of 2.3 would be very unlikely to be normal. Again the numbers given in the article are correct, but the hard numbers are largely only correct in so far as the commercial lab that you use. The ranges listed for WBCs and RBCs are pretty much the same from lab to lab so those numbers you can like extrapolate but the chemistry values will vary significantly. If you tie yourself into a box by wanting a specific number, you are really missing the point. I think you may find this article helpful: http://animalmedicalcentreofmedina.com/lib...y%20Failure.pdf

An necropsy (aka autopsy) is really the best way to find out what happened. While it can't bring her back, knowing if it was a possible toxin may be important to make sure it can be removed if still present. DIC, a ruptured splenic tumor, thromboembolism, toxin would all possibly cause the symptoms you noted. GDV (bloat) would seem unlikely but still possible. An autopsy would tell you for certain.

The tough part about this question in a forum like this is that you will get a lot of annecdotal reports which are helpful but may not be reflective of the real benefit of a product. I had a Greyhound that had 1 dental cleaning in his life and ZERO extractions and was not fed raw and was only brushed occassionally. He did get lots of dental chews! : ) If the dental vaccine was available back then and I gave it to him it would appear to be a HUGE success for him when in reality... he was one of the few Greyhounds that actually have good teeth! : ) In the end the dental vaccine is not something I would recommend across the board for every dog. Having said that, if I had a Greyhound with bad teeth and periodontal disease, I would consider its use. I'm not saying GT isn't a greyt source of information... it really is! But I wouldn't base a decision on whether or not to use a product on a few annecdotal reports.

Diagnosing an enlarged liver on a physical examination not always a straight forward thing. Especially in a Greyhound with a very deep chest. The liver also won't fluctuate in size significantly from 1 day to the next so if a liver is truly enlarged... it is likely to stay that way for awhile b/c it rarely swells overnight. There are LOTS of possible reasons for an enlarged liver but first thing you would want to know is if it is truly enlarged. I'd consider an x-ray of the abdomen to evaluate the size of the liver. With the ALT and ALP being normal that makes liver disease less likely but not impossible. ALT will elevate when there is damage to a liver cell but diseases can effect the liver without always damaging liver cells. ALP elevations are a LOT harder to deal with b/c mild/moderate elevations can be completely normal in older dogs or can be indicative of disease. I'd get an x-ray and if the liver is not enlarged... you have no worries. : ) If it is enlarged... I might have a radiologist take a look at the x-rays to confirm the enlargement and then you can decide if anything else such as an ultrasound should be considered. My guess is w/ normal bloodwork... the liver likely isn't overly distended but an x-ray should tell you for certain.

As Lynn said... too many variables to consider. Some severe infections could really affect life expectancy... mild infections may have no effect whatsoever. You'd have to talk to the vet who treated the dog to really know.

I would have no problems using it longterm if it was needed. As Batmom said, bloodwork will be necessary to continue using it and rechecking it periodically is important! Consider some other things as well like a glucosamine supplement, Adequan injections, Duralactin which are all safer (although less potent) longterm options.

Here was some information presented at a internal medicine CE conference regarding protein and kidney disease: PROTEIN There is agreement among veterinary nephrologists that protein restriction is warranted in dogs and cats with signs of uremia, based on clinical observations which indicate that some of these signs are alleviated. The ideal diet for imposing the restriction should minimize generation of nitrogenous wastes while providing a quantity and quality of protein that avoids protein malnutrition. Published reports which compare commercially available renal diets for relative success in approaching this ideal could not be found. The level of azotemia warranting protein restriction seems to be a matter of opinion. Many veterinary nephrologists advocate protein restriction in cases of CRD when BUN values exceed 75 mg/dl. Although protein restriction seems to relieve signs of uremia, this effect involves extrarenal factors. A separate issue is whether dietary protein causes kidney damage. Although compelling evidence has accumulated indicating that high protein diets cause kidney damage in rats, such is not the case in dogs and cats. In the remnant kidney model of renal failure, dogs fed a high protein diet for 2 years had no higher mortality than dogs fed a low protein diet. 1 In old uninephrectomized dogs fed either a high protein or low protein diet for 4 years, mortality was slightly higher in dogs fed the low protein diet, and kidney lesions were not different between groups.2 In remnant kidney cats in which caloric intake was controlled, no adverse effects on kidney function or morphology were detected on cats on a high protein diet, compared to a low protein diet.3 Reports of controlled studies investigating the effects of protein intake on naturally-occurring CRD in dogs or cats could not be found. Here is a journal article discussing this issue in humans: Dietary protein intake and kidney disease in Western diet Contrib Nephrol. 2007;155(0):102-12. 41 Refs Roberto Pecoits-Filho1 1 Centro de Ciências Biológicas e da Saúde, Pontifícia Universidade Católica do Paraná, Curitiba, Brazil. r.pecoits@pucpr.br Abstract Components of the diet related to changes in eating habits that characterize the modern Western world are important factors in the increasingly high prevalence of chronic disease, including obesity, diabetes, hypertension and as a consequence, chronic kidney disease. The healthy diets recommended for the general population to promote longevity (such as the Mediterranean diet), are defined based on epidemiological and intervention studies and are usually characterized by a relatively higher amount of protein than the usual Western diet. Unfortunately, very few clinical studies focused on diet-based strategies of prevention of kidney disorders. Furthermore, this review will propose that the concept that protein restricted diets decrease the risk of developing kidney disease in the general population is not supported by the scientific literature. Indeed, preliminary studies showing a positive effect of relatively high protein diets on risk factors for chronic kidney disease (particularly on obesity, hypertension and diabetes) point to the need for future studies addressing diets that could prevent the increasingly high prevalence of kidney disease in the Western world. On the other hand, there is a potential role for protein restriction in patients with established kidney disease, particularly in patients with significant decrease in glomerular filtration rate. The exact protective action of protein restriction in patients with established renal disease needs further analysis, taking into account the more broad effects of protein restriction (lower phosphate, acidosis, uric acid) and a more current definition of malnutrition.

Read the thread posted above to hear why I personally wouldn't recommend NGAP for dentals. The nice thing is you actually get a reply from the director of NGAP in the thread (which he also included in the 2007 NGAP newsletter). However, if you notice his reply actually doesn't dispute any of the points that I raised. NGAP uses IV Domitor for most if not all of their dental cleanings. NGAP does nto intubate for routine dental cleanings. NGAP performs some standing anesthetic free dentals and NGAP will supplement a shy Greyhound with thyroid supplement no matter what their level is. Notice I am NOT saying that they don't check T4s... I am saying they supplement the Greyhound no matter what the level is. Now, before you make your decision... think of the most Greyhound savvy vet that you know or would be comfortable contacting. Your primary vet, or Dr. Suzanne Stack or OSU or whoever it is that you would be comfortable contacting. Now review these practices with that person and ask them if that is something that they feel is practicing a level of medicine that they are comfortable with. IMHO the person that you contact is very important because you need to be able to trust their judgement and opinion. Now you know the cost of a dental at your vet, the cost of the dental at NGAP. You now also know that NGAP doesn't intubate for dental cleanings and gives IV Domitor only to pretty much all of their patients. Now it is up to you to assess the value of each. I will say that the one way I do think NGAP and I do agree is in leaving bad teeth in the mouth. I've seen a lot of bad teeth left in the mouths of Greyhounds over the years but that is not a mistake I have seen or heard of NGAP making. They do a nice job of removing the teeth that need to be removed. I just disagree strongly with the practices that I listed above.

I agree with your vet completely... I would really try aggressive homecare and try to avoid anesthesia. If it ultimately came to the dog really needing a dental, I would likely consult with OSU and possibly refer so I think your idea of consulting with Tufts is a good one!

I understand your idea of "wanting to be cautious". Anesthesia is NEVER risk free (I never take recommeinding or performing anesthesia lightly)! When I say "you are punishing her for being old" I do not mean in anyway to imply that you are doing this deliberately... however, if we leave periodontal disease untreated adn she is otherwise healthy that is basically what is happening. We are neglecting a health probem because of her age. Also... the teeth won't get better with time, only worse so if we wait we may end up with a dog who needs a teeth cleaning, multiple extractions adn is now a year older. Obviously you need to be comfortable with whatever decision you make... I'm just providing food for thought!

Is he on any medications for nausea? If not... I'd ask your vet about the following: 1. Metoclopramide 10mg tabs: you can get 30 or 60 from Wal-mart for $4. This is an anti-nausea medication. 2. Famotidine (aka Pepcid) 20mg tabs: you can get 30 or 60 from Wal-mart for $4. This is an antacid and can help with upset stomach. I would start both of the medications ASAP. Other things you can consider if these don't help: 1. Injection of Anzemet: used to treat chemo nausea in humans... only lasts about 24 hours though. 2. Ginger 3. Acupuncture 4. Gastricalm: a newer oral medication which can help upset stomach 5. Mirtazapine: a newer medication which is an appetite stimulant and anti-nausea med in animals. 6. Pepto-bismol 7. Megestrol: a hormonal supplement which is an appetite stimulant. I've only used this once or twice and would reserve it for severe cases. 8. Prednisone: generally not my first choice but a steroid that can stimulate appetite. 9. Winstrol: an anabolic steroid that can stimulate appetite. I may have missed a few but that is a long starting list.

severe periodontal disease could actually accelerate the kidney disease. there are certainly some patients that I would not pursue a dental cleaning in... a previous poster mentioned her Grey went into respiratory arrest with the last anesthesia... obviously that would worry me. I do not use age as a discriminating factor by itself, however. As I mentioned before using age to justify not pursuing anesthesia is simply punishing the dog for being old. If I had a patient with kidney problems that needed a dental cleaning... assuming the dog was stable... I would likely bring the dog in 24 hours prior to the procedure and start some IV fluids running. I would pursue the dental the following day with a premedication of something like Butorphonal IM and valium IV (or midazolam IM) and then induce with propofol and get the dental done. As I mentioned before... I jsut did surgery on a 16 year old whippet with a heart murmur that did wonderfully! As I said, there are cases that I might opt not to pursue a teeth cleaning but those are rare. Another option would be to see a dental specialist who really is very efficient at doing everything b/c all they do is teeth all day every day. An echocardiogram as another poster noted is nice but if there is no heart murmur adn teh dog is otherwise healthy I don't know if it is ultimately necessary... but doing it won't hurt. If an echo was pursued, I would strongly recommend pursuing it with a board certified cardiologist (not a GP or a internist who "does cardiology").

Just my $0.02 but I would really consider a proper cleaning. I understand your concerns about an older dog and anesthesia but in the end if you use that as a reason not to pursue a procedure then you are really punishing the dog for being old. If the dog has a good heart and normal bloodwork then the anesthetic risk should be low. I just did surgery on a 16 year old whippet with a heart murmur who did wonderfully.

Just because the dog doesn't scream doesn't mean it doesn't hurt! While staples do not result in uncontrollable pain... they do hurt. I would challenge every poster on here that declines any sedation or local for staples to 1st get the same number of staples themselves. If you can take 4 staples in the hand or leg and tell me it doesn't hurt, then I guess you can continue to get staples without sedation or a local. On the other hand, if you tell me that it actually hurts and you would prefer not to be stapled again then you will see why this vet recommended or demanded at least a local. As for the argument of the local causing as much pain as the staples/sutures... I would disagree. If you use bicarbonate to neutralize the pH of the lidocaine, it takes 90% of the bite out of the lidocaine. To me the argument of "he doesn't appear to be in pain" is why an animal's pain with MANY procedures was ignored for so long. We know physiologically that they feel pain by the same pathways that we do. Instinctually animals will try to hide pain and typically will tough out much more than we do but that doesn't mean that they are not in pain. Recently there was a vet in there 60s or 70s that lost their license because the vet did not provide appropriate pain relief to a dog after performing back surgery. What was his defense? "The dog didn't appear to be in pain". He lost his license b/c he failed to show how a slipped disc and the surgery to repair it could NOT result in signficant pain. I think preventing/controlling pain is one of the most important things a vet can do so sorry if I rambled a bit... just kind of a soap box issue.

I would tend to think that the "jumping off the x-ray table" probably has little to do with any of Bella's signs. Of course as you have heard many times "I wasn't in teh room" so obviously I can't know that... but the pitting edema is not a typical response to trauma. It often is a response to vasculitis. With HGE we actually normally see an elevated red blood cell count due to dehydration even though they have very bloody stool so obviously a low red blood cell count is unusual. I assume from the history that the coagulation test was done on Tuesday or early Wednesday? Based on the history I would have some concerns for disseminated intravascular coagulation (DIC). However, I would have expected the coagulation panel to be abnormal if that was the case (unless the coagulation panel was done before the DIC started). I would highly encourage you to ask your vets to contact Dr. Couto at OSU (or if he is out of the office someone in the Greyhound program). The general number for OSU is 614-292-3551. From there voice mail will get them where they need to go (there is a number for vets to push... I just don't remember which one). Dr. Couto has done a lot of research on bleeding Greyhounds and is probably the best resource available. Are the platelets also dropping with the red blood cells? Is the BUN elevated which would also indicate an upper GI bleed? Has she had any black tarry stool or has the stool always contained frank red blood? Have they discussed doing tick titers with you at all?

If there was no trauma... then this his a pathologic fracture of some sort (most likely osteo unfortuneately) and the leg will need amputated. Of course wait to hear from OSU but you need to make this decision ASAP. There isn't enough Tramadol and Rimadyl around to overcome the pain of a broken leg!

Just thought I'd post some opinions of some specialists from the Veterinary Information Network on TPLO vs. lateral suture repair. Outside of the posts below, you might want to consider contacting Dr. Dyce at OSU or Dr. Radcliffe (private practice) as they are probably two of the top Greyhound ortho specialists around. See if either of them strongly recommends one procedure over another. Also... with the 2nd post below I'm not implying in anyway that you are looking for "the cheap way"... I was just sharing some of the posts and this was one of them. In general, I think the consensus of most of us would be that TPLO would be the best alternative for a dog this size. While many large dogs can have very good function with extracapsular repairs, the degree of degenerative joint disease seems to be much greater than with TPLO. You ask about cost. While obviously costs will vary from area to area, TPLO is always a much costlier option (sometimes by 2-3 times). I always remind folks looking for the cheap way that if the suture repair fails they get to spend more money doing the TPLO that should have been done in the first place :-) In addition to saying the same comments that both Doug and Greg made, I ask owners what kind of outcome they want for their pet. It they want their dog to return to pre-injury function, and not have progressive degenerative joint disease in that knee, then TPLO is the only option. I would also really look at this dog's alignment. Is he bow-legged in his conformation? Does he have excessive tibial plateau slope? If so, then any other procedure besides TPLO will fail, since TPLO is the only procedure to address limb malalignment issues. It's a perfectly good question Jered. As you will be aware, the recent literature has not found much evidence-based medicine to back up anything we do with cruciate ruptures so I don't have compelling evidence to present you in that vein. However, this board is a pretty good snapshot of the general consensus in the rest of the profession. Between the regulars here, Kathy, Vic, Jim, Gary, Michael, Aaron and others, we've all done 100s of extracapsular repairs on all kinds of dogs. Many have done well. Others, especially of the larger breeds, have done mediocre...or worse. Personally, I got tired of reexamining extracapsular repairs 12 months later and finding a big, arthritic stifle joint with varying degrees of disability. With TPLO, all of us report a quicker return to function, better athletic function and no more big, arthritic stifle joints. This is especially important to me because in my own practice the average age of these patients has dropped in the last decade from 7.8 years to 5 years (and getting younger). It's not for every dog....I don't do TPLO in dogs under 20-25 kg and I think twice about it in dogs over 10, but it's an option in the big guys....and an option that virtually every major academic institution and referral center in North America and Europe is offering. As Greg put so succinctly, there are no good, large scale, well-blinded, prospective/controlled studies comparing various techniques, so most of what we do is based on the weakest form of EBM (evidence based medicine), namely personal experience and anecdote. Conventional surgical procedures (such as lateral suture, fibular head advancement, etc.) all share the concept that the way to replace the function of the torn CCL is by building a new one, ie, some structure that is mechanically oriented in a way similar to the original CCL. The goal in this type of operation is elimination of cranial drawer. What we have learned over the years are two major things: (1) These repairs don't hold up in a consistent way (and also have inconsistent clinical results); and (2) Dogs don't injure their CCLs the way people do. So while conventional reconstruction works well in humans, it leaves us short in a lot of cases. Because of their stance, dogs naturally develop a lot more shear force (tibial thrust) than humans do (mostly compression). Our current thinking is that this shear force results in a repetitive stress injury to the CCL. This dog/human difference then explains several things: Dogs having partial tears that progress (rare in humans), and the frequency of bilateral problems sans trauma. Understanding this biomechanical paradigm, it makes sense that if we simply replace the torn CCL with substitute, the new ligament will be subjected to the same mechanical forces, and thus likely loosen/fail over time the same way the native CCL did. This is in fact what we find, and hence the development of geometry modifying procedures (TPLO, TTA, CWTO, etc) to alter local anatomy in such a way as to eliminate the shear force trigonometrically. Once done, the CCL (or any replacement) becomes moot. We don't worry too much about drawer with these operations since that is passive laxity only significant when the dog is in lateral recumbency. With TPLO and TTA (tibial tuberosity advancement) we achieve functional stability in the weight bearing position (no shear). On a theroretical basis at least, there is no justification for a size cut-off when choosing a conventional reconstruction vs. geometry modifying. But from a practical and cost basis, the differences in clinical outcome are less dramatic (we think) in small dogs than in larger dogs (very similar situation to the question of whether to do hip replacement or excision arthroplasty in a smaller dog with end-stage hip disease). So fewer geometry modifying operations are done in small dogs. As you noted, the greater complexity of TPLO and TTA can translate to more or at least more serious complications (and cost). This is always a part of my discussion with clients therefore when we review available options for treating their dog's knee injury. Hope that helps...

I would do a TPLO if it were my Grey. Less longterm arthritis with TPLO than with traditional therapy. I would make 100% certain that the diagnosis is correct though as ACL rupture was one of the most commonly misdiagnosed injuries that we saw at Ohio State.

My understanding is that you may now be finding it in stores... or may be soon.

From what I understand Cosequin DS is going OTC b/c they released Dasaquin as their "new and improved" prescription product.

Michigan State is the only place I would send thyroid panels!

I would think most would be aware of it... but here is what I would ask your vet: 1. If he/she believes that phenobarbital can lower thyroid levels. If he/she says "No" then I would share with them the article abstracts I posted. If they say "Yes" then ask them why do they think Henry may be hypothyroid vs. just having a lower thyroid level from his phenobarbital.

There is an easy way to adjust for being rawfed and the BUN... next time you are going in for a blood draw... have it done fasting. No food for at least 12 hours prior to having it checked adn that will generally allow the BUN to normalize if it is only diet related. : )

It sure can! Phenobarbital is known to lower thyroid levels! I would really discuss this with your vet. Most of his "symptoms" sound more likely to be related to his phenobarbital then to hypothyroidism to me. Here are some articles that you can reference if needed. J Am Vet Med Assoc. 1999 Aug 15;215(4):489-96.Links Effects of phenobarbital treatment on serum thyroxine and thyroid-stimulating hormone concentrations in epileptic dogs.Gaskill CL, Burton SA, Gelens HC, Ihle SL, Miller JB, Shaw DH, Brimacombe MB, Cribb AE. Department of Anatomy and Physiology, Atlantic Veterinary College, University of Prince Edward Island, Charlottetown, Canada. OBJECTIVE: To determine whether phenobarbital treatment of epileptic dogs alters serum thyroxine (T4) and thyroid-stimulating hormone (TSH) concentrations. DESIGN: Cross-sectional study. ANIMALS: 78 epileptic dogs receiving phenobarbital (group 1) and 48 untreated epileptic dogs (group 2). PROCEDURE: Serum biochemical analyses, including T4 and TSH concentrations, were performed for all dogs. Additional in vitro analyses were performed on serum from healthy dogs to determine whether phenobarbital in serum interferes with T4 assays or alters free T4 (fT4) concentrations. RESULTS: Mean serum T4 concentration was significantly lower, and mean serum TSH concentration significantly higher, in dogs in group 1, compared with those in group 2. Thirty-one (40%) dogs in group 1 had serum T4 concentrations less than the reference range, compared with 4 (8%) dogs in group 2. All dogs in group 2 with low serum T4 concentrations had recently had seizure activity. Five (7%) dogs in group 1, but none of the dogs in group 2, had serum TSH concentrations greater than the reference range. Associations were not detected between serum T4 concentration and TSH concentration, age, phenobarbital dosage, duration of treatment, serum phenobarbital concentration, or degree of seizure control. Signs of overt hypothyroidism were not evident in dogs with low T4 concentrations. Addition of phenobarbital in vitro to serum did not affect determination of T4 concentration and only minimally affected fT4 concentration. CONCLUSIONS AND CLINICAL RELEVANCE: Clinicians should be aware of the potential for phenobarbital treatment to decrease serum T4 and increase TSH concentrations and should use caution when interpreting results of thyroid tests in dogs receiving phenobarbital. J Vet Pharmacol Ther. 2000 Aug;23(4):243-9. Links Changes in serum thyroxine and thyroid-stimulating hormone concentrations in epileptic dogs receiving phenobarbital for one year.Gaskill CL, Burton SA, Gelens HC, Ihle SL, Miller JB, Shaw DH, Brimacombe MB, Cribb AE. Atlantic Veterinary College, University of Prince Edward Island, Charlottetown, Canada. A multicentric prospective study was conducted to monitor the effect of phenobarbital on serum total thyroxine (T4) and thyroid-stimulating hormone (TSH) concentrations in epileptic dogs. Serum T4 concentrations were determined for 22 epileptic dogs prior to initiation of phenobarbital therapy (time 0), and 3 weeks, 6 months, and 12 months after the start of phenobarbital. Median T4 concentration was significantly lower at 3 weeks and 6 months compared to time 0. Thirty-two percent of dogs had T4 concentrations below the reference range at 6 and 12 months. Nineteen of the 22 dogs had serum TSH concentrations determined at all sampling times. A significant upward trend in median TSH concentration was found. No associations were found between T4 concentration, dose of phenobarbital, or serum phenobarbital concentration. No signs of overt hypothyroidism were evident in dogs with low T4, with one exception. TSH stimulation tests were performed on six of seven dogs with low T4 concentrations at 12 months, and all but one had normal responses. In conclusion, phenobarbital therapy decreased serum T4 concentration but did not appear to cause clinical signs of hypothyroidism. Serum TSH concentrations and TSH stimulation tests suggest that the hypothalamic-pituitary-thyroid axis is functioning appropriately.

Thyroid Stimulating Hormone = TSH I would try to track down the previous copy of his complete thyroid panel another poster had mentioned first. I would also strongly consider requesting that a premium thyroid panel be sent to Michigan State and request an interpretation by the endocrinologists there. If the only clincal sign is a seizure, I would be pretty hesitant to start my own Greyhound on thyroid supplementation without an elevated TSH to support the diagnosis. Just my $0.02.