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greyhndz

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  1. greyhndz

    Buddy

    The Gods were smiling on Buddy when Praveen and Karen offered to adopt him 11 years ago. No one in the world could have given Buddy a more loving, patient, nurturing home. Buddy was my Lexi's daddy, and not only will he always be in my heart, but Praveen and Karen (aka Grampa and Grammy to Lexi) will be there too. Godspeed, Buddy! Jordan and your daughter Lexi
  2. I've had a lot of luck with melatonin for storm phobia as well as anxiety disorder. I'll usually give 3mg as needed, though I know a larger dose can be safely given.
  3. Adenocarcinoma is one of the most common types of mammary tumor. It simply means a tumor arising from epithelial cells. This is just a pathologic diagnosis.
  4. Just caught that one. I agree with the consensus about ex-naying the immodium. If a dog (or human) has intractable diarrhea and no underlying bowel disease, maybe, but if he's not even having diarrhea, what's the purpose? If you don't yet have an answer to the problem, I wouldn't compound it by giving him something that could slow bowel motility considerably, putting him at risk of obstruction. If Spencer does indeed have true IBD, "bowel motility" isn't the only issue, and the treatment for IBD (proven by biopsy) is quite different. Having looked at human abdominal films for 20+ years, I'm trying to figure out how the vet can discern "increased motility" by a plain film. You can do a contrast study (like an upper GI with small bowel follow-through, or barium enema) which watches the progression of the contrast throughout the GI tract, and can get a sense of transit time. There are also special studies done via endoscopy. But hypermotility is often a clinical diagnosis - loud, sometimes high-pitched bowel sounds, frequent and/or loose stools, signs of abd. discomfort. I'm kind of coming in at the end of this - has Spencer been formally diagnosed with IBD, and is he on a treatment plan of some kind? A hypoallergenic diet? I'm trying to dig up some articles that might be helpful (and reader-friendly), but the other thing that comes to mind regarding the abd. distension associated with loud bowel sounds would be: is there some type of partial obstructive process in the bowel that might cause distension above that level, relieved when the fecal material passes through the partial obstruction? Is his belly filling with fluid rather than air -- is he leaking protein out of his gut which pulls fluid along with it (ascites)? (How are his serum albumin and protein levels? Cobalamin?) Has he had an ultrasound, looking at bowel wall thickness for signs of inflammation? Is the distension occurring above the level of the pyloric valve -- that is, is there "delayed gastric emptying", with food/fluids taking an excessive amount of time to leave the stomach, resulting in distension? This can be confirmed by an upper GI or more specialized radiologic studies. Medications such as Reglan or Propulsid are helpful for this problem. To throw another fly into the ointment (ew), this is some info from an article too long to cut and past, but I wonder if this has been considered: (BTW - borborygmi = excessive loud, high-pitched bowel sounds) Stress-associated Colitis (Irritable Colon Syndrome, Irritable Syndrome) Stress-associated colitis is a condition with similarities to irritable bowel syndrome and presents with signs of intermittent, often mucoid, diarrhea, with urgency, occasional vomiting, tenesmus and hematochezia. In some cases borborygmi, flatulence, "bloating", and abdominal pain are described. This often occurs in nervous/highly strung dogs e.g., toy breeds and competition dogs. The etiopathogenesis is poorly understood, but a number of hypotheses have been suggested: - Primary intestinal motility defect - Heightened sensation of intestinal distension/motility - Psychological factors - Undiagnosed organic disease There are no specific diagnostic tests for stress-associated colitis, and diagnosis is made by consideration of the signalment together with exclusion of all other organic diseases. Treatment involves eliminating stressful events if possible, behavioral modification and (in some cases) drug therapy (anticholinergics, sedatives, and antispasmodics, e.g., hyoscine, diazepam or peppermint oil). The syndrome of fiber-responsive colitis has recently been reported (Leib et al., 2000). The etiopathogenesis is poorly understood but may well have similarities to stress-associated colitis (see above). As the name implies, therapy involves dietary management with a high-fiber diet (>8% crude fiber or 15% total dietary fiber DMB). It may be interesting to test various sources of soluble and insoluble fiber. So, basically, I think your trepidation is right-on. Masking symptoms isn't going to solve the problem, but it could potentially exacerbate it. If you haven't already, can you hook up with an Internal Medicine specialist who is comfortable diagnosing and managing bowel diseases? I hope I haven't been redundant by suggesting things that you've already done. I know you're anxious to have answers and to get on track with a treatment plan. If I can research anything for you, please let me know, or PM me. Jordan
  5. Excellent article from the Veterinary Surgical Oncology website: Clicky here first (warning: surgical diagrams at bottom of page) A good link to a veterinary text describing reproductive tumors: Clicky If this were my pup, I'd be looking for a surgical oncologist (or at the least, a board-certified veterinary surgeon experienced in managing diseases of the reproductive and urologic system). This can be very intricate surgery, and if you want to maintain normal urinary function and continence, you need a surgeon who knows her/his way around the pelvic floor. Best wishes to your friend and her pup! Jordan
  6. I was in the presence of greatness today.... Yup, the "gloved one"! Purple is really Winslow's color. Very royal. First off, I have to say that Winslow looked GREYT! He's a big hunka fuzzy hound. I've never felt such soft, fuzzy hair on a GH before. You'd never know that he's been through surgery this week. He bounded over to the door when I came in. And then he went right for the tote bag with the toys in it. It was just awesome meeting Winslow, Glynis and Craig. And boy, he's got them whipped! I vaguely remember hearing the tinkling of the little bell that he uses to summon mummy and daddy when he needs a drink or a greenie. Seriously, more loving parents you will never find. Their world revolves around Winslow, and he loves it! He's truly a character, and an enigma -- and just a really cool, great big fuzzy, blogging, sponge-painting lovebucket. Safe travels tomorrow, and I know everyone is putting out vibes for a good pathology report and no need for any additional treatment. 'night, "gloved one"! Glynis, Winslow and Craig (and "the glove") Winslow doing what he does best Just a quick snooze... And a little nookie happening between Crocheted Jerry Murray and Miss Broodie!
  7. Cool! Have a fun visit. Sorry I won't have a chance to meet you, too!
  8. Hey, I'm heading down on Saturday. If you want to rendezvous, we can shoot down in my car! Jordan
  9. Normalcy? What's that? I'm going to respectfully disagree with your vet on several points. (BTW, if you can PM me your e-mail addy, I can send you articles that are too long to post on the forum) After reviewing the veterinary literature, here's the general consensus (this is mostly applicable to human medicine as well): Any proteinuria requires some type of follow-up, at the least a urine recheck in about 2 weeks. If 2-3 samples continue to show proteinuria, further evaluation is warranted. (Or, if the protein on dipstick is high -- such as Max's 3+, the vet should consider testing after just one repeat U/A.) Complete urinalysis (including microscopic) is essential, and your vet did that. But urine culture is also indicated. There are two tests to confirm presence of protein: SSA, which is a special urine test that a vet can either run in their own lab or sent to an outside lab, depending upon how their in-house lab is set up. And UPC. Crystals in the urine wound not affect the presence or quantitation of protein; however, RBC or leukocytes (white blood cells, indicative of inflammation or infection) may indeed skew the results. I don't know that 6-10 RBC would make a significant difference because that is a small amt - the lab could probably answer that question. But would those few RBC cause 3+ protein? I can see 1+ but the literature suggests that 3+ protein mandates investigation (SSA or UPC, the latter being an accurate quantitation). The veterinary literature also recommends a sterile bladder tap (cystocentesis) for a reliable, uncontaminated specimen. Lower urinary tract diseases, such as UTI, stones, crystals, can result in proteinuria, but I would have expected the micro to have shown leukocytes (inflammation or infection) or bacteria (infection) were that the case. Also, remember that the SG of 1.050 is very high. The urinalysis might look quite different were it less concentrated. Also, concentrated urine and/or inadequate fluid intake contributes to crystal or stone formation. It would be helpful to aggressively hydrate Max (perhaps by subQ fluids) and repeat the U/A and micro exam to see how it changes. Definitions: proteinuria - presence of protein in the urine. Crytalluria - presence of various types of crystals in the urine. Hematuria/blood; pyuria/leukocytes; bacteriuria/bacteria. As far as UTI not being present if no odor is detected, I can't find any literature to support that -- certainly not in human literature. It's one of those things where, if there's unusual odor, great - that's a sign to make note of. But lack of odor does not at all rule out infection. A good, properly-obtained urine specimen for culture does. And not every dog becomes incontinent, especially if their fluid intake isn't adequate. And not every dog with UTI will have either fever or elevated WBC. Calcium stones may well show up on a plan abdominal film, and it doesn't hurt to take a look. Depending on the UPC, you may still be looking at an U/S. As far as whether stones in the bladder need to be removed, I still have study that part of the literature. I'd like to see Max aggressively hydrated to see if the stones or crystals pass spontaneously. Here's a snip from a study on managing crystals/stones: Previous research by Stevenson et al49 has shown that, at least in healthy dogs, a reduction in both dietary calcium and oxalate will give the lowest risk for CaOx formation as assessed by RSS. Thus, the treatment diet was formulated to provide controlled levels of both calcium and oxalate. It was also designed to contain a relatively low level of protein and moderate levels of fat and sodium, with the purpose of reducing urinary calcium excretion. It was produced in a canned format that delivers a high level of dietary moisture, with the objective of increasing urine volume as demonstrated in a previous study by Stevenson and associates.50 Feeding this diet to the stone-forming dogs resulted in significant increases in moisture intake and the production of more dilute urine with a lower calcium concentration. Thus, the diet appeared to meet the aim of reducing urinary calcium concentrations, which could be attributed to decreased calcium excretion, increased urinary dilution, and reduced dietary calcium intake. Urinary oxalate concentrations were also lower in both groups when fed the treatment diet. Since dietary intake and urinary excretion of oxalate were similar to baseline, it is likely that the reduction in urinary oxalate concentrations was the result of urinary dilution.... Conclusion The results of this study indicate that hypercalciuria and hyperoxaluria are important factors in the formation of CaOx uroliths. Since the stone-forming dogs excreted more calcium despite a lower dietary intake, it is suggested that they might hyperabsorb calcium from the intestinal tract. This study has highlighted the importance of urinary calcium and oxalate in CaOx formation and has identified several dietary components (sodium, potassium, calcium, and phosphorus) that may influence disease risk. It has also demonstrated the ef�fectiveness of dietary intervention and showed that a diet that increased moisture and sodium intake and reduced calcium and potassium intake reduced the risk for CaOx formation in the majority of affected dogs. You know, the adage in medicine is that you don't look at the labs, you look at the patient. And you treat the patient, not the labs alone. If there's a significant abnormality, repeat it. If it stays abnormal, you investigate it but don't assume the worst. Keep the lines of communication open. Write down your questions. Write down what you've researched. I have a feeling you're bringing more data to the table that your vet is! Don't hesitate to disagree with his plan in a respectful manner. And remember that you, too, can contact the other Greyhound Clinic vets as OSU for guidance. I'm delighted to hear that he snorkled down food tonight. I hope mom did the same, and also sampled a little "adult beverage". Jordan
  10. OK, 'Fess up! Who's the Friday visitor? I'm going down Saturday to be in the presence of greatness. I am WAY psyched that I can finally meet Winslow, Glynis and Craig. I'll try to remember to take photos. I'm even bringing a hot date for Crocheted Jerry Murray!
  11. I agree with Lindsay's agreement. A dose or two of metacam will likely not make a difference, and when you weigh the small risk with the importance of keeping Max out of pain, I, too, would give it to him. Have you tried tramadol for his pain? Maybe the vet needs to reassess his pain management plan and find something that will work a bit better for Max. I hope tomorrow brings you the answers you need, and a plan!
  12. And I agree with you both. Greyhounds (Borzoi, other large-boned sighthounds) are slow to reach maturity. Having a friend who has raised AKG greyhounds from puppyhood and their knowledgable breeders, they prefer to wait until at least a year - longer if possible. Of course, my friend has always had her "entire" dogs in a setting where they couldn't breed (no unspayed females, and always on lead or in a safe yard). She believes that the dogs have better bone growth, muscle development and stay in better coat for showing purposes. This probably doesn't really relate to your own pup's needs, but ensuring healthy bone and muscle sure does if you plan to do lure coursing, agility or other demanding sports. That being said, all bets are off if he turns into an obnoxious little stud puppy. PS - Apparently when Saluki are neutered, the feathered dogs grow a very thick undercoat coat. Check out beautiful Sky, owned by my friends Patty and Steve. Before snip-snip: After snip-snip: (kinda reminds me of Father Time....)
  13. Winslow, Glynis and Craig! Where are you heading in NH? I'm here in Concord, pretty central to everything. Would you like a place to stay? We would SO love to see you while you're up here, and I've plenty of room in the house to keep the King in the manner to which he is accustomed. Jordan
  14. Diagnosing Cushings would entail more than just one lab test, and it sounds as if your vet just did a CBC and chemistry profile. Chronic steroids don't cause Cushings; they can cause "Cushingoid" physical changes - weight gain, thin skin, muscle atrophy, etc., but this is not the same as Cushings, which an excess production of cortisol by the adrenal gland, as opposed to an exogenous source such as oral steroids. So it's very doubtful that your pup actually has Cushings. I absolutely agree that steroids are a horrendous drug for anyone (human or animal) to be on. In many cases, though, steroids can gradually be eliminated, or tapered down, by using another class of medication to suppress the immune system. Cyclosporin is one, but as you said, is very $$$$. There are others which are considerably cheaper, such as azathioprine (Imuran) which come generic and can be purchased at a discount at pharmacies online like Costco. There are others, such as methotrexate and leflumonide, which also come generic and can be found at a good price. Many primary care vets just don't have enough experience with autoimmune diseases to feel comfortable prescribing and managing these meds, though. This is where a consult with an internal medicine vet or a vet dermatologist could really help - you don't have to make multiple visits to the specialists, but sometimes just one visit to confirm a diagnosis and start a treatment plan will be enough, and the specialist can then guide your own vet on med management. This would entail a visit which would be $$$$, but it might also save a lot of trial-and-error with your own vet. BTW, I, too, have autoimmune disease and have been in remission (without any steroid use, ever) for > 2 years, so it may indeed be possible to achieve this with your pup. OTOH, my IG has immune mediated polyarthritis as well as kidney disease, and despite being on an immunosuppressant (leflumonide) has crashed every time her steroids have been tapered to within a week or two of stopping, so for quality of life purposes, she does have to stay on a daily low dose. Lexi has an internal medicine vet to manage her autoimmune disease, but this is almost always done by phone, and my own vet takes care of Lexi's day-to-day care while consulting with the IM vet for questions or problems. Important question: was this diagnosis confirmed by biopsy?
  15. [i'm not a veterinarian but do practice human medicine. I also have an iggy with glomerulonephritis.] An elevated creatinine, which 1.8 technically isn't, doesn't only reflect renal function. There are many other things which cause variability in creatinine. Two things really stand out from what greytkat has told us: he's been on an NSAID (meloxicam) which is notorious for affecting kidney function (but is usually reversible when the NSAID is stopped), and he has a recent injury resulting in muscle breakdown. I don't know what antibiotic he was on, but several can also have an effect on renal function. His diet, hydration status, time of day of urine collection -- all of the above can cause mild elevation or variability of creatinine without there being any underlying renal disease. Explanation of factors affecting creatinine I don't recall if greytkat has mentioned whether Max has PU/PD (urinary frequency and increased volume; increased water intake). I honestly don't see a clinical significance in a large variability of creatinine (0.9 - 1.8) as long as both are within the normal values for a greyhound. This broad spread is easily explained by the factors listed above. Another lab to check would be Glomerular Filtration Rate (GFR) - in human medicine, this is routinely performed anytime serum chemistries are run (which include BUN/creatinine). A couple of OSU articles if they haven't already been referenced: OSU article on creatinine in GHs OSU - lab values Hope this wasn't too medical-esey!
  16. Yup, agree totally with above. Can't diagnose renal disease just based upon a urine dipstick showing +++ protein. Dipsticks are notoriously unreliable. I would not consider the creatinine of 1.8 alarming at all, just at upper limits of normal. If the BUN is normal (which I assume since the BUN/creatinine ratio is normal) then it's unlikely there's been any signif. decrease in renal function. The urine protein/creatinine ratio (UPC) will confirm whether or not Max is spilling protein into his urine. This is obtained by getting just one urine sample. If it's normal, I would not take this any further, and I'd tell the vet to chill. If it's elevated, he'll need a renal ultrasound and possibly additional workup (I'd ask for a referral to an internal medicine specialist). I would absolutely NOT start on any kidney diets or medications without a diagnosis being confirmed, meaning via UPC and possibly ultrasound. And even if he did prove to have some type of renal disease, it can often be controlled very well by diet and medication. So, don't freak out.
  17. Fiona looks wonderful! (except of course for that big, silly-looking whisker sticking out of the right side of her face). What a relief to know that she's healing exactly as you'd hoped for. Zeke - well, he's DA MAN! But the raccoon stuffie has got to go. Can you slip in a fox stuffie when she isn't looking?
  18. You know, Mary, you should really write up a short story on Zeke's feats of do-goodly-ism, to send to CG for their "Hero Hounds" feature! CG submission info And maybe just a wee bit more ice cream tonight?
  19. So glad to hear that Fiona is getting back to her happy, waggy self, and is eating mama's home cooking . And did Zeke enjoy his hero celebration last night?
  20. No, no, no mama... Everything you've said makes it obvious that you are an uber-prepared houndmama. Short of pulling out a ouija board and crystal ball ( ) there was no way you could have seen this coming. No hindsight allowed, because when it comes to wildlife, there's no foolproof way to outthink a desperate critter. You take every precaution in keeping your pups safe. This was a horrid accident that you're in no way responsible for. So be as gentle with yourself as you'll be with Fiona while you nurse her back to health. Oh, and for Zeke? Maybe a whole ice cream cake and a medal of honor?
  21. Mary, you are amazingly prepared for anything! Some interesting points about rabies: because it's transmitted in saliva (and not in blood), even if a pup has no wounds, there's still the risk of his having the feral animal's saliva somewhere on his body. It's a long stretch, but theoretically, if you come in contact with the fresh saliva on his coat, and you have even a small wound on your hand, the virus could be transmitted. I know... it really *does* seem to be a long stretch, but most State Veterinarians or ER staff will tell you that even a very small risk isn't worth taking. If you had the coon's carcas, it could be sent to the state lab and rabies could be definitively ruled out (or in), but when you don't have that option, you have to eliminate any risk by assuming the worst. Read through the CDC guidelines on various types of exposure, as well as the likelihood that various types of feral animals will be rabid. Raccoons unfortunately have to be assumed rabid unless proven otherwise by brain biopsy. CDC guidelines on rabies exposure Try to contact your ACO, or even discuss with your vet. Take care! Jordan
  22. Healing thoughts for Fiona - and for you! There's no way you could have predicted this, so be gentle on yourself! Very important, though: have you been vaccinated against rabies? Even though you didn't come in direct contact with the raccoon, you probably DID come in contact with saliva while holding and examining your pups. This is exactly how rabies can be transmitted, and since you don't have the raccoon to have it tested, you really, really need to get yourself to your doctor or ER to start the series. (You'll be given immune globulin in addition to Imovax to provide you with rapid immunity.) If you have any questions, contact your local ACO for recommendations, but here in NH we'd definitely immunize you. If you have had the rabies series, you'd just need a booster. So please, Mary, while Fiona is getting the care she needs, YOU need to do the same! I've given the rabies series innumerable times to patients in the ER and our office - feel free to PM if you have any questions. Jordan
  23. Dandi has been on clomipramine 75mg twice daily for about 2 yrs, for anxiety disorder and fear aggression. The usual dose of clomipramine is .5 - 1.5mg/lb twice daily, so depending on the dog's weight, 100mg might not be inappropriate. I'll also add that I haven't seen any side effects whatsoever, but unfortunately I think it's not been terribly effective for Dandi, so he's going back to the veterinary behaviorist this week to talk about other options. Especially if the dog has been on clomipramine for a while, there should be little in the way of side effects. And I agree that this drug needs to be titrated up and tapered down.
  24. This might be a helpful link It's a HSUS site with numerous resources out there for financial assistance.... ETA more: United Animal Nations and more UAN Pet Fund AAHA Too many to list, so go to this google page for more links
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