scott@vtx-cpd.com
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Replying to Synnove S. 27/10/2021 - 08:23
Synnove.
Thank you so much for your question and your kind words.
Regarding bladder wall culture, this really has to be a tissue biopsy. Taking a roll prep from the bladder wall surface would probably still only represent what was going on in the bladder. The culture really has to be from the tissue to get an understanding of what is going on in the actual bladder wall. This can be done with surgical or cystoscopic biopsies.
The main issue with treating the inflammation and not infection is that there are many other factors at play regarding host immunity that will also be dealing with the infection. Whether bladder colonization causes clinical disease ultimately depends on bacterial gene expression. Bacteria contain genomic islands encoding fitness factors that promote commensalism and/or virulence factors and dictate the severity of the UTI.
The NSAIDs are just dealing with the inflammation. The hope would be that multiple other body factors will be dealing with the infection. There is no doubt that these situations when there are clinical signs, will require antibiotics.
I hope that helps.
Let me know if you have any other questions.
Scott š
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This reply was modified 4 years, 6 months ago by
scott@vtx-cpd.com.
Replying to Jeanette Tungesvik 27/10/2021 - 13:24
Hello Jeanette.
This is a brilliant question. Basically, I would not treat in this case if there are no associated clinical signs.
Subclinical bacteriuria is not uncommon, even in individuals with no known predisposing factors. Rates of 2.1ā12% have been reported in healthy dogs, with higher rates (15ā74%) in groups such as dogs with diabetes mellitus,
morbidly obese dogs, puppies with parvoviral enteritis, dogs with acute disk herniation, chronically paralyzed dogs and dogs treated with cyclosporine or glucocorticoids. Study of subclinical. No evidence of an association between
subclinical bacteriuria and risk of development of cystitis or other infectious complications has been reported in dogs or cats, although study has been limited. A study of 101 healthy female dogs identified bacteriuria in nine (8.9%) and found no association with subsequent cystitis development over a 3 month follow-up
period. Bacteriuria was not associated with fever or survival in a study of paralyzed dogs. In humans, there is abundant support that antimicrobial treatment is not needed for asymptomatic bacteriuria. Treatment guidelines such as Infectious Diseases Society of America Guidelines for the Diagnosis and Treatment of Asymptomatic Bacteriuria in Adults and European Association of Urology guidelines on urological infections do not recommend treating asymptomatic bacteriuria in almost all patient groups. While treatment might eliminate the current bacteriuria event,
recolonization often follows. A systematic review in humans concluded that while bacteriuria may be
eliminated in the short-term, the effect is not sustained and recolonization is common, leading to no impact on overall morbidity or mortality.I would definitely not treat and monitor for now. I don’t think that there would be much value in culturing this sample.
Do you think the dog is underweight due to nutrition?
Hope that helps a bit.
Scott š
Replying to elaine elder 12/10/2021 - 17:52
Hey Elaine!
They do indeed! Various studies have shown that α2-agonists reduce the perioperative levels of stress-related hormones and thus attenuate the stress response of surgery in dogs. Alpha2-agonists, typically xylazine, have been reported to induce an increase in serum glucose by suppressing insulin release, stimulating glucagon release, or both, in β and α cells of the pancreas, respectively. However, medetomidine given at doses of 10 and 20 μg/kg BW, IV, decreased insulin values significantly but was not found to alter plasma glucose concentrations in normal beagles. Differences in plasma glucose concentrations are likely associated with the greater specificity of medetomidine, compared with that of xylazine, at the α2-adrenoreceptors. The hyperglycemia associated with xylazine has been attributed to the actions at both the α2- and α1-adrenoreceptors.
The following study did demonstrate this effect in cats:
Effects of dexmedetomidine on glucose homeostasis in healthy cats
Abstract
Objectives
Alpha(α)2-agonist administration has been documented to increase blood glucose concentrations in many species. The aim of this study was to further describe the effect of dexmedetomidine on glucose and its regulatory hormones in healthy cats.Methods
A randomized crossover study using eight healthy cats with a 14 day washout period was used to assess the effect of dexmedetomidine (10 μg/kg IV) and saline on glucose, cortisol, insulin, glucagon and non-esterified fatty acid (NEFA) concentrations at 0, 20, 60, 120 and 180 mins post-administration. Glucose:insulin ratios were calculated for each time point.Results
Within the dexmedetomidine group, significant differences (P <0.05) were detected: increased median (range) blood glucose concentrations at 60 mins (11.55 mmol/l [5.9ā16.6 mmol/l]) and 120 mins (12.0 mmol/l [6.1ā13.8 mmol/l]) compared with baseline (6.05 mmol/l [4.8ā13.3 mmol/l]); decreased glucagon concentrations at 120 mins (3.8 pmol/l [2.7ā8.8 pmol/l]) and 180 mins (4.7 pmol/l [2.1ā8.2 pmol/l]) compared with baseline (11.85 pmol/l [8.3ā17.2 pmol/l]); decreased NEFA concentrations at 60 mins (0.281 mmol/l [0.041ā1.357 mmol/l]) and 120 mins (0.415 mmol/l [0.035ā1.356 mmol/l]) compared with baseline (0.937 mmol/l [0.677ā1.482 mmol/l]); and significantly larger (P <0.05) glucose:insulin ratios at 60 mins compared with baseline. Insulin and cortisol concentrations were not significantly changed after dexmedetomidine administration.Conclusions and relevance
Feline practitioners should be aware of the endocrine effects associated with the use of α2-agonists, particularly when interpreting blood glucose concentrations. The transient effects of dexmedetomidine on glucose homeostasis are unlikely to significantly affect clinical practice.Hope that helps.
Scott š
Replying to Anisha A. 14/10/2021 - 15:21
Hello Anisha.
I hope you are well and enjoying the course.
I put your question to Felipe in the live Q&A last night. It was the first question I asked him in fact!
The recording will be available by the end of the week.
If you have any other questions let me know.
Scott š
Replying to Rebecca C. 18/10/2021 - 19:16
Hello again.
Hope you are safe and well. I have popped some thoughts down regarding your other questions too:
The amount of blood vs. EDTA can definitely have am effect on the sample. What tubes do you use. It might be having a chat with the lab/manufacturer about the variability. Collection of a small blood volume with placement into a standard EDTA tube will cause shrinkage of red blood cells, because EDTA is hypertonic. This will cause a false decrease in the mean cell volume (MCV) and false increase in mean cell hemoglobin concentration (MCHC) of red blood cells. Crenation of red blood cells (echinocyte formation) will also be evident on the blood smear. This is a common artifact that we see in hematologic samples. Too much blood compared to EDTA will increase the risk of clot formation.
There is not an exact gauge guideline. Venipuncture should be minimally traumatic to minimize platelet activation and should be done using a minimum of a 23G needle, 21-22G is also fine for small animals. I would not go lower than 23G.
Regarding smears; any smears (blood or FNA) are best kept out the fridge once air dried. It is best to get them to the lab (as with everything) as soon as possible.
Hope that helps. Let me know if you have any questions.
Scott š
Replying to Shona M. 25/10/2021 - 19:04
Hey.
Our half term was last week in Scotland… so kids were not so much of an issue up here! š
Will get the recording up ASAP.
Scott š
Replying to Lesley M. 25/10/2021 - 19:46
Hey!
No pressure to speak. I am just conscious that I sometimes speak too muck and want to make sure people have time to ask questions too.
Hope you enjoyed the session.
Scott š
Replying to Emma A. 25/10/2021 - 23:51
Hello.
Thank you so much for your lovely feedback.
I will pass these questions on to Jon and get back to you ASAP.
Scott š
Replying to Anisha A. 14/10/2021 - 15:21
Hello Anisha.
I hope you are safe and well.
I will make sure to ask Felipe this question tonight at the Q&A.
Hope you are enjoying the course.
Scott š
Replying to Alison Docherty 25/10/2021 - 13:44
Hello!!!!
How lovely of you to join us again!
Hope all is not too mad up there in Livingstone!
Scott š
Replying to SAM LILLEY 20/10/2021 - 23:01
Hey Sam.
Big shout out for popping a picture on your profile too!
Nice to see everyone’s face.
Have a lovely week.
Scott š
Replying to Jeanette Tungesvik 21/10/2021 - 11:03
Lovely to hear from you Jeanette!
I am looking forward to learning too!
Hope you have a lovely week.
Scott š
Replying to Laura M. 24/10/2021 - 15:04
Hello!
It is a great question. The ones we use are very specific to the machine we have in the lab:
https://www.woodleyequipment.com/product/562/InSight-Urinalysis-MS-11-Urine-Strips
Generally, you should always use veterinary-specific dipsticks. Regardless of the dipstick you use, some of the test panels are not reliable in our patients. Urobilinogen, nitrates and leukocytes, are not accurate in small animal patients, as they are neither sensitive nor specific.
Just another couple of quick points:
The ketone panel on the dipstick test is only for acetoacetate and acetone (and not beta-hydroxybutyrate), although it is extremely rare for diabetic ketoacidosis patients to not produce any acetoacetate. In our feline patients, any hyperbilirubinuria is abnormal, but this may be normal in a dog depending on urine concentration.
Hope that helps.
Scott š
Thank you Emma.
I have popped the abstract below. It is an interesting discussion. I have certainly sent dogs for surgery that have recessed vulva’s and recurrent urinary tract infections:
J Am Vet Med Assoc
2021 Oct 1;259(7):744-748. doi: 10.2460/javma.259.7.744.
Characterization of recessed vulvas in dogs
Jean-SƩbastien Palerme, Eric Zellner, Sara Leonard, Austin K Viall, Darren J Berger
PMID: 34516259 DOI: 10.2460/javma.259.7.744
Abstract
Objective: To determine the prevalence of vulvar recession in a large population of dogs and to compare the reproductive and physical differences between dogs with and without recessed vulvas.Animals: 250 female dogs presenting to a tertiary referral institution.
Procedures: Female dogs > 6 months of age presenting to a tertiary referral institution were enrolled. At enrollment, a full medical history was obtained with particular emphasis on the presence of lower urinary tract (LUT) disease in the 3 months prior to presentation. All dogs underwent a full physical examination including perivulvar cytologic examination and scoring of the degree of perivulvar skin coverage on the basis of an 8-point scale. Dogs with scores of ā„ 7 were classified as having recessed vulvas. When available, urinalysis data were also included.
Results: Recessed vulvas were identified in 36 of 250 (14%) dogs. Dogs with recessed vulvas had significantly higher body condition scores and body weights than unaffected dogs. In addition, recessed vulvas were more common in spayed than sexually intact dogs. Dogs spayed at ⤠1 year of age were almost 3 times as likely to have vulvar recession, compared with dogs spayed at > 1 year of age. No significant difference was identified between affected and unaffected dogs with respect to the prevalence of LUT signs, urinary tract infections, or perivulvar dermatitis.
Conclusions and clinical relevance: Although recessed vulvas were relatively common in dogs, they did not appear to be associated with an increased risk of LUT disease or perivulvar dermatitis.
Replying to Daphna S. 14/10/2021 - 15:44
Hello.
Harry has popped some answers to your questions below:
1) The RER formula discussed is unfamiliar to me ā in my workplace/uni/textbooks Iāve always come across BWx30+70 (for animals between 2 and 30kg). Is this not considered correct anymore or dose the RER calculation in the lecture refer the something else entirely?
– There are a whole range of RER/MER formulas proposed and are frequently updated as new research comes out. A lot of formulas will have an exponential function (i.e. bodyweight) which takes into account allometric scaling ā the fact that the calorie requirement of animals does not increase linearly with body weight- i.e. smaller animals need a higher calorie requirement/kg than larger animals.
– The formula(s) in the presentation were taken from the National Research Guidelines- Nutrient Requirements of Dogs and Cats. These guidelines are generally considered the reference source and are an assimilation of years of research into calorie/nutrient/water requirements. However, although the guidelines are often updated, there is a potential for it to be out of date!
– Overall, I donāt think it overly matters which formula is used as they are very rough estimations and vary between dog-dog and on a day-day basis. As long as a rough estimate is made using the formula(s) and then increased/decreased to that individuals animal requirement, it should be fine.
– Personally, I do tend to use the 30*BW+70 formula frequently, principally because some calculators struggle with the exponential (BW0.75) part on other formulas, opening the opportunity for errors. I think it does depend on your individual practice/hospitalās situation whether introducing more complex calculations is feasible, or whether this is going to lead to errors/confusion (which is arguably a more important consideration!).2). Considering the graphs discussed in the lecture which demonstrate that āmaintenance rateā Hartmanns provides x3 times more salt than the animal requires, not having seen in practice any other calculation other than the traditional 2ml/kg/hr, never having seen medications + food being deducted from fluid requirement calculations or calculating for lean body weight and using Hartmanns for the vast majority of our cases (we only stock Hartmanns and 0.9% NaCL) ā Iām just wondering whether weāre extremely overloading all out hospitalised patients constantly and hindering their improving and getting better?
– Personally, I think there are two important points with this:
– Firstly, yes, we probably are fluid and salt loading the majority of our animals and overall, we would likely be better moving towards trying to quickly transition onto oral intake of water (cf. intravenous) and monitoring to ensure that animals are maintaining hydration. However, the reality is that we do not have enough research evidence to say how significant the consequences are and unfortunately will be unlikely to be able to carry out such research in veterinary medicine. Furthermore, the risk with intravenous fluids is likely to be of much more importance in animals that are salt/fluid sensitive (i.e. animals with kidney/heart disease) compared to animals that have had a routine operation (i.e. a lipoma removal). When we look at human medicine, there is generally suggestion that fluid overload (and maybe more so than underload) is correlated with a poorer outcome. However, the exact consequence varies between study and are likely at a lower (more nuanced) level than we would be able easily detect in our animals (most veterinary studies have small numbers of participants). For example, in one study looking at Plasmalyte vs. 0.9% Saline in critically ill adults, the 30 day mortality was 818/7942 (10%) in the Plasmalyte group vs. 875/7860 (11%) i.e. using 0.9% Nacl (cf. Plasmalyte) āonlyā resulted in 1% more deaths. Such a small % difference would be difficult to assess in veterinary medicine and may even be brushed off as an āinsignificant amountā. However, the other way you could look at this is āyes only 1% more people died with 0.9% NaCl than Plasmalyte, however that was 57 actual peopleā who died as a result of the using 0.9% NaCl vs. Plasmalyteā. So, yes, although we should be aiming to avoid this, particularly in at risk demographics, the true risk (if any) is currently unknown in veterinary medicine and, most likely, is a relatively small, but not insignificant, risk.– Secondly, I think the most important question is āwhat is feasibly achievable/manageable for my practiceā? Iām a big proponent of āminimising cognitive loadā. I.e. everyone has a set amount of āmental power/energyā for making decisions and the more things you have to think about (i.e. the bigger the cognitive load) the less mental power/energy you have for other things ā potentially opening up the opportunity mistakes. For example, if it is a horrendous Saturday morning clinic where the phones wonāt stop ringing, somebody has phoned in sick, the waiting room is full, the label printer has stopped working, the parvo puppy has chewed itās IV out, and the vet student failed to bring cake on their last day, the more you have going on and the less mental power/energy you have for making decisions. This may mean that, when someone subsequently asks you to draw up medetomidine and butorphanol for a sedation, you draw up 0.5ml of medetomidine instead of 0.05ml by mistake ā it happens, everyone is human, everyone has a set amount of mental power/energy and itās important to minimise the cognitive load to help minimise error. Therefore, if you are in a nice quiet practice where the vet student has remembered to bring cake on their last day then great, you have the time to make it the ānormā to sit down and work out the exact fluid calculation taking into account lean body weight and other sources. Conversely, and probably the situation pretty much everyone is in at the moment (i.e. where the practise is very busy and calculating in-depth fluid calculations is not the norm), I personally think it is more important to have a set, simple rule for everything, to minimise everyoneās cognitive load and avoid errors. However, more detailed fluid calculations could be something that is introduced over time and made easier with flow-charts/calculations sheets/excel forms etc.
– Overall, the presentation is more an example of āthis is what we should be aiming forā but must be very much tailored to everyoneās individual situation, especially with the limitations weāre facing at the moment. Long story short ā if your practise is too busy to frequently check on in-patients because of the workload, donāt have the time (mental energy) to calculate exact fluid requirements taking into account lean body weight etc., or it is not the ānormā to do so, itās probably better that the animal goes on 2ml/kg/hr of Hartmannās to minimise the risk of error and to concentrate on other aspects of care.3) Would we expect to see changes to electrolytes test results after a certain amount of time on Hartmanns 2ml/kg/hr, due to the high quantities of sodium and chloride, or would results be affected by a much longer increase in intake?
– Again, I donāt think we have any idea of the exact relationship. Anecdotally, I have definitely seen sodium increase in animals on high rates of fluids (and believe the IV fluids was the cause). Most commonly this has been in animals with kidney problems and, off the top of my head, Iāve seen it the most in post-obstructive cases (i.e. blocked cats). Itās always hard as a vet to judge the post-obstructive diuresis phase in blocked animals, but my suspicion is that we generally get it wrong and give them more fluid than is needed. Iāve seen sodium creep up in a lot of these, but more commonly see signs of fluid (rather than electrolyte) overload- i.e. pleural effusion, abdominal effusion, pulmonary oedema etc.Hope this helps.
Let me know if you have any questions.
Scott š
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This reply was modified 4 years, 6 months ago by
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