scott@vtx-cpd.com
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I have attached the results you have asked for. We ran some urine as well? Why would that be useful?
Scott x
So… based on the clinical presentation my neurology specialist pal made the following comment:
“Although cerebellum is compatible with some of the current clinical signs, the fact that he also was unresponsive and no proprioception may indicate that the brainstem is also affected. Either way, I agree with you that intracranial seems the most likely. As you said, ischaemic encephalopathy and neoplasia sound like the most likely differential diagnosis… There may be a potato arising/compressing the caudal fossa (brainstem +/- cerebellum)”.
I will follow up at the clinic and see if I can get more information about the actual case outcome.
Hope that helps.
Scott x
Lameness has many causes, but due to the multiple joint effusions the differentials focused on causes of non-traumatic inflammatory joint disease. Degenerative joint disease was a consideration (but thought less likely due to age), but more likely septic or immune-mediated (erosive and non-erosive) polyarthritis.
It is always important to distinguish between hyperthermia and pyrexia.
Increased body temperature may be a result of pyrexia caused by infectious agents (bacteria, protozoa, fungae and parasites), immune-mediated disease, neoplasia, non-septic inflammation, tissue damage, necrosis, pharmacological agents (e.g. colchicine and bleomycin) and idiopathic pyrexia. Causes of hyperthermia; inadequate heat dissipation (heat stroke, hyperpyrexic syndromes), exercise hyperthermia (normal exercise, seizure disorders) and pathologic or pharmacological origin (lesions of the anterior hypothalamus, malignant hyperthermia, hypermetabolic disorders).
No access to pharmacological agents was reported. Heat stroke, seizure disorders and malignant hyperthermia were excluded as there was no history of exposure to strenuous exercise, history of seizures or administration of halogenated anaesthetics or depolarising agents. Lesions of the hypothalamus and hypermetabolic disorders could not completely ruled out.
Pyrexia was thought to be more likely as the dog did not seem to attempt to dissipate heat and was most likely to be related to the joint effusions at this stage.
What initial treatment and investigations would you consider?
Scott x
I missed the signalment! Sorry:
A 2-year-old, neutered female, 12kg, Whippet.
The primary problems were considered to be the lameness, joint effusion and increased body temperature. The lameness was considered most likely to be secondary to the joint effusion. Additional problems were the muscle atrophy, anorexia, reluctance to exercise, dehydration and were thought to be secondary to the same disease process causing the primary problems.
Spot on with the problem list, I would always create the problem list and then prioritise them before coming up with my differential list.
Scott x
So the basic principals are…
In peripheral vestibular disease, the nystagmus can be horizontal or rotary and the fast phase is always away from the lesion. In central disease the pathologic nystagmus can be in any plane (including vertical), can change direction with different positions of the head, and the fast phase can be toward the lesion. Therefore, identification of a vertical nystagmus or a nystagmus with the fast phase toward the lesion is an indication of central involvement. However, caution should be exerted when labeling a patient with central disease based on vertical nystagmus alone since it is easy to confound nystagmus with a slight rotary component with vertical nystagmus. One comparative clinical study also suggested that the number of beats of the resting nystagmus was significantly higher in peripheral vs. central disease. A resting nystagmus rate of more than 66 beats per minute was found to be very specific (95%) and sensitive (85%) of peripheral disease.
I have contacted one of our neurology specialists to get a final call location!
Scott x
Also, was the nystagmus evident before sedation? Sorry for all the questions!
Sx
Hello.
Thanks so much again for the question. Could you double check the ACP dose. The only reason I ask is that that would be quite a high dose and may explain the prolonged sedation. Just a thought.
Scott x
Thank you so much for your reply!
I will see if others have thoughts before replying!
Scott x
You can use this link to upload videos and pictures. Once uploaded paste the like that it generates in another comment.
Scott x
Thanks again.
I have answered below your questions below:
So the sodium is both lost through urine with diuresis and diluted by water being drawn into vasculature from intersitital fluid. Does that mean we shouldnt worry as the body as the sodium, just not in the extracellular space?
There will be electrolyte losses in the urine. When animals are significantly hyperglycaemic, a big effect will come from fluid being drawn into the intravascular space. Overall this is a dilutional effect so we need to worry less about body sodium overall.
Insulin will also cause hypokalemia- because it shifts potassium into the cells. which is why insulin is given with potassium supplementation? but is also potassium lost through increased diuresis? i get abit confused here as diabetics is said to be hyperkalemic due to lack of insulin, but then they have increased diuresis with the hyperglycemia as well.
Again, electrolytes will be effected by the diuresis, but there are more significant effects going on in the body. The potassium will be normal when DKA patients are first diagnosed as the acidosis will also have an effect. The increase in H+ will cause potassium to move extracellularly. Basically the movement of potassium in and out of cells is much more significant that the effect the diuresis has.
Hope that helps.
Scott 🙂
Thank you so much for this. Really interesting question.
Diet, drugs or supplements all might be effective in improving signs and slowing the progress of CDS. Canine studies have demonstrated that mental stimulation in the form of training, play, exercise, and use of manipulation toys can help to maintain quality of life as well as cognitive function, but are most effective together with an appropriate nutritional base. This is consistent with studies in humans in which education, and brain and physical exercise, have been found to delay the onset of dementia.
Currently there is one pharmaceutical in North America, selegiline (Anipryl, Zoetis Animal Health), that is approved for the treatment of CDS in aged dogs. Selegiline hydrochloride is a selective reversible monoamine oxidase B inhibitor, which was found to significantly improve cognitive signs in aged dogs. In the canine brain, selegiline increases 2-phenylethylamine, a neuromodulator that enhances dopamine and catecholamine function. Its metabolites l-amphetamine and l-methamphetamine could further enhance cognitive function and improve behavior. Selegiline also might contribute to a decrease in free radical load in the brain.Propentofylline, a xanthine derivative, is licensed in Europe and Australia for the treatment of dullness, lethargy, and depressed demeanor in old dogs. It could increase blood flow and inhibit platelet aggregation and thrombus formation. In a laboratory trial with aged Beagle dogs, it had no effect on behavioral activity.
No drugs are approved for treatment of CDS in cats; however, both selegiline and propentofylline have been reported anecdotally to be useful.
Another therapeutic strategy for cognitive dysfunction in dogs, cats, and humans is diets and natural supplements that might reduce the risk factors that contribute to brain aging and cognitive decline. It is likely that an integrative approach is required to achieve and maintain brain health, such as diets supplemented with polyunsaturated fatty acids, antioxidants, and mitochondrial co-factors. Two veterinary therapeutic diets that have been developed for the management of CDS have been demonstrated in laboratory studies to improve learning and memory in dogs. A diet from Hills Pet Nutrition (Canine b/d) is supplemented with fatty acids, antioxidants (vitamins C and E, beta carotene, selenium, flavonoids, carotenoids), and dl-alpha-lipoic acid and l-carnitine to enhance mitochondrial function. When the diet was combined with environmental enrichment, the greatest level of improvement was achieved. I have a funny feeling this diet is no longer available. In a clinical trial, significant effects were obtained from the diet alone. A diet from Nestle Purina Research (Purina Pro Plan Bright Minds) is supplemented with botanic oils containing medium chain triglycerides to provide ketone bodies as an alternate source of energy for aging neurons. A dietary supplement from Nestle Purina (not yet commercially available) with antioxidants, (vitamins E and C, and selenium), arginine, B vitamins, and fish oil significantly improved learning and memory tasks in cats aged 5.5 to 8.7 years.
A number of nutritional supplements also might be effective in the management of CDS based on laboratory and/or clinical studies. Senilife (CEVA Animal Health), which contains phosphatidylserine (a membrane phospholipid) and Gingko biloba, vitamins Eand B6, and resveratrol, is labeled for both dogs and cats but only has been evaluated in canine studies to date. Activait (Vet Plus Ltd), which contains phosphatidylserine, omega-3 fatty acids, vitamins E and C, l-carnitine, alpha-lipoic acid, coenzyme Q, and selenium, has been evaluated in a canine clinical trial. A feline product also is available with alpha-lipoic acid removed. S-adenosyl-l-methionine (Novifit, Virbac Animal Health) might help to maintain cell membrane fluidity and receptor function, regulate neurotransmitter levels, and increase production of glutathione. Apoaequorin (Neutricks, Neutricks, LLC), is a calcium-buffering protein found in jellyfish that improved learning and attention in dogs in laboratory trials. Immunotherapy has also been evaluated in aged dogs, involving the vaccination of aged animals against the A-beta protein. Although the study was not successful in reversing cognitive deficits, this approach might have future treatment potential.
Hope that helps.
Scott x
This is really interesting!
It is clearly an area that we need to do more work on to understand.
I am pleased she is doing better!
Scott x
Thanks so much for the question… it is a good one!
The combined effects of hyperglycemia, ketonemia, acidosis and many co-morbid processes often causes significant electrolyte derangements in both DKA and HHS. Hyperglycemia-induced osmotic diuresis results in severe fluid and electrolyte losses. Ketones contribute to the solute diuresis via excretion of ketoanions, which obligates urinary cation excretion of Na, K and ammonium salts. Decreases in Na can also follow hyperglycemia. For each 3.44 mmol/L increase in glu, serum Na decreases by 1 mmol/L. If a patient has severe hyperglycaemia with normal serum sodium, their true sodium is probably high. This formula may underrepresent the effect on Na. Low Na concentrations can also be seen with hypertriglyceridemia, “pseudohyponatremia.” Insulin deficiency also contributes to solute loss as insulin stimulates salt and water reabsorption from both proximal and distal tubules and phosphate from proximal tubules.
In summary, the large increase in glucose in the circulation will draw water into the vasculature from the interstitial fluid and have a dilutional effect on the sodium!
Hope that helps.
Scott x
This is a brilliant question. Thank you for posting. I have tried to answer as many of the points as possible below:
There is a good post started about Slippery Sam catheters generally. I think there is a question now over using these catheters beyond initial unblocking.
Overall, the presence of a urinary catheter can predispose to infection as a result of ascending migration of bacteria into the bladder. Contamination of the bladder can also occur during catheter placement. I think it is also important to remember that the duration of catheterisation should be as short as possible. In humans the prompt catheter removal is considered one of the most infection prevention tools.
I think you are right about the repeated sedations, especially when it is questionable why the cat is having the urinary catheter changed at this regularity. A closed collection system is definitely the best way of managing these cases.
Overall, I am struggling to understand the need for regular catheter changes. One catheter placed aseptically and removed when no longer needed should be sufficient.
Hope that helps.
Scott x
This is a really good point. I have just been downstairs to check out what the data sheet actually says currently…
I think the issue was that when these catheters first came out there was no issue using them as longer term indwelling catheter. It was only after there was some instances of detachment that there became an issue. As Gail has said, the data sheen now specifically says that:
“the catheter and silicone hub are not permanently affixed to each other. The hub can be secured to the patient using the secure holes, but it is advised not to leave the catheter in place for more than 6 hours and the patient must be observed at all times”
The biggest problem comes now that the data sheet says this, we would have little come back if the catheter detached and we had to surgically retrieve from the bladder.
Hope that helps.
Scott x
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