if im certain there is no obstruction and room with cervical palpation/dilation I normally start of low and increase doses based on bitch response. I often find that they respond before you reach 0.5iu, but i have gone to this level once in a labradoor who wanted to sleep rather than welp 🙂 I also give calcium in addition which I find help increase contractions.if my patients don’t respond to a lower level of oxytocin I always want to check that calcium is adequate too.
=)
The x ray is of good quality and the dog seems to have excess fat so a high BCS.
there is small amount of osteophyte formation on some of the vertebrae which is to be expected with age.
the dog is intubate and microchipped
the heart is slightly enlarged as occupying more then 1/3 of the thorax on lateral and DV.it is also more than 2.5 rib spaces in size. the heart has increased sternal contact of the sternum.
i think is looks like some increased bronchial signs and multifolcal patterns on the lung field. maybe mix with bronchial and interstitial pattern?
my dxx would be
pulmonary oedema with cardiomegaly
tracheal collapse and negative pressure oedema
neoplasia
Thanks liz thats really helpful =). my first case is about a salbutamol MDI toxicity in a dog that developed hypokalemia and slight hyperglycemia. with everything eg treatment etc mentioned in the other structured fields. im not sure what to discuss.
would you talk about things like eg in human literature overdose of salbutamol has caused DKA but that this patient only had mild hyperglycemia or that other reports oral burns 36 hours post ingestion. so after the initial signs were stabilised, but our patient didnt develop anything whilst hospitalised 48 hours?
Thank you scott.
So either Lipid sink theory where increasing lipid in the body prevent lipophilic substances to attach to the body tissue by providing binding to the intralipid
or
enhanced cardiac metabolism: where the myocardial contractility might be subdued by drugs and contractility might improve my giving fatty acids?
sorry the dose was 0.02mg/kg- they contacted the ACP rep who said that it would be out of the system at 10 hours. the dog was having nystagmus but much brighter around 11pm. 12 hours after but started to lift his head around 9 pm. and ACP was given 10.30am.
there was no nystagmus or any circling or other neuro signs apart from hindlimb weakness and collapse prior to sedation.
if you contacted one of your neurology guys you might know what happend to the case. He went to wear referrals for further imaging, so it be interesting to see what they found
Hello Scott, how old was the animal, old/young? was it a shar pei?
Problem list:
anorexia,
reluctant to exercise
shifting lameness- discomfort on all limbs
bcs 3/9
tachycardia, possible pain related as dehydration 5%
Pyrexia
effusion both stifles, carpal and hocks
dehydration 5%
Thank you for your answer scott.
just to see that i got this right
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?
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.
I agree that generally we cannot say high lactate is lactoic acidosis or poor tissue perfusion, but in the interpretation along side this patients blood gas Metabolic acidosis the high lactate could be one of the causes for its blood gas result.
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