scott@vtx-cpd.com
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Areti!
So lovely to hear from you. Thank you so much for your questions as always.
I have popped some ideas under your questions below:
1)how long would you withdraw from meds causing lower T4 before consider testing for hypothyroidism?
It depends a little bit on the medication and the half-life of the medication. I would normally give a good couple of weeks free of medication before testing thyroid hormone levels. If there are any equivocal results I would wait a further 2 weeks and test again!
2)if you find elevated TgAA with normal fT4 what should you do? do you start tx or retest later on?
Positive TgAA results are associated with lymphocytic thyroiditis but may be present in the circulation long before a dog becomes clinically hypothyroid. As such, TgAAs provide no information on thyroid function. TgAA positivity, uncommon in dogs with non-thyroidal illness, is suggestive of underlying pathology. A positive TgAA does, indirectly, support a diagnosis of hypothyroidism. However, if the free T4 is normal I probably not treat at that point and re-test at a later time point as you suggest.
3) I am a bit confused with lymphocytic thyroiditis. Is it not the cause of hypothyroidism? or is it a concurrent condition? as on the chart of how to interpret results says if low fT4 and positive TgAA then lymphocytic thyroiditis with hypothyroidism. Are they not the same? (hope not silly question)
Acquired primary thyroid disease accounts for the overwhelming majority of dogs with hypothyroidism. The two main causes on a cellular level are lymphocytic thyroiditis and thyroid atrophy (equally common). Lymphocytic thyroiditis is a destructive autoimmune process characterized by multifocal or diffuse infiltration of the thyroid gland by lymphocytes, macrophages and plasma cells and progressive replacement by fibrous connective tissue. By contrast, idiopathic atrophy is described as a degenerative process with minimal inflammatory change and gradual replacement of thyroid tissue by adipose and connective tissue.
Ultimately both will result in hypothyroidism.
Lymphocytic thyroiditis is slowly progressive, causing signs of hypothyroidism after about 75% of the gland has been destroyed. Its progression can be divided into four stages. The rate of progression through these stages is variable, and not all dogs develop functional hypothyroidism. Approximately 20% of TgAA-positive euthyroid dogs develop hormonal evidence of thyroid dysfunction within a year of testing, but only 5% become clinically hypothyroid. Most dogs remain TgAA positive and asymptomatic, while a small number later test negative without evidence of thyroid dysfunction. Some TgAA-positive hypothyroid dogs later become TgAA negative, supporting the concept that thyroid atrophy represents an end stage of lymphocytic thyroiditis. Theoretically, the complete destruction of all thyroid tissue leads to a reduction in immune stimulation, absence of histologic thyroiditis, and conversion to autoantibody negativity.
Yes, low free T4 and positive TgAA are part of the same process and supportive of hypothyroidism. However, patients can be hypothyroid with a low free T4 without being positive for TgAA (see about). Please let me know if this is not clear.
4)would you start oral suppl. of T3 only if on higher end of dosage and no response or would you check for concurrent diseases first?
I would definitely check for a concurrent disease first. It would be very unusual to have to use T3 supplementation.
5)How do you support the diagnosis in breeds with lower circulating t4 especially in Greyhounds?
The key thing has to be compatible clinical signs and clinicopathological tests (is the cholesterol increased). TSH, free T4 and TgAA would then all be used to support a diagnosis. The fundamental thing would only to look for this condition in dogs with compatible clinical signs.
6)is there anything we can do in patients with congenital hypothyroidism? what is the prognosis/life expectancy?
With appropriate supplementation, they can do well and actually can have a relatively normal life. It all depends on how quickly the problem is detected as if not detected early, the growth abnormalities may be left as permanent changes.
7)and last question, when we say about concurrent illness, do we mean only serious diseases or could be anything like a simple infection on a nail base for example?
It really could be anything, definitely does not have to be a severe concurrent disease.
Thanks again for your questions. If any of this is not clear, let me know.
Scott 🙂
Lovely to hear from you all!!!!
Also lovely to hear what a small veterinary world it is!
Let me know if you have any questions at any time.
Scott 🙂
Hey.
I think the bottom line is that there is probably not a universal gold standard.
If the PDSA are recommending, I would honestly go with that. They are very careful and considered about the information they give to clients. I would consider this good information.
Do you have a website for your business? I would love to check it out.
Scott 🙂
What an interesting question!
Thank you so much Amy. I hope you are safe and well and enjoying the course.
I have looked in the literature and I am not able to find any actual peer-reviewed data. This genuinely may be because there is none. I will ask some ECC specialist colleagues to see if they know of any.
I did find some information on the Hills website which was helpful:
https://www.hillspet.com/dog-care/healthcare/how-to-help-a-choking-dog
I will ask our friends at Hills if they know any more.
Sorry not to be more helpful!
Scott
Emma,
We did do imaging. I will try and upload that today.
Scott
No problem.
Yes, I think if haematuria problematic I would trial treatment.
The human literature supports this.
Let me know how the dog gets on.
Scott 🙂
Thanks again for sharing Ashley.
I have popped images of the skin lesions below:
Let us know how the dog gets on. Great shout regarding RVC referral.
Scott x
Interesting!
Would be interested to hear the comments on the post result… that is still quite a stonker!
Scott 🙂
Hey Inga.
Really sorry about delay!
Really interesting question and one of my favorite drugs!
What other drugs is the dog on?
Tranexamic acid is an antifibrinolytic drug. It therefore reduces bleeding but, in certain situations, it may expose patients to a risk of thrombosis. It is used for the treatment of various types of bleeding, including menorrhagia, haematuria, certain surgical procedures and trauma. Its harm-benefit balance is favorable in certain situations associated with serious bleeding. The harm-benefit balance is different in minor bleeding: the expected benefits are smaller because the condition is not serious, and the risk of thromboembolism may be higher without the haemodilution associated with severe bleeding.
Clinical trials (human) conducted in serious haemorrhage or in patients undergoing surgery with a high risk of bleeding have not shown an increased risk of thrombosis with tranexamic acid. In practice, as of early 2013, the harm-benefit balance of tranexamic acid is favorable in severe traumatic bleeding. But when bleeding is not life-threatening, the thrombotic risk is too poorly documented to justify exposing patients to a plausible and inadequately evaluated risk.
I could find one specific human haematuria paper that overall did not represent a massive benefit (https://pubmed.ncbi.nlm.nih.gov/28916142/).
It has also been suggested that there may be a specific contraindication with bleeding in the urinary tract as tranexamic acid prolongs the dissolution of fibrin deposits already formed. Macroscopic haematuria is therefore
regarded as a contraindication for the use of tranexamic acid because this may lead to clots in the urinary tract with possible obstruction. I am not able to find any reports of this in the animal literature.So, in summary! I would probably only use it if the bleeding was severe and causing more severe side effects like a drop in PCV.
Hope that helps.
Scott 🙂
Hey.
Both pre and post results are often increased in cPSS but they do not have to be. Most of the time the post prandial is the most elevated value and is most helpful/diagnostic.
Hope that helps.
Scott x
Hey.
Really interesting question but really frustrating cases! I have seen a couple and not had any survive sadly. Anderson Moores are currently the leading centre for research and have some useful information:
https://www.andersonmoores.com/vet/CRGV.php
Anderson Moores will also offer a type of free PM service if the dog is PTS. THe main components of treatment are supportive:
1. IVFT to maintain perfusion/hydration. Be careful not to fluid overload if AKI. It is helpful to place urinary catheter and measure urine output. If anuric then furosemide could be considered but must be used with care.
2. I would administer antibiotics (amox/clav) IV is unwell and hospitalised.
3. other supportive care would include anagesia and maropitant.
4. I would be careful with doing too much topically with the skin wounds. I am a massive fan of Vetericyn spray for these sorts of situations.
5. Keep a close eye on electrolytes and obviously manage deficiencies appropriately.
6. There have been reports of the use of therapeutic plasma exchange (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6060235/). This procedure is only available in the UK at the RVC and Vets Now Glasgow.
Can you send some pictures of the skin lesions?
Hope that helps.
Scott 🙂
Thank you so much for sharing the radiographs.
I would agree with Liz’s comments.
You mentioned harsh lung sounds. Is there a crackle or a wheeze to be heard? 🙂
Scott
Great thoughts everyone!
I know the megaoesophagus was the easier one, but I wanted to share as it was a good example! I think they can sometimes be quite tricky to spot! We did manage to get this radiograph conscious. Sedation and GA can in themselves cause megaoesophagus, so I always try and get conscious when I can. We found no underlying cause, so I think idiopathic.
The pneumomediastinum was a real surprise in the other case! We really struggled to understand. The CT did not give us an answer… could it have been the blood sample!??! This dog presented with significant vitamin D toxicity. Hypercalcaemia resolved but respiration worsened. Severe interstitial pattern on CT. Sadlt we put dog to sleep, we got consent for PM, so will keep you posted. Still no explanation for the pneumomediastinum…
Pneumomediastinum is the abnormal accumulation of air within the mediastinum and it can be caused by a variety of mechanisms. Tracheal disruption can leak air into the mediastinum, and has been reported with cervical trauma, mechanical ventilation, transtracheal aspiration, tracheostomy, tracheal intubation and overinflation, or central venous catheter placement. Similar to tracheal trauma, oesophageal or pharyngeal rupture can result in pneumomediastinum. Subcutaneous emphysema from any location can eventually enter the mediastinum via the cervical soft tissues and thoracic inlet. Less commonly, air can enter the mediastinum from gas accumulation in the retroperitoneal space. In some cases, the cause of pneumomediastinum is not determined (spontaneous pneumomediastinum).
The presence of air in the mediastinum creates enhanced contrast and detail, allowing radiographic visualization of individual mediastinal structures (best seen on lateral images), including cranial vena cava, brachiocephalic trunk and left subclavian artery, oesophagus, and azygos vein. Visualization of the tracheal wall is enhanced due to the presence of both intraluminal and extraluminal air.
Scott x
Really interesting Gail.
Thank you for sharing your experience of gabapentin!
Scott 🙂
The trazodone/gabapentin in blocked cats is a brilliant idea Jack.
I am going hunting for literature now… if it is not there then this might be the first official vtx study!
Is the liquid gabapentin Bova?
Scott x
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