Hi, my name's Fiona. I'm a boarded medic working at North Down Specialist Referrals in Surrey. And thanks so much for joining me in this webinar, and with the webinar ve entitled What's new in Hyperthyroidism.
As we all know, hyperthyroidism is the most common feeling endocrinopathy that we see. And straight up, it's an endocrinopathy, it's very close to my heart. As a previously hyperthyroid person myself, I've had lots of these treatments and I've been through some of this process.
So I feel really, A kinship with these guys and I really hope that, by talking about things that are new, that we can have a big opportunity as a group to make a difference to these patients that we obviously see quite commonly. So the clinical signs of hyperthyroidism clearly will be no surprise to you guys. So, generally speaking, these cats, are showing evidence of their kind of hypermetabolic state, they're polyphagic, they're losing weight, you may be seeing increased activity levels that might manifest itself as restlessness and vocalisation.
. It is likely that the hyperthyroid cats that we identify nowadays are less significantly affected than the cats that were identified when this disease was considered more novel in the 1980s. I am probably due to more diligent owners, and lots of vet vigilance, annual checkups, etc. It is suggested that about 10% of hyperthyroid patients present in what they call an apathetic state, so and with lethargy and reduced appetite, .
But the vast majority of them will look like they're in a kind of hypermetabolic state. It's often stated that hyperthyroid cats don't feel unwell. And always difficult to avoid anthropomorphizing, but as someone who's hyperthyroid myself, I beg to differ.
It doesn't feel very nice, at least it didn't feel very nice for me. I am so I kind of presume that our feeling patients might feel the same. The clinical signs of this disease can be unpleasant both for the patient but also for their owner.
I am so. They're begging for food, they're restless, they're yowling, they're waking up at night, etc. I am.
It's unusual for cats to die of hyperthyroidism. Probably the main potential way in which that can happen is development of congestive heart failure associated with the cardiac changes seen in this disease. I am, but euthanasia is also a potential consequence due to perceived poor quality of life, both for the patient and for the client.
And so, although it's a really common disease, it's one that we're really familiar with, and it's probably unpleasant for our patients and it can certainly be unpleasant for our owners. So in this lecture, we're going to touch base on diagnosis and treatment options, and then we're going to talk more about some of the the newer stuff, sort of the part of what's new in hyperthyroidism in this lecture, thinking about the relevance of renal disease, and also the importance of hypothyroidism and when we're thinking about managing these patients. So hyperthyroidism generally, as we know, is a benign process.
And important to remember that the majority of patients have bilateral disease. So 70% of patients will have a bilateral process affecting both lobes of the thyroid gland, . It's important to remember that because sometimes appreciating the bilaterality of it with our fingers on digital palpation isn't always easy.
So if one gland is substantially larger than the other, it doesn't mean that the other is definitely not affected. And sintigraphy demonstrates that really, really nicely. It's just a tool that isn't widely available for us clinically.
But if we know or think that the condition is likely to be bilateral, and we know that in 70% of patients it will be bilateral, that should make a difference to how we think about treating these patients and thinking forward to surgeries and all these types of things. Important to hone your skills on thyroid palpation. A goitre is palpable in the vast majority of hyperthyroid patients.
The literature would suggest somewhere between 80 and 100% of of hyperthyroid patients. But when you get good at thyroid palpation, and I would strongly suggest that really any patient over the age of 8 or so should be having its thyroid specifically palpated. And you can feel the thyroid in a lot of these cats.
The literature varies a bit, but probably I am in a sort of senior cat, and you will have somewhere between 20 and 75% chance of palpating the thyroid. When you detect what you think is an enlarged thyroid, the bigger the thyroid is, the more likely it is the cat is truly hyperthyroid. So by the time you're feeling a 5 millimetre nodule, it's very, very likely this patient has thyroid pathology and has hyperthyroid.
And the size of the thyroid nodule doesn't correlate terribly well with the functionality of it. So, if you're diagnosing a patient with a subtle thyroid nodule, or one with a massive goitre, it doesn't mean the one with a massive goitre will have a total T4 that's substantially larger than the other, for example. But yeah, it's worth having a revision of different thyroid palpation techniques.
There's two main ones. And if you're sort of wondering whether the cat could be hyperthyroid from its clinical signs and you don't appreciate it with the first technique, it's definitely worth having the other one in your arsenal because it will increase your likelihood of picking up in these guys. So as you all know, hyperthyroidism in the cat, I am hyperfunctional thyroid tissues, so we get overproduction of the thyroid hormones, and by the principles of negative feedback we get suppression of the hormones prior to that being released from the hypothalamus and the pituitary gland.
And diagnosis of hyperthyroidism is generally fairly straightforward, of course. So 90% of hyperthyroid cats will be able to be diagnosed on a total T4 alone. OK, lots of these and senior cat profiles will include a total T4 in all their older cat profiles.
But usually it's a pretty straightforward diagnosis to make. The important exceptions to that rule is where the disease is perhaps early or mild, so the cat doesn't have raging clinical signs perhaps, and or where there's a concurrent and non-thyroid or illness. And so in pretty much any illness, we can see suppression of the thyroid hormone as a consequence of that other illness.
So be that chronic kidney disease, be that a chronic enteropathy, and be that and terrible dental disease. So the presence of other disease in your patient may reduce your total T4, making it less likely to pick up a true hyperthyroid state that is existing. In instances where your total T4 has not enabled you to make a diagnosis of hyperthyroidism, but you remain suspicious, then looking at free T4 is a good next step.
The reason why we don't recommend doing free T4 as a sole test is that it can be elevated in other illness. So in up to 20% of patients with other illness, the free T4 will be high, . In a hyperthyroid cat where the free T4 is high, we expect the total T4 to be at the high end of normal, really, OK, so they certainly the upper part of the reference range.
In an unwell cat with an elevated free T4, we expect the total T4 to be, you know, a long way away from the upper part of the reference range, so probably in the middle or lower part of the reference range. So this is the reason why I would absolutely not recommend using free T4 as the only test, although the sensitivity of this test is good, the specificity is bad. And so the chance of you erroneously making diagnosis of hyperthyroidism is higher if you're only looking at free T4.
So to T4 is a first step, adding the free T4 if you don't make the diagnosis on the the initial test but you remain suspicious. The diagnosis of hyperthyroidism is generally fairly straightforward. Let's look next at the treatment options.
So essentially the treatment options for these guys, there are 4, right? So the first option is anti-thyroid medications by mouth. Nothing particularly new in this sector, the only newish thing is the fact that there is an oral suspension, which can make it much easier for some clients, but otherwise these drugs have been around for a long time, we all know the side effects, they're very strongly efficacious, etc.
Etc. . A second option, is, diet, so that's an iodine restricted diet.
Has very much waned in popularity since its initial release. And it's fairly unusual to use it at this point. Lots of reasons for that.
The food has to be fed absolutely exclusively, so no treats, nothing like that, which can be really difficult in a multica household or just in a household where the cats enjoy treats as interaction with their owners. I am palatability of the diet isn't wonderful, so lots of cats will reject the diet. And although the, diet typically will cause, control of the thyroid hormone levels, the clinical improvement in these patients sometimes isn't quite as robust as we might expect in other settings.
So at this point, I very rarely see patients on the diet, and I would really reserve it for patients that have failed medical treatment and cannot have definitive therapy for some reason. So perhaps the, the cats, have had adverse side effects on oral medication and we need to have another short term plan, or potentially a long term plan, but it's an unusual thing to, to, reach for as a first choice in this setting. And next option, of course, radioactive iodine, and generally considered to be the gold standard by most people.
And the fourth option, is thyroidectomy, so surgical removal of the thyroid gland. And so 4 different choices. I am.
What defines the choices? What do we choose most commonly? So this is a nice study from Paul Higgs, from around 10 years ago, 600 odd vets.
I am unsurprisingly, the first choice for most of these patients is oral medication. I am vets said the next choice they would tend to make would be thyroidectomy, it's radioactive iodine coming in at the bottom of the pile, at only 6%. And this study was performed before the widespread use of umYD, the iodine restricted diet, so it doesn't really feature in this study.
But basically, oral medication is absolutely the forerunner in terms of the choice that people and reach for when diagnosing a hyperthyroid cap. Things that the participants of this study cited as important considerations for them when selecting treatment choice and owner compliance and ease of administration were cited as number one. Great, that makes a lot of sense.
Although, I guess you could argue that actually the commitment to orally medicate your patient lifelong is actually less appealing than some of the definitive options. So I don't think it's the, the sole choice that that guides people's decision making, obviously. Comorbid disease, cost of treatment, and cost of monitoring or other big contenders.
So costs clearly another really important consideration. And how does it stack up looking at these four options? Medical treatment, which is the most commonly selected choice, is one of the less expensive options.
So, depending where you are in the country, etc. You're probably looking at somewhere between 1000 and 1500 pounds for the tablets alone or the suspension alone over a 2.5 year period, roughly, does not take into account the cost of monitoring, which would have a very significant contributing to the cost there.
I am. The iodine restricted diet is fairly similar to the cost of medical treatment, I suppose you then can save money on not buying the cat any other food, but so they're fairly equivalent. The definitive treatment options, thyroidectomy or radioactive iodine are more expensive on upfront costs on face value.
So depending on where you are in the UK, probably looking at somewhere 10,000 pounds and 2000 pounds for thyroidectomy, presumably you don't have any significant complications afterwards, like postoperative hypoparathyroidism causing hypocalcemia. And radioactive iodine, and it probably, again, depending on where you are in the country, somewhere between 2 and going towards 3000 pounds. The cost of radioactive iodine has jumped quite a lot in the past few years, primarily due to availability issues with the radioactive iodine.
And so that's how these treatments compare on initial glances. But if we start to then think about what's the average survival of a hyperthyroid cat. And then most cats with hyperthyroidism don't die of hyperthyroidism, they die of other things associated with older age, because of course, most of these patients are in their senior years.
So the average hyperthyroid cat will live between 2 and 4 years. If you have a patient who lives longer, the apparent sort of cost saving, if you like, with medical treatment or dietary treatment disappears, OK? So although the upfront cost of the definitive treatments like surgery and radioactive iodine may be off-putting, if you're diagnosing a younger cat with hyper hyperthyroidism, who's thus hopefully likely to live longer, .
When you tot up through this cat's journey of life, the definitive treatments may actually end up being less expensive. So something really important to sort of consider. The other really important thing to consider, which has definitely been understated historically, is that hyperthyroidism is a progressive disease.
So cats who come into you with hyperthyroidism will essentially become more hyperthyroid as the years pass. If you are managing the cat with medical treatment, or potentially with diet, let's say, you're going to have a harder and harder time controlling this cat's hyperthyroidism. So oral medication doesn't really take into account the progressive nature of this disease.
This is a great study by Mark Peterson, basically charting hyperthyroid cats through the remainder of their life. So if we look at the graphs in turn, and we can see here that about 70% of patients have bilateral disease, and these patients are all classified on the basis of centigraphy, so this is like robust data. On presentation, some of these cats, so about 35% of them had unilateral disease, but the proportion of them that have unilateral disease declines over time.
And the proportion of patients who have multifocal disease, so hyperfunctional thyroid tissue beyond the thyroid lobes, increases a lot. So at the point of diagnosis, the prevalence of tissue elsewhere, which I guess we would probably call ectopic tissue, right, is about 3%. By the time you're looking at this group, 4 or 5 years post diagnosis, a third of them have tissue elsewhere.
And so again, this has got to be relevant when we're thinking about how we're going to treat these patients. Because if you're having problems medically controlling a patient who's been hyperthyroid for 4 years, and you're not managing to control the problem medically, and then you think, well, perhaps I'll now go for surgery. Surgery on a patient who has ectopic tissue elsewhere is destined to failure.
So this is really important data. Mark Peterson in this paper suggests that we should move away from the concept of thinking about benign thyroid disease versus thyroid carcinoma and sort of argues that I'm, you know, advanced, benign thyroid disease is really difficult to tell apart from a thyroid carcinoma. Both of them who are present in many sites, both of them can be large and very functional.
So they suggest that we move towards a classifying sort of big and hyperfunctional patients that's something called SIMRAD, so it's an acronym for severe hyperthyroidism, huge disease, intrathoracic disease, multifocal disease, or refractory to anti-thyroid drugs. So they suggest using this term shimrad. And basically these are patients that are causing you a nightmare because you're struggling to control them.
So at the point of diagnosis, we don't really have a problem controlling hyperthyroidism generally, right? So it's unusual to have any issues establishing medical control in a newly diagnosed patient, but if you're then managing this patient for 5 years down the line, the chance of you having big problems slash not being able to keep their total T4 at a sensible level is about 20%. So it's a progressive disease, and these things can become a problem because if you're going up, up, up with the dose of medical treatment, and as time goes by, you may encounter the negative side effects of the drugs.
So if you have to ply them with large doses of methimazole, carbimazole, you may well end up in a situation where you're causing GI side effects and stuff, and the tolerance of the drug is lost, and then you're in a bit of a sticky situation. So this is a sort of newer way of thinking, but being mindful of the fact that this is a progressive disease and that if you are managing a patient for 4 years plus, you may well find it difficult as the years pass, . It's an important thing to be aware of, and it's a strong push towards thinking about definitive treatment, particularly in younger cats.
So where you're diagnosing a cat that's 1011, even 12, that hopefully has quite a long life ahead of it still, and you should probably be guiding the owners with more and more like pushing them a little bit more strongly towards a definitive treatment. And the definitive treatment of choice in my eyes has to be radioactive iodine. The recurrence rate of, hyperthyroidism following bilateral thyroidectomy is somewhere between 5 and 50%, depending on the study.
So it's not insubstantial. So if you do a bilateral thyroidectomy, everything's going fine. Two years later, the hyperthyroidism re-emerges.
You know, you obviously you could then manage the patient medically, but maybe back into the same situation. So I think knowing that this disease is progressive and that it may become more challenging to control as the disease sort of grows like so to speak, has to motivate us to present radioactive iodine and more strongly to owners with younger cats. So this is the kind of newer thing, something certainly I wasn't taught, when I was in the earlier stages of my career, and it's a really strong, rationale for using radioactive iodine, particularly in younger patients.
In a couple of studies have looked at the owner's perception of how they were guided through the hyperthyroid cap process if you like. What people say and what people do can of course be different, but one of these studies suggested that 50% of people said that costs had no impact on what treatment they were selected. And importantly, a substantial number of clients said that radioactive iodine had never been discussed with them.
It's really difficult talking about finances of clients. I definitely find it difficult and it continues to challenge me in my career, and I think we all can be guilty of trying to, Guests, clients, financial situations avoid making them feel uncomfortable or that they're not able to offer their pet the care which might be presented as gold standard. But it's important that we do present all the options and explain the pros, cons and each of them, and of course the costs of them.
And so, you know, clients need to be making informed decisions. Something else that was cited in Paul Higgs' study by the vast majority of vets, when in that they were thinking about when selecting a treatment for their hyperthyroid patient was the presence of comorbid disease. Super important.
The one which springs to mind for all of us, I'm sure I am is chronic kidney disease. So let's look more into this. So we all know chronic kidney disease is common in older cats, common cause of death, 1 in 3 cats over the age of 12 will have chronic kidney disease.
We know all the figures. Hyperthyroidism is of course a disease of older cats, so unsurprisingly, the two coexist commonly in our older feline population. The problem of course comes in that hyperthyroidism can mask, chronic kidney disease.
So when you become hyperthyroid, everything goes into overdrive. So you get, a huge, increase in your cardiac output, sort of up to 60%. So due to changes in stroke volume and heart rate, and, your renal blood flow goes up, your glomerular filtration rate goes up, and as a consequence, your creatinine drops.
So we may not recognise that a hyperthyroid patient has dysfunctional kidneys because the kidneys are essentially gonna going in overdrive and because of the hyperthyroid state. When we then go ahead and treat these hyperthyroid patients and return them to you thyroidism, we see this renal dysfunction emerge, so called unmasking the chronic kidney disease. And it's what we were all taught for, you know, many years, right?
And it does happen. It's true. Probably happens in around 25% of hyperthyroid cats.
On average, it's about a 1 in 4 chance when you treat hyperthyroid cats, that you will unmask renal disease. It's a useful figure to give to a client. So can you predict for an individual patient, whether they are likely to be one of the patients where chronic kidney disease is unmasked when their hyperthyroid state is controlled.
And so urea and creatinine are not very reliable. OK, so urea is affected by the hypermetabolic state, so protein metabolism can increase your urea. But the PUPD seen in the disease can reduce the area.
Creatinine is derived from muscle mass, so when you have a low muscle mass, your creatinine can be lower, so creatinine is, often lower in a hyperthyroid patient. If they had, elevated creatinine in the hyperthyroid state, it is likely they have true chronic kidney disease. But otherwise the creatine isn't very, very useful.
Urine specific gravity unfortunately can be affected by the hyperthyroid state itself, so these cats can often be heat intolerant and drink a lot as a consequence, so dilute urine as a consequence of that. They can have a nephrogenic diabetes incipidus, in the hyperthyroid state. So a reduced urine specific gravity is really common in hyperthyroidism and does not mean that they will go on to have unmasked renal disease.
If you see a hyperthyroid patient and their USG is high, so more than 1035. It's less likely they will go on to have unmasked renal disease, but unfortunately not impossible. So USG is a bit more useful than your creatinine, and if it's high, it's less likely they'll go on to have unmasked renal disease, but otherwise, kind of all bets are off.
And protein in the urine is a common consequence of the hyperthyroid state, often resolves when you address the hyperthyroidism, so that's not very helpful. What's the deal with SDMA SCME is kind of like the new kid in the block. And what does the literature say about how useful that might be?
So I'm sure you probably know SDMA is more sensitive for detecting renal dysfunction, so SDMA will be elevated when you've lost about 40% of your renal function, and whereas creatinine should only be elevated when you've lost 75% of your renal function. So SDMA does elevate sooner. Idex data derived from going towards half a million cats, which is huge numbers as far as veterinary medicine is concerned.
Showed that hyperthyroid cats were less likely to have elevated creatinine than other kind of adult senior cats, which is what we talked about. So we said that hyperthyroidism creates a sort of hypermetabolic state, increases GFR, suppresses the creatinine, that all makes sense. But interestingly, there was a much, closer, connection between the SDNA elevations in these two populations, .
SDMA isn't affected by muscle mass, so that's one thing that it has over creatinine, so to speak. But it is a product of intracellular cattabolism. So where you're in a hypermetabolic state, it's it's possible that your SDMA could be elevated because of this.
So it does suggest there could be problems where hyperthyroidism could affect your SDMA levels. STMA is exclusively excreted by the kidney, which is good, but it also means that it could be vulnerable to the same changes in you know blood flow and GFR that things like creatinine do as well. So in reality, does STMA perform better than, you know, creatinine and neurons specific gravity at predicting which patients might go on to have unmasked renal disease.
This is a study by, Mark Peterson, which basically, looked at cats who had treated hyperthyroidism and compared the ones that went on to have unmasked renal disease with those who did not. So. What we can see is that the, the blue group are the patients who remain non-azotemic after treatment, so they have radioactive iodine, they've returned to your thyroidism, but they're they're non-aoemic.
The red group are those who go on to develop azotemia. And what we can see is the patients who go on to develop azotemia, about a third of them had elevated SDMA prior to treatment. So in this study, basically a third of the cats who had unmasked renal disease had elevated SDMA prior to initiating their hyperthyroid treatment.
And not really any other cats did. So in this study, it said that if you had elevated SDMA prior to hyperthyroid treatment. It was a strong indicator that you would go on to have unmasked renal disease, but only a third of the cats that went on to have unmassed renal disease had elevated estimates, elevated STA is a strong indicator that you would go on to have unmassed renal disease, but only 1/3 of cats showed it.
. Like everything else in the world, I am, is, is still up for debate. OK, there are other studies that absolutely disagree with this. So this Borisova study is a small study, of only 10 cats, but they did see, you know, a group of hyperthyroid cats that had elevated SDMA prior to their hyperthyroid treatment that normalised after redirective iodine.
I think probably where it stands is the SDMA is, is not perfect at predicting those that will have unmasked renal function. It seems quite likely that thyroid status, renal function and SDMA have a complex interplay. There is an inconsistent relationship between GFR and SDMA in hyperthyroid caps.
I it's probably I am. The best indicator at predicting unmasking renal function, but it absolutely cannot be taken as red and cannot be used in isolation. So more information needed, I would definitely say to a client where the cat had elevated STMA prior to treatment, I think there's a reasonable likelihood that your patient will go on to have amassed renal disease, but we'll just have to wait and see.
OK, and unfortunately they just have to wait and see. I am saying is how it is, when thinking about, predicting which patients will have unmasked renal disease, once you treat their hyperthyroidism. It doesn't really matter.
That that's the key point, right? So, it was cited for years and years and years and years that if you unmasked chronic kidney disease once you treated a hyperthyroid patient, that they would have a less good outcome. OK, we were taught this for years and years and years.
And it doesn't seem to be true. So this is Tim Williams study from 2010, a really important study basically showed that in the patients that had an unmasked renal disease following the treatment of their hyperthyroidism, there was no difference in their long-term outlook compared to the cats that did not have unmasked renal disease. So typically cats who have unmasked renal disease following hyperthyroid treatment have mild CKD, so typically it's gonna be like an iris stage 2, something like that.
And you just manage them as you would manage any other CKD patient. And the average outlook for a patient in that setting will be somewhere between 1.5 and 4 years.
Most of these patients are senior patients. I am in their later years and, you know, something's gonna get them basically. So unmasking renal disease absolutely should not be feared.
It doesn't make a difference to their outlook, and this is a key point, a massive change in the past sort of 15 years from what went before. But because we've had it drummed into us that unmasking chronic kidney disease worsens their outlook, and people are frightened of that happening. So in this study, that's from almost 10 years ago, it said 50% of vets deliberately undertreated hyperthyroid cats with unmasked renal disease, so they chose for them to have higher T4 levels during the treatment phase of their disease, basically to keep the creatinine a bit lower.
I want to explain why doing that is not the best of plans and for quite a few reasons. If we use the analogy of a dehydrated anaemic dog, so let's say this dehydrated anaemic dog comes into the clinic with a PCV of 22%. OK, so the dehydrated patient is missing basically fluid, right?
So the PCV of this patient is arttifactually elevated because the height of the red blood cell column in the hematocrit tube is proportionally higher because essentially they've not got enough fluid on board. OK. If you rehydrate that patient, and basically restore the fluid volume of this patient.
The number of red blood cells the dog has is exactly the same. So this dog's oxygen carrying capacity is exactly the same, but the number will drop, OK, because the height of the red blood cell column relative to the height of the plasma column will be less, OK? The number is less, but the number of red blood cells is exactly the same, OK, and the dog is in a better position, much better to be a properly hydrated anaemic dog than a dehydrated anaemic dog.
If you chose not to rehydrate the patient to avoid reducing the PCV, the only person you are treating in inverted commas is yourself, OK? You're leaving the PCV artfactually elevated to make yourself feel better, but actually the dog will feel better once you have rehydrated it. And choosing to leave a cat.
Hyperthyroid to keep the creatinine number a bit lower. Again, the only, the only person that sees that number is you, the cat doesn't care. The cat isn't going to have any more functional nephrons, as a consequence of you leaving it in a hyperthyroid state.
So, choosing to undertreat a hyperthyroid patient with CKD so that the creatinine number stays a little bit lower, it is not a benefit to your cat. It's it's probably actually the opposite, so. It's considered highly likely that the presence of a hyperthyroid state is actively bad for your kidney.
OK. So you get RAS activation. We know that aldosterone is you know, toxic to the kidney.
I they will, they And glomerulli will have hypertension within them, more prone to glomeosclerosis, proteinuria, we know proteinuria and predicts a shorter outlook for patients with CKD and it's highly likely that hyperthyroidism accelerates, the decline of renal function. So you and I know that deliberately undertreating hyperthyroid cats with chronic kidney disease to make the number lower doesn't make sense for lots and lots of reasons. It doesn't make sense because cats with unmasked kidney disease following hyperthyroid treatment don't have a different outlook.
Doesn't make sense because, you know, you're just generating a lower creatinine number to make yourself feel better, not the cat. And doesn't make sense because the hyperthyroid state will probably accelerate the decline of the renal function. So even when they have an unmasked renal disease, it's really important that you treat their hyperthyroid state as actively as you would have, had their creatinine ischemia, etc.
Being normal. And so really important take home message. I am and a really important message out there.
I'd love you to share it with the rest of your team. Now we we know what hypothyroid dogs and hypothyroid people look like, but I'm not really aware of having seen cats that look like this. So what do hypothyroid cats look like?
Annoyingly, they just look like normal cats, OK, so hypothyroid cats do not present in in the grossly obvious way that many hypothyroid dog patients do. But although they look normal, physiologically, they are experiencing negatives as a consequence of their hypothyroid state. So if you compare a new thyroid cat to a hypothyroid cat, the hypothyroid cats have lower heart rates, higher body weights, higher creatinines, etc.
Now the tricky bit is if you are monitoring a hyperthyroid cat that you're actively treating, be that you're giving it methimazole or you've done a thyroidectomy, something like that. You'll be pleased if you see weight gain, right? So some of these things, a lower heart rate, a higher body weight, would be things that you would almost be what you'd be hoping for when you address the hyperthyroid state.
So identifying hypothyroidism on the basis of examination and clinical signs in a cat is not going to happen. But the problem is hypothyroidism is really important and it's really important, you need to recognise it. And so it's thought now that of the cats who developed an unmasked azotemia following hyperthyroid treatment.
2/3 of those patients may be hypothyroid. So lots and lots of the cats which we are treating for their hyperthyroid state. Maybe accidentally ending up hypothyroid, and that is not doing them any favours.
But maybe you're thinking, yeah, but you told me unmasking renal disease doesn't alter prognosis. And for a new thyroid cat, that's absolutely true. So, new thyroid cat undergoing hyperthyroid treatment, unmasking renal disease does not affect outcome.
But when you make that cat hypothyroid and easyotemic, It impacts outcome. So Unmasking renal disease, after treating hyperthyroid cat, as long as it's your thyroid, not a big deal, but if your cat is hypothyroid. The prognosis is worse.
Now the good thing about that is hypothyroidism is really easy to address, right? So if the patient's on anti-thyroid medication, you just back off a bit. If the patient's had radioactive iodine or thyroidectomy, you can supplement it with levothyroxine.
And when you do that, you will drop their creatinine, OK, so the creatinine drops by on average 20%, 50% of. Amic patients, I'm in this study, and when they were supplemented to restore their thyroidism from their hypothyroid state, they weren't aotenmic anymore. OK, so supplementing them will often magic the the renal situation better.
And in this small scale study, and it changed the prognosis. OK, so. It's a bit of a switcheroo from, you know, 15 years ago, we were all told that, unmasking renal disease when you treat a hyperthyroid cat was a disaster and should be avoided at all costs, and we know that's absolutely not the case.
And we never even batted an eyelid about hypothyroidism. We didn't even think about it, but actually, it's really important and Prognostically for these patients is really important. And when we have in a patient, particularly one where azotemia has developed after hyperthyroid treatment, we should be interrogating them for hypothyroidism because being hypothyroid will worsen their outlook, and we can fix that.
So hopefully you're on board with me and I'm, you're sort of coming over to my side of the table. But how common is hypothyroidism? It's just something I'm rabbiting on about, or is it something that we actually see?
It's really common. OK, so in the patients, in the hyperthyroid patients that we are treating, a large number of them are hypothyroid. So in medically managed, cats, around a third of them are hypothyroid.
This is a really common endocrinopathy. We're probably all managing plenty of these cats. So probably quite a lot of the cats we're managing are hypothyroid, and we have, we don't know about it, we haven't thought about it, and it's important.
OK, so this is common. Hypothyroidism can be transient after the definitive treatment, so after surgery we need active iodine, it can be transient while the pituitary sort of recovers to produce enough TSH and while the remaining thyroid tissue kind of reactivates. So it can be that it can take sort of 36 months to sort of wake up again.
So the hypothyroid state can be transient for up to 6 months maybe. After surgery or radioactive iodine, so you could wait and see in those patients, but if they experienced a precipitous renal unmasking after their surgery and they looked hypothyroid, I would definitely jump in and treat them as if they, as if they were. On the flip side, it can be that hypothyroidism can take quite a long time to emerge.
OK, so, and if you've got a medically managed patient, you might see it, you know, pop up at some point in the future where it wasn't there 3 months into treatment, for example. So it's definitely a dynamic state. So how do we detect hypothyroidism?
So it seems straightforward, right? We should have hypothyroidism, the thyroid's not doing enough. We've got low thyroid hormones, elevated TSH, it should be straightforward.
So if we check the total T4 of patients, and these patients are all classified by sintigraphy, so I really kind of active functional information, and annoyingly, only half of the truly hypothyroid cats had a low T4. OK. .
Annoying, I am. And you think, well, how can that be? The problem is that when you look at the reference range for a T4, let's say between 12 and 52 or whatever your lab says, and that's the population reference range.
Each of us actually has quite a narrow and individual reference range, so you will hover in a much, much smaller part of that reference range. So you could be hypothyroid, but still within the reference range, but, but your individual T4 has dropped out with your individual reference range, and it's just the population reference range can't capture all that individual information. So only 50% of hypothyroid cats had a total T4 below the population reference range.
And the other problem is that, cats who have chronic kidney disease will often have suppressed total T4 because of their other disease. So basically a low T4 is not a great way of picking up hypothyroidism in cats. So only 50% of hypothyroid cats will have a low T4.
And you can have a little T4 for other reasons. And so what about free T4? We know that we use that when picking up early or mild hyperthyroid cats, for example.
The great thing is, TSH is brilliant at identifying hypothyroidism in cats. And so in this study, which is a pioneering study by Mark Peterson. All the hypothyroid cats had elevated TSH and none of the other cats.
So TSHH works brilliantly in cats to identify hypothyroidism. And interestingly, although it's a canine assay, it works way better for picking up hypothyroidism in cats than it does for picking up hypothyroidism in dogs, where TSH is only elevated about 70% of dogs. But yeah, TSH is basically what we need to identify hypothyroidism in cats.
So take home message, TSH is the test of choice. OK, elevated TSH identifies hypothyroidism in cats. And, reference range total T4 or free T4 absolutely does not exclude hypothyroidism in a cat.
Now historically, we've been told to aim for a total T4 in the lower half of the reference range when treating hyperthyroid cats with medical treatment, for example. But the problem is that that's not going to pick up hypothyroid cats. We know that half of hypothyroid cats will have a total T4 within the reference range, probably going to be in the lower half, right?
So TSH is really important, OK. You might want to add it routinely, so every hyperthyroid check you do, you just do a TSH and T4, so you get both pieces of information from the off. Or you might say, well, if the T4 comes back in the lower half of the reference range, then I'll add the TSH and the lab should be able to do it on the sample you've already sent them.
But TSH basically should be a really important feature of your hyperthyroid cat monitoring. So this is like newest information. I would love you to take this home as like the big take home message from this lecture.
TSH in cats is really important, hypothyroidism in cats and kind of hyperthyroid treated cats, super important. And then alter your treatment to normalise the TSH. If the cat's on medical treatment, back off a little bit.
If the cat has had surgery or radioactive iodine, some time ago, I don't think it's transient, and then jump in with levothyroxine and do using the oral suspension will be the easiest way to do it because you can titrate that quite finely. So, take home messages so far, I would love you to take home that, definitive treatment, particularly radioactive iodine, should be, we should lead with that, particularly for young cats, and remember that hyperthyroidism is a progressive disease, and, and it can become bigger, more multifocal, more difficult to control as the years pass. I don't be scared of unmasking renal disease.
I am the prognosis should be the same, but we really, really vigilant, looking for hypothyroidism in cats, and when you have treated their hyperthyroidism, be on it, make TSH part of your, practise management for monitoring these cats, and you will change some of their lives. Just wanted to end with a little case example. So this is a 10 year old female neutered domestic short hair, a short history, a few days of acute onset blindness, according to the owner, non hyperthyroid, cat's been on carbimazole for 8 weeks and when the TT4 was checked, 2 weeks ago, I was in the middle of the normal range, TSH sadly was not checked, .
On examination, bilateral goitre was there before, systolic heart murmur, which was their diagnosis 8 weeks ago, not been investigated further, weight and body condition stable. And this is your cat. OK, so hopefully you can see just on the gross image, you can see the retinal vessels and you can see that sort of billowing kind of curtain appearance of the back of the eye.
So grossly you can tell that this patient has bilateral retinal detachments. Here is a funduscopic image showing the same. So the patient has, retinal detachments, differentials for that big player hypertension, OK, various causes, including hyperthyroidism, surprise, surprise.
OK, other possibilities, things like, trauma, chorior retinitis, neoplasia, etc. . That in this patient it's going to be absolutely key to check the blood pressure, knowing the patient has an underlying predisposing cause.
And hypertension is quite common in hyperthyroidism, so probably around 15% of hyperthyroid cats are hypertensive at the point of diagnosis. But really important to recognise that a further 20% will develop hypertension as their journey progresses. So even when the patient is thyroid moving forward, hypertension can develop.
So could this be the explanation for this little cat? Yes, so marked hypertension, systolic blood pressure, 210. And how do we interpret that?
So this table is from a really useful, blood pressure consensus, statement from Aero, 2018. And this is the current, recommended classification. So this patient has a systolic blood pressure of 210, so definitely classed as severely hypertensive.
Always a problem when we have hypertension though is, is it true hypertension? Is this patient truly got high blood pressure, or could it be in situational hypertension or so called white coat hypertension? And this consensus guideline that this paper is taken from have some great and flow charts on.
How to interpret blood pressures, when to recheck them, when to institute treatment. I am, and I'm going to show you one in the next slide. So their recommendation very, very sensibly is that when you recognise that a patient has hypertension, your assessment of that blood pressure will be affected by whether target organ damage is present.
So this patient has retinal detachment, we know hypertension is a really important cause of retinal detachment. We've got to take this blood pressure as likely to be true, particularly when we add in the fact the patient has a known predisposing cause for hypertension. So really immediate treatment is appropriate for this little one.
Now unfortunately this patient did not have its blood pressure quantified at hyperthyroid diagnosis. So we have no idea whether this patient's hypertension could have been intervened with at an earlier point to potentially have avoided these retinal detachments. But we also know that hypertension commonly develops later, so after your thyroidism has been established.
Which makes it really tricky when you're, monitoring these patients because we need to be on these patients' blood pressure regularly because if you're a patient that's normal intensive at diagnosis and becomes hypertensive at a later point, we have to keep monitoring the blood pressure of these long-term thyroid patients to try and catch them, to try and avoid kind of irreversible consequences of hypertension, like retinal detachments. These hyperthyroid guidelines from Dami and set out the recommended plans, so they say blood pressure at diagnosis, and then basically at every check thereafter. So, and when you see them back 23 weeks later for their first C4 blood pressure, when you see them a month later, blood pressure, 3 months, blood pressure.
So blood pressure monitoring should definitely be part of the long term management of these patients. It's very clear what the recommended drug for hypertensive cats is, amlodipine, and there's also some great guidelines to tell you what dose to use, basically, if their blood pressure is more than 200, they need 1.25.
That's regardless of how many kilos your cat is. And if the blood pressure is less than 200, then probably, half of that, so 0.625, will be fine.
There are a couple of good studies looking at Talmazartan, as an anti-hypertensive, it is pretty effective, but it hasn't been tested at higher blood pressure levels. I am, so it's unclear. I would say amlodipine is, is definitely the first line.
Recommendation. It may be that in the future, particularly if Telmazartan comes sort of back online more readily available, it might be more work is done into this, and Telmazartan is a good anti-hypertensive. It's just we don't have enough information about it to regard it as an alternative first line treatment.
So just around this little cat, I just want you to remember that hypertension is important in these patients. Hypertension can damage the eyes, the brain, the heart, and the kidneys, but the . Retinal detachments which can develop typically are non-salvageable situation and the patient will not see from that eye and it's often a bilateral condition.
I am so super important to make sure we're monitoring the measuring the blood pressure of all hyperthyroid patients that diagnosis and monitoring it moving forwards because we know it can develop later. And so I hope this little cat sticks in your mind, and that we can, you know, catch a few of these guys earlier and stop it from happening. So just important to remember through their hyperthyroid journey.
So I really hope that you have learned some stuff, picked up some useful stuff. I hope that the newer bits and bobs about the importance of hypothyroidism. I am in particular, I am, and, you know, how to deal with renal disease when you unmask it.
I hope they stick with you and that you can spread them to the wider practise team and that we can really up our game and looking after all these little hyperthyroid cats. And thanks so much for joining me.