Hello everyone and thank you very much for joining me this evening while I discuss paraoplastic syndromes, which I'm sure you've probably all come across while dealing with your cancer patients. So this evening we're gonna discuss all things paraneoplastic. Syndrome, we go through the most common paraplastic syndromes, how do we identify them and how do we treat them.
So what is a perineoplastic syndrome? Well, these are cancer associated alterations in the body structure and or functions that are not actually they're not directly related to the physical effects of that primary or even the metastatic tumour. They are most commonly caused by a tumour producing lots some small molecules that are then released into the circulation, such as hormones, cytokines or these peptides.
And it can also be the host response to the tumour which is then often immune mediated. So many many many perineoplastic syndromes parallel the underlying malignancy. So successful treatment of the cancer actually can lead to the disappearance of this paraoplastic syndrome and recurrence of this syndrome after successful treatment might actually indicate the tumour reoccurrence, so such as with a With lymphoma, we have successfully put this patient into remission.
They have been in remission and, with a normal calcium level during the entire of their treatment and then following on, we've monitored their calcium and then all of a sudden, we end up with a hypercalcemic result. And this can then indicate that the lymphoma has relapsed. A paraneoplastic syndrome might actually even precede the first clinical, any clinically detectable tumour, and it might actually be the then the first sign of malignancy, so you might have the hypercalcemia before you've even detected any cal cancer.
And patients with a perineoplastic syndrome may end up with a greater morbidity than that actually associated with the tumour. There are lots of paraneoplastic syndromes, and I've included this table that is out of Withow. And they link all of the paraplastic syndromes with associated tumours.
And as you can see, there's loads. There's so many of them. And for the purpose of the talk this evening, I am just going to focus on the 6, just so we can go into them a little bit more detail about what's going on and how to treat them, So we can just, yeah, we can delve a little deeper rather than having to skim through lots of different ones.
So the first one we're gonna talk about this evening is cancer, anorexia and cachexia. So there's lots of several me there's lots of lots of mechanisms that actually lead to weight loss in cancer patients. Hyperexia and anorexia is common in cancer patients that do have an advanced disease, or you'll see them even at the beginning of the disease as well.
And this is often a result of, an enhanced inflammatory state and cytokines. So cytokines such as interleukin 1 and interleukin 6 can cause us a whole manner of problems and they can interfere with the normal balance of appetite, so, they will. Can cause the loss of appetite or the stim they reduce their stimulating effect on appetite, so this patient will be feeling full and feeling like they don't want to eat anything but when actually they really, really should be eating something.
So cachexia is a profound destructive process, it causes lots so much ske skeletal muscle wasting, there may or may not be loss of the fat mass. And they causes so many harmful abnormalities in, fat, protein and carbohydrate metabolism. And this this alteration can actually precede tumour detection, as we'll see in a couple of slides, so this process can actually be going on for months, prior to actually detecting that this patient even has cancer.
And all of this happens in spite of, adequate nutrient intake. So as I said, tubber necrosis factor, interleukin 1 and interleukin 6 all play roles, and they induce anorexia, they increase, energy metabolism, they accelerate lean body mass, . Boss mass.
So there's also a lot of other contributing factors to Kexia as well, if there's ongoing vomiting, nausea, diarrhoea, and if there's any renal or intestinal protein losses. So there has been evidence that cachexia and sarcopenia is prevalent over all BMI categories in humans and dogs with various malignancies, and various body condition scores, were all showing that they did have, that there was cachexia present. And as I've just mentioned that.
The, the signs of cake or the, the, the metabolism alterations can actually happen prior to detection of cancer. And in one study it was shown that in in the 12 months prior to neoplasia being diagnosed that some dogs were losing, 5, 10, 10% of their body weight, prior to the diagnosis of cancer. So cats, is shown with various malignancies, and some, a lot of them had a body condition score of less than 5 out of 9.
Most of these cats have been diagnosed with GI lymphoma or oral squalls oral squamous cell carcinoma, and these are tumours where food intake or absorption may have actually also been the cause of the weight loss as well. And in there was lots of muscle wasting in 93% of cats, and this included cats that did actually have a higher body condition score of over 5 out of 9. So as we can see that, cachexia is, prevalent across all of the tumour types.
Low body weight and low body condition scores are negative prognostic factors for survival. It's so, so sad, and some of these patients are, seem so well and they, they have a waggy tail and they still want to eat, but they just, the weight, you can see pretty much just see the weight is falling off them and it is so sad. It can dramatically affect these patients' quality of life.
They, they just, they're just wasting away and their energy is much reduced, and, they just don't have the quality of life that we would, that we want for these guys. And it's often seen as the end stage of the disease, is probably like, and is likely to contribute to euthanasia for this patient. So but hopefully successful management of the cancer should see an improvement in that patient, but it can be really difficult to get these guys under control, and get the cancer under control and successfully treated and then get these guys back into their body condition, that we would like for them.
What can we do to assist these guys? We can try some appetite stimulants, anti-nausea medications, and assisted feeding. So, firstly, we could try some appetite stimulants, but we really, really, really absolutely need to make sure that all of the factors have been considered before we start using these.
Is this a dog that is in the hospital? It's absolutely terrified. There's other dogs barking.
There's people coming and going, he's not got a minute to himself to kind of be quiet and calm, to actually eat something. Take that dog out of that environment, take him somewhere nice and quiet and just see if he will, they will eat on their own. Is that patient painful?
Do they, have they got their mouth sore, they've got tumours in their mouth, do they have neck pain? Are they just generally feeling rubbish? Are we dealing with that?
. Are they nauseous or vomiting? Are they, are they undergoing treatment? Are they, is there any other reason they hypercalcemic, which is why they're not also not wanting to eat.
We need to make sure that we control nausea and vomiting as well before we even start thinking about appetite stimulants. So we, first line we normally go for mirtazapine. We have tablets, and we formulated tablets into smaller sizes and a transdermal gel now, which is wonderful for cats.
So the Mirattas, which is the Mirtazapine transdermal ointment, is available for cats, and we use this once a day and it is applied to the pinna of the ear. There's a line on the box that actually guides the owner to actually show how much of a treatment, how much ointment actually should be used for that cat. And we should be careful with administration and making sure that you that yourselves or the owners are actually wearing gloves so that you're not absorbing it into, into your, into you.
Entice or Eora, which is Camoralan, is available on licenced, in America, unfortunately, not over here, but you can acquire both of them by, sorting out a VMD special import certificate, and there's a couple of different companies that are able to import them. So we can, we can get hold of it, and we do use it in the hospital, and it can work very, very well as well. And then Peractin or ciproheptadine is still available, and we tend to use this as the last as a .
The third option, for an appetite stimulant, but it is, still available. So feeding tubes can be absolutely a godsend, and can intake can help with the intake of calories, and fluids and medications. So we can have some of these patients that are desperate for treatment and owners are just really struggling to get medications into them cos they won't eat or they're difficult to tablet.
So having a feeding tube in can actually can aid with medications. An esophageal tube is most suitable, and these can stay in place for months if they're cared for correctly. You can get food down them, you can get most medications down them.
And we should consider preemptive placement, especially if these guys are going ahead with surgery or. A GA for imaging or anything else, we could get one of these placed, at that time as well. And yeah, the only, the downside to these tubes is that it does require anaesthesia.
So even if these patients, for these patients that have been in the hospital for a couple of days, they've had all of the other procedures and stuff done, and now we need to re-anesthetize them for placement, but, the benefits can be, absolutely fantastic. So if these guys are at home, we want the owners to be monitoring how much food their pet is actually consuming, and it might be that they just need to spend a bit more time with their pet to encourage them to eat and, hand feeding always seems to go down well, regular diet changes, as I said, all of these, all of these . Substances that are floating around in the body that can affect their appetite and satiety, and all of these effects can actually change the patient's taste, perceptions as well.
So it might be that they, they've been on a regular diet for years and absolutely love their food, all that treat, and all of a sudden they absolutely will not eat that food anymore and you try them with something different and that that's what they want. We could use some warming up of the foods. It might be that we need to separate other pets, from them, especially overnight if they are slow to eat, or we could do some microchip feeders as well.
I mean again, consider that any neck pain, can they actually get to the food? Do they have a bus of collar on or something that is actually going to stop them getting to their food? And we really, really should be avoiding .
Force feeding of these guys, absolutely not, it's something that can lead to aspiration pneumonia, and in a sick patient, it's not ideal, obviously, and it can also lead to food aversion, and this is really catastrophic, and it can take months and months for this to actually rectify. So, and then in patients that are already very poorly, we don't really, we don't want to add something else extra to them where they actually then don't want to eat. We want these guys actually what willing, willingly eating.
You'll see lots of different things about which food you should use for patients that have cancer and they have this, and they have that, and you should feed this level of protein, this level of fat, and, I've got this table from, a textbook to kind of a bit of a guide as to what levels we should be aiming for. And, ideally what we want is a really, highly digestible protein, that's something that should really exceed maintenance for normal adult animals and highly digestible, good quality, . Foods and Hills have just recently brought out a new prescription diet, which is Oncacare.
This was only launched, I think it was April of this year, which is 2023, and it's been developed to be like super high, highly palatable, that I've got highly digestible protein in as well, so hopefully we can see some good things come from this too. So moving on now to mast cell tumours and GI ulceration, so as you can see these beautiful mast cells, with their beautiful granules are stains ever so beautifully. These granules contain histamine, heparin, and enzymes.
So mast cell tumour degranulation results in the release of these radioactive substances, so histamine and heparin. The release of these substances can be spontaneous because mast cell tumours just like to do these crazy things sometimes. Oh, it can be triggered.
Have we been handling that mass? Have we taken a sample? Have we put a needle in there to get a sample?
Have we actually even just started chemotherapy, or, have we, has that patient had some radiotherapy? So hyperhiaminemia is regarded as one of the main factors contributing to GI ulceration and perforation. And this is because histamine, it binds to the parieyl cell H2 receptors, and this actually then leads to an increased gastric acid secretion.
And it also exerts direct effects on the GI mucosa and causes all sorts of other problems and increased vascular permeability. Localised protein exudation and increased mucosal blood flow, so all of these factors together contribute to the GI ulceration risk. And these can then lead to hematosis or melena in some extreme cases.
So we want to aim to minimise any complications from histamine release from mast cell tumours. So if we have a mass that we are not sure what it is, and we suspect that it's potentially a mast cell tumour, this patients had a mast cell tumour before, we want to be, . Using some antihistamines prior to taking any samples, so yeah, antihistamines can be used to help with minimise these complications.
So as I said, if it's a suspicious mass, patients had a previous mast cell tumour, let's use some antihistamines. If there is gross mast cell tumour, that is actually non-resectable. And prior to sampling of a primary mass, or during staging, so we know this dog has a mast cell tumour, we've got it confirmed already, but we're taking this dog for staging, we want some FNA's of the liver, spleen and local lymph nodes.
We will give an antihistamine prior to sampling as well. And even during the time between tumour identification and resection at surgery. So the antihistamines that we tend to use are H1 blocker, er, which is chlorophenamine or diphenhydramine, and the chlo chlorophenamine is just Pyriton.
We tend to use these alongside a H2 blocker such as famotidine or a proton pump inhibitor such as omeprazole. So in a patient that has a previously resected mast cell tumour, and everything has been completely resected, there is no gross disease still left, there are clean margins, everything was done perfectly. We don't need to continue antihistamines after that.
They're moving on to hypercalcemia of malignancy, so this is the elevated blood calcium level, secondary to a neoplastic process. This is common in dogs with an anal sac adenocarcinoma and lymphoma. It tends to be in the T cell, .
Varieties of lymphoma and the most common site of this is the cranial mediastinum. And it's also seen in dogs that do that have multiple myeloma as well. It's less frequently seen in cats, but can be seen with cats with lymphoma and squamous cell carcinoma.
So there are two mechanisms to cause hypercalcemia of malignancy in our patients. So the first one is the humeral hypercalcemia of malignancy, and this is caused by soluble mediators that are then released from tumour cells into the circulation. This acts on the bone and kidneys and the intestines via the endocrine and paracrine pathways.
PTHRP is most commonly involved with this. So PTHRP acts on target cells, so bone, stimulates bone reabsorption, mobilises the calcium, leading to hypercalcemia. So on the kidneys, it increases the renal tubular calcium resorption, and it inhibits phosphate reabsorption and increases its excretion.
And it then converts inactive vitamin D to active vitamin D, and all of this increases the calcium, leading to hypercalcemia. And with the intestine, it uses the vitamin D from the kidneys, and this actually increases the intestinal calcium absorption, again, leading to hypercalcemia. The other mechanism is focal bone destruction, and this is mediated by paracrine factors secreted by tumour cells that are infiltrating bone.
These are cytokines and growth factors that increase bone reabsorption by either directly stimulating the osteoclasts or interaction with osteoblasts which then which then upregulate osteoclass activating factors. And this tends to be associated with skeletal metastasis or multiple myeloma. So the clinical signs in dogs tends to be inappetent, nausea, PUPD and that's in most of the cases, vomiting, muscle weakness or twitching, which is actually less common.
And in cats we will likely see anorexia, vomiting, er PUPD is less common in cats than it is in dogs. So these clinical signs are mainly the PUPD heat hypercalcemia induces an automatic diuresis and inhibits the anti-diuretic hormone, and it's an action on the tubular cells of the collecting duct within the kidneys, so that leads to polyuria. So polyurea plus nausea and vomiting leads to that patient becoming dehydrated, which leads to then a reduced glomerra filtration rate, and increased calcium reabsorption and worsening hypercalcemia.
Renal damage can can result from renal vasoconstriction, mineralization of renal tubules, basement membranes or in the intertesticium, tubular necrosis or degeneration, and initial fibrosis and some of this kidney damage and esotemia may not actually be reversible. So, diagnosing a hypocalcemia, . Measurement of an ionised calcium is much more accurate than the total calcium, so ideally we would want a nice ionised calcium result.
Calculations that we, there are calculations around that we can use to correct, to change the calcium into an ionised calcium, but these aren't really recommended. We would much prefer an ionised calcium result. But, however, total calcium in dogs and cats that do have, hypercalcemia of malignancy do tend to be higher than any of the aetiology.
So if you are seeing a high total calcium, it is most likely to be a neoplastic process. And then the normal range of calcium, of the total calcium is 9 to 11 milligrammes per deciliter, and an ionised calcium of 1.12 to 1.42 millimoles per litre.
If hypercalcemia malignancy is is suspected, so they, they've already we've got the clinical signs, we've got a history, and we've done some baseline bloods and we've noticed a Hypercalcemia, total or ionised calcium. So we should be really carefully examining these patients, so we want careful palpation of peripheral lymph nodes, just to show you if we do have a lymphoma, and careful digital rectal examination, to assess for any anal sac adenocarcinoma. We would want further blood tests and urine, for full analysis, and then thoracic radiographs and abdominal ultrasound, to examine for any neoplasia.
If there's no malignancy then found, we could move forward then with a cer cervical ultrasound and then measurement of serum PTH, PTHRP and Calcitro. We can then move forward then with bone radiographs and bone marrow sampling as well. So the most effective treatment for dealing with hypercalcemia is to remove the cause of the hypercalcemia, so deal with the cancer.
It might be that we have to, we go ahead with chemotherapy for a lymphoma patient to induce remission or surgery to remove that tumour, such as an anal saccadenocarcinoma or moving forward, we could use radiotherapy as well. So concurrent supportive care can be initiated if then if the patients are clinically. Excuse me, clinically ill with the hypercalcemia, if they are aotemic.
If they are non-surgical, such as with an anal saccadenocarcinoma that has metastasized or is non-surg completely non-surgical or is unlikely to respond to chemotherapy or other treatments, or even if they have stopped responding to chemotherapy or other treatments. So if this patient has mild hypercalcemia and kind of minimal clinical signs, they're still pretty well on themselves. We could, we would use some saline, 0.9 saline diuresis, and this, the aim of this is for rehydration, and then to slightly volume expand to increase the GFR and the filtered load of calcium.
So we use saline as it's because of the high sodium content, and this can compete with calcium. For renal tubular absorption, so this then further enhances calcioesis. With moderate to severe hypercalcemia and some of these and the patients that are showing lots of clinical signs.
We would go again with the 0.9% saline diuresis to rehydrate initially and then maintain on 0.9 saline again for diuresis at usually 2 to 3 times maintenance.
We can add infuzamide, the loop diuretic, to further promote calcium loss, and this can be used IV orally. But we can only use this when this patient is fully hydrated, this should just stop. To hope, yeah.
Only use when, when, yeah, sorry, make sure that we are only using with these in patients that are fully hydrated to make sure that we can promote the proper calcium loss. We can use bisphosphonates such as alendronaladronate, which is a tablet or zoledronic acid, which is an IV formulation. Permidronate is still available, it's a little bit more difficult to get a hold of at the moment and with that is an IV infusion also.
These medications decrease the activity and function of osteoclast cells and therefore decrease the breakdown and resorption of bone, therefore lowering the blood calcium. Due to renal excretion of these drugs, we need to assess renal function prior to use. They are known to produce renal pathology such as proton urea, altern creatinine clearance, and acute renal failure.
So we want to check minimum urea creatinine prior to use. IV fluid therapy, saline should be administered alongside these, to minimise the potential side effects. So the permigenate and Zyzyedronic acid are diluted in saline for administration, and we tend to follow up with some saline for a little while afterwards as well.
So we wouldn't use these in cases that were about to start chemotherapy or have surgery. So we have a, if we had a hypercalcemic patient with nail sack tumour that was about to go to surgery, we would rely on the surgery to remove the cause of the hypercalcemia, so we wouldn't go ahead and, use these treatments prior. If after the surgery, the patient was still hypercalcemic indicating that there was still residual disease or we weren't inducing remission, that's when we can consider using these.
Glucocorticoids can quickly induce a rapid reduction in serum calcium, by increasing the urinary output of calcium. And it's essential that a diagnosis has been obtained prior to use, especially if this patient is a suspected lymphoma, or the hematopoietic tumour, . Steroids can really interfere with the ability for us to confirm the diagnosis, so make sure you've got all of your samples, your bloods, your FNAs of lymph nodes, organs, everything, prior to actually starting these, prior to starting steroids.
Antiemetics are probably going to be used and we would use Meropotent, as hypercalcemia can cause nausea and vomiting as well. And it might be that we also need to add in some appetite stimulants, but remember antiemetics should be used first, and then making and then we can go ahead and give some appetite stimulants, as I discussed earlier. Salmon calcitonin has been used to treat hypercalcemia in dogs, but it's got a short half-life, high incidence of side effects including anaphylaxis, especially with repeated doses, and it's really expensive to actually use.
I've only used it once and all of my time, doing oncology and medicine. So yeah, it's not something we would use as a first line at all. So, as we mentioned before, The presence of a of a paraoplastic syndrome, kind of goes hand in hand with how, how well the disease is actually progressing or not progressing.
So reoccurring or increasing hypercalcemia may indicate that the disease has relapsed or there has been progression. So we monitor our our previously hypercalcemic patients, monthly or every 6 weeks, as part of our remission check. So we have a couple of lymphoma patients who were hypercalcemic at presentation.
Ended up with normal calcium during the whole of their treatment, so we continue to monitor them, I said, every 4 to 6 weeks, just to monitor their calcium, and if, if these levels ever start changing and increasing, this is likely to then to Show that this patient is likely coming out of remission. And these patients that are hypercalcemic ongoing, we should be assessing renal function as well regularly just to make sure that is there anything else that we need to be . Doing for these patients.
So moving on to hypoglycemia? So the most common cause of hyperglycemia is an insulinoma, which is a pancreatic beta cell tumour. And these functional insulinomas typically produce an excessive amount of insulin, but occasionally they can produce the insulin gross factor 1 and 2.
So non noninsulinomas or non- islet cell tumour causes can include primary liver tumours, smooth muscle tumours, but there's also reports of hyperglycemia also occurring with hemangiosarcomas, lymphomas and leukemias, mammary carcinomas, melanomas and plasma cell tumours. So tumour cell production of insulin growth factor 2 is the most common mechanism for hypoglycemia in these non- islet cell tumours. This is because the IGF 2 stimulates insulin receptor cells and glucose utilisation.
So other causes include production of IGF one as this increases glucose uptake and decreases the production of hepatic glucose. If we can have hypermetabolism of glucose, production of substances that actually stimulate insulin release. Production of hepatic glucose inhibitor and insulin binding by monoclonal immunoglobulins, such as with a plasma cell tumour, insulin receptor proliferation, and rarely ere we could end up with ectopic insulin production.
So diagnosis, higher insulinomas are usually diagnosed by documenting hypoglycemia alongside an inappropriately high serum insulin levels. So these bloods we will, we would pull at the same time, so that they would be, concurrent. These tumours tend to be small and visualisation and an ultrasound can be difficult, so, a CT is ideal.
And for these non-isle cell tumours, most of these intra-abdominal tumours are tend to be quite large, and that we can actually identify them on the abdominal palpation or ultrasound as well. So for insulinomass, surgery is the recommended treatment, the patients shouldn't have a prolonged fasting period. They may require IV detrose prior or during surgery.
And pre-op steroids might actually be able to help with glucose levels to try and stabilise them a little before we actually anaesthetize for surgery. So for medical management of insulinomas, some of these may need IV glucose, and anything over 5% glucose or dextrose solution requires jugular catheter for administration. We want these patients having small regular meals that are high in fat and protein and complex carbohydrates to slow down just to sort of regular, glucose, provision.
And it might, it might mean that these, the owners are having to feed them once or twice overnight. So this again is where, maybe the microchip feeders or timer feeders, are ideal for feeding overnight. Steroids can be used as well, as these are insulin antagonising and they actually increase gluco neogenesis and they.
And they can actually help to decrease the peripheral tissue glucose utilisation. And we would start at 0.25 milligramme per kilogramme orally twice a day.
And we have dioxide, which we would start at 5 milligramme per kilogramme twice a day and work our way up a little. And this actually suppresses insulin from the beta cells, inhibits cellular uptake of glucose. And stimulates hepatic leuconogenesis and glycogenolysis.
These patients have actually adapted pretty well to the low blood glucose levels, so, we don't need these levels to actually return to, a normal levels. We just need to make sure that we're dealing, that we're preventing any, complications from hypoglycemia. So the last one we're going to talk about, oh no, the second to last one is hypoestrogenism.
This hasn't actually been reported in cats, from what I could find, and is most associated with the Sertoli cell tumour. So 25%, 25 to 50% of dogs with a sertoli cell tumour will show hypoestrogenism. Half, approximately half of the otoli cell tumours develop in crystal cryptoid testicles, and then clinical hypoestrogenism develops more commonly in these.
A sattoli cell tumour must remain a differential diagnosis, even if there's no palpable testicular mass. It may, but they, it may actually also occur with semenomas, interstitial cell tumours and ovarian granulosa tumours. A CT or ultrasound can be used to screen for an inguinal or abdominal tumour, especially in these riptal patients, and as you can see this is a massive tumour on this, patient here, and this was confirmed as a sertoli cell tumour.
Yeah So the clinical signs we'd expect to see with hypoestrogenism is bilateral symmetrical alopecia, cutaneous hyperpigmentation, epidermal thinning, appendulous prep use, penile atrophy, and atrophy of the contralateral testicle. As you can see with this picture, I apologise for the quality of the picture. You can see the the alopecia and, on this patient.
Oestrogen can also have a myotoxic effect, so bone marrow toxicosis, leads to a progressive bone marrow hyperplasia or aplasia leading to an aplastic anaemia as well. And so consider hypoestrogenism, as part of your. Work up for some of these patients that do come in .
With bone marrow. Oh, excuse me, that's for your some of your pancytopenic patients. So these guys may then present with anaemia if they may be weak with weakness, lethargy, pale mucous membranes, and tachycardia, thrombocytopenic with petti and neckhymosis, maybe GI bleeds and epistaxis, and leukopenia, so they may end up with have some form of an infection or even sepsis.
Treatment is surgery, and that's the treatment of choice to remove that tumour. And clinical signs may take several months to resolve, but eventually, hopefully they, they should resolve with coat regrowth and skin skin normalising as well. So hyperviscosity syndrome is the last one, and this is caused by an increase in blood viscosity, and it may occur due to myeloma related disorders, such as hyperpotinemia, and this tends to be seen with multiple myeloma, leukaemia and lymphoma.
It can also occur due to polycythemia vera and perineoplastic erythrocytosis. So hyper viscosity syndrome, of the myeloma related disorders, and this is because there, there has been production of or of a single over overproduction of a single type or component of immunoglobulin, referred to as the M component, and serum electrophoresis is required to categorise the class of immunoglobulin, that is actually involved. So clinical clinical signs result from the sludging of the blood in the small blood vessels, and all of these extra proteins or cells causing the sludging of the blood, and this leads to then an ineffective delivery of oxygen and nutrients around the body and it can actually also lead to coagulation abnormalities as well.
So clinical signs include retinopathies, including retinal haemorrhage and detached retinal detachment, and can often result in acute onset of blindness. Patients may be ataxic with an altered demeanour that may end up leading to seizures that also then need management. They can end up with a bleeding diathesis and just you end up with some keep an eye out for any particular or any bleeding.
And hypertrophic cardiomyopathy and congestive heart failure has also been noted as well. So treatment again is treatment of the underlying cause is the, is essential to rectify these conditions. Plasmaphoresis is indicated in the if the syndrome is caused by serum proteins.
And I can remember we have had one we've had a multiple myeloma patient and the patient whose bloods are actually on the side of the screen there, that we did end up removing. A a blood unit from him, . And then replacing that one then actually performing a pack red cell transfusion with him, just so we can actually remove a a decent portion of plasma.
But if they If the complications are caused by erythrocytosis, we can, do phlebotomy and then fluid and then replace the volume that has been removed with fluid therapy. I said under treatment of the underlying cause is essential and ongoing monitoring is required to assess the remission status. And I said, these bloods on the side were from a patient with multiple myeloma, that we followed and monitored during the course of his treatment.
So just to add a few little books onto the end for some further reading and I didn't want to go into lots and lots and lots of detail with lots and lots of different ones because we could have been here absolutely all night. But if you do have any questions, or you want to, if there's anything I can help you with, give me a contact me on my email, or directly through to Northwest Veterinary Specialist and myself or one of the other oncologists, and one of the oncologists would be happy to help. Thank you very much.
Have a lovely evening.