So this lecture is part one of a two part distilleries, focused on care of the periparterane. And this first part will consider the major metabolic disorders that affect sheep in the UK and Ireland predominantly, but a lot of these conditions are global metabolic disorders and seen all over the world. So I'm David Charles.
I'm a farm practitioner by background, now I'm doing more consultancy, and I'm a RCVS recognised advanced practitioner in sheep health and production. So when we. Are called by by one of our clients, or nowadays, quite often, we might just even get a WhatsApp, or sometimes we'll just get a picture of a sheep through originally.
It's important to think about the important history questions that we need to take when we're thinking about periparteran problems. It might be that the farmers have got some down ewes, might be that they're just ewes that aren't quite doing right, and you know they're close to lambing. So that seasonality and that awareness of the different systems that your clients run is so important as well, and that's where that that farmer relationship is so important.
But we're gonna wanna make sure that we know how many individuals are affected. Is it just the one you? Is it a whole group?
Is it a particular group? Important to know whether they're pregnant or not. Just because we're close to lambing time, we can't assume that every EU is pregnant, it could be an issue affecting the barons.
If they are pregnant, have they been scanned? Is it, are they primyparis, multiparis? When is the expected labing date?
Good to know the age you've used, good to know the breed of rams used as well, that might affect what we're thinking in terms of the potential lamb sizes or any foetal maternal disproportional mismatch. Important to know if these youths have been housed in the peripartuate period, if they're still out at pasture. We want to know what they're feeding, if they're supplementing what they're supplementing with, what kind of forage they're on.
We want the farmer reported clinical signs. What's made the client ring you in the first place to say that they've got a problem. And it's important to know if there have been any fatalities, have they lost any yet, or are they ringing you early on in the problem?
And when we think about the metabolic disorders. Always frame it in this context, that a periparerent metabolic disorder arises when or if there is a failure for the EU to have their nutritional requirements met during the late gestation and or the early lactation period as well. I think for a lot of us, people only think of metabolic disorders is something that affects yous.
Before lambing, some of the conditions we'll talk about today, actually, we tend to see them post parturingly, and some of them actually we can see pre and post parttuation as well. And a lot of it is about nutrition, and it's about water access, it's about feed intakes, and it's about getting everything right in the management of these sheep. Metabolic disorders, 99 times out of 100 are a management problem.
And we have lots of different systems in the UK, lots of different systems globally. We can see a fairly typical. The British lambing system on, on the right there, this is a this is a farm that I work with.
They, they lamb in a polytunnel, but you know, it's that straw base, quite well stocked and obviously the stocking density reduces the further through the lambing period we get is use of lambs go into individual pens. Or this is actually a French system on the left here, and again you can see it's quite similar, but again we're thinking, where's the feed face, where are the water access points? If there's supplementation, where's the supplementation, where's the forage?
So as I say, it's all about nutrition. We could do, we could do multiple hours of webinars just on sheep nutrition, but we're gonna frame this in the context of metabolic disorders and just cover some of the highlights before we get into the conditions and the management advice that we can give. Late gestational requirements for the you.
Twice maintenance ME. That's approximately 16.8 megajoules of ME for a 70 kilogramme lowland e.
1.6 kilogrammes of dry matter a day are achievable and the. Back of a piece of paper calculation is 2 to 2.5% of your body weight.
So supplementary concentrates are required to get sufficient megadues of ME when that dry matter intake is quite limited. And so what we have to do. We have to maximise the forage component that's taken on and then supplement with concentrates.
We do not want to be in a concentrate heavy ration. A 75% forage to 25% concentrate diet is digested by the rumen and the rumen flora a lot better than a high concentrate low forage ration. That's really important to remember and that's where ration formulations often go wrong.
We've got to think about the space and the access to the feed as well. The same as if we were doing a talk on dairy cow nutrition or metabolic disorders of dairy cows. Yes, the ration that's formulated and is recorded on the piece of paper is important, but the ration that matters is what the sheep actually eats and what they can get access to.
We want a minimum of 50 centimetres per ewe trough space, so that actually all the ewes can eat at the same time. Remember in late gestation, you need more space than, say, post weaning. We need to think about the rationing content, I've got to remember that increased energy demand that comes from growing lands as well.
And when we do think about how we're using those concentrates, we never want to use more than 500 grammes of concentrates per year per feed at a time, otherwise we significantly increase the risk of ruminal acidosis. Which can be a whole metabolic disorder problem in itself. But the big 3, the big 3 metabolic disorders of the peripareran period.
Ovine pregnancy toxaemia. Hypercalcemia, hyperglycemia, or staggers, as a lot of people will colloquially know it. But let's start with the big one.
Ovine pregnancy toxaemia, colloquially known as twin lung disease. Not necessarily the best name because we do see it in use pairing singles, we do see it in triplets. The quads that we do see, obviously they have a greater risk as well.
So, what happens when we have a pregnancy toxaemia, when we're thinking about the aetiology, what happens? Well, the first thing to remember is that in contrast with what we see in our dairy cattle, problems with negative energy balance and hypoglycemia that lead to hyperketonemia. They're observed in the late gestational period in sheep.
We tend to see urine pregnancy toaemia. Prepartuition compared with ketosis in cattle would be generally a post-partuic problem. Why?
Well, a large driving factor behind that is 70% of foetal growth occurs in the last 6 weeks of the gestation period in sheep. The principal source of energy to the foetus is maternal glucose, and in early pregnancy. The ewe can meet the demands of foetal development, but as we progress through the gestational period, the in utero demand for glucose rapidly increases, rising as high as 30 to 40 grammes per foetus per day.
In fact, if they're bearing twins, therefore, that's 60 to 80 grammes of glucose per day. And as the foetus or foetuses grow, there's less space for the ruin to expand in the abdomen, limiting that feed intake. Think about where we're talking about limited ability to intake forage and dry matter, but that reduces the metabolizable energy available per day.
But the daily glucose requirement is increasing. Most commonly we see this as a problem of ewes carrying multiple lambs in utero, but we know there can be management errors, there can be human error, there can be nutritional formulation problems that can lead to clinical cases and ewes carrying singles, and that's why I much prefer one pregnancy, toxaemia is a problem rather than twin lamb disease. This doesn't just affect uses with twins.
So we get the mobilisation of the body fat and the production of ketones greater than they can be utilised. But what we really get is the creation of a state of hypoglycemia, the hydrolysis of triglycerols from the adipose tissue to free fatty acids or nefers. And also to glycerol And these could act as the energy source for foetal growth.
The 3 fatty acids are converted into acetylOA. But when there's excess acetylchoA, so more that can be used up in the citric acid cycle, because there isn't enough oxylo acetate quite often, then the excess acetylchoA is converted into ketones. The increased production of the ketones, well, it suppresses natural glycogen production, that leads to overine pregnancy toxaemia.
We see the metabolic acidosis, we could find the hyperglycemia on the test. We know we find the hyperketonemia, and we know we see the signs of the emia as well. And actually, we know, if we dig deeper into this, the metabolic acidosis is because aceto acetate and beta hydroxybuyric acid, the BHBs that we often test for, well, they're strong acids driving that metabolic acidosis.
And then we also get the osmotic diure diuretic effect of the ketones that leads to increased losses of potassium and sodium bis at the kidney and advanced cases do become uremic and we can see signs of uremia on clinical exam as well. But when we're called out to a case or when we're advising a client over the phone. Given those 1st, 1st bits of advice, convincing them that you need a visit often as so much of this advisory work now is, and so much of farmers can be is we can do a lot more remotely before we then get the farmer to let us come on the farm and do a more detailed investigation.
Well, we need a good history. Are they feeding to scan? Are they doing stepped feeding, gradually introducing the concentrates?
Are they feeding more concentrates, more energy, greater Russian to those carrying twins and triplets than the singles? What's the body condition score? We know it's more frequently observed in us with a body condition score below 2.5, or greater than 4 out of 5 on a standard body condition score scale.
And we know it's got some fairly characteristic clinical signs as well. Remembering that ovine pregnancy toxaemia, it's a multi-stage disease that progresses over time, so the stage one signs. Often it is at gathering or at feeding.
Reluctance to move, hanging back from the group, not coming to the feed face, not coming in when they gathered. A level of inoppetence. They're probably normothermic.
But we're seeing these early signs of hypoglycemic encephalopathy. So you might see if you look closely minor tremors, hyperesthesia, if you're close and handling. And start to get a level of ataxia.
Some early signs of star gazing, a reduced menace response, and we will see an apparent, but not a functional blindness. And we know that progresses often over 24 to 48 hours to stage 2 signs. All the signs of stage one, often exacerbated.
We'll always see now. The development of the apparent blindness, but we're still gonna have a normal PLR that's important to remember later on in the talk. It might progress to a true central blindness.
They can progress to a la recumbency. JB Crilly's paper shows 73% of cases have a high pain score, so we might see that accompanied by Brooksism, hypersthesia, we'll see depression, reduced mentation, we'll see decreased reminal tone, decreased abdominal tone. Ruinal atomy on auscultation, we might see diarrhoea as well, sometimes.
To try and save themselves. We'll see abortions occur, and we know if they're not treated, these animals will progress to die. If we're on farm, we can do pen side patient side testing.
Using a handheld ketone metre testing for BHPs, well, subclinical disease, 1.1 to 2.9 milli per litre, beta hydrodroxybutyrate, clinical condition, greater than 3.0 milli per litre.
The literature tells us testing free fatty acids or fructosamine is the most effective test. However, we don't yet in the UK have the ability to do hen side or on-farm free fatty acid or fructosamine testing, so it can be impractical, and the majority of people will be using the BHB monitors and the BHP test for a rapid diagnosis to inform the important decision making. Make sure if you are using one of these machines that we're picking one that is calibrated and proven to be effective for testing BHBs and ketones in sheep because they're not all, so that's important to note.
If we do a postmortem, they're usually non-specific. It's often a multi-gravi U. We might see evidence of decomposition, breakdown of the tissue.
We might see a more friable liver as well, and we might start to see notable autolysis or signs of uremic damage to the foetuses in the uterus as well. If we catch them early, then this is a condition that we can treat and see good results for, but the best results come from treating stage ones. So early interventions when we see those early signs.
And to me, that's why this is a condition. That relies on good farmer education, good support of farmers, good creation of protocols in conjunction with our farmers and, Having the right product on the farm ahead of the lambing season. We want to provide glucose precursors for energy.
We need to correct dehydration, correct those electrolyte deficits. We might want to remove the glucose drain. There's a growing body of evidence for the importance of providing NSAIDs.
People will talk about using palatable food as. A treatment for Avo pregnancy toxaemia will go on to consider why that isn't the case, why it should only be used as an adjunctive therapy or supportive care, alongside steps 1 to 4. And in advanced cases, we must remember there are welfare considerations of this disease, and we must consider when it's appropriate to perform euthanasia on the farm.
But if we look at these in more detail. Step one We need to provide glucose precursors. We need to rapidly elevate the plasma and CSF glucose concentrations, and we need to do that rapidly and effectively before the hyperglycemia causes irreversible brain damage and neurological damage.
If there are advanced neurological signs, then intravenous glucose can be effective for a, a rapid spike, but it's not that long lasting, but it can help protect the CLS. Glucose precursors Obviously, they're used for gluconeogenesis in the liver. But they do yield glucose at different speeds.
So a very popular option, so in most trade, most merchants would be just a straight propylene glycol drench. A lot of the agricultural retail and lamb drenches contain just propylene glycol, maybe a few vitamins. It's a traditional treatment, but it's not the fastest.
So propylene glycol converted to pyrubate enters citric acid cycle and is then converted to glucose. But we now know that there are faster ways of elevating the plasma and TSF glucose concentration by using a different glucose precursor and using glycerol based products. So glycerol bypasses the citric acid cycle and therefore it can yield glucose in a much faster fashion.
In one study by Alon Natal, they found glycerol elevated the glucose concentration in 1 hour, whereas it took 9 hours to see the same effects when using just propylene glycol. In the 2015 study, a comparison of a combination product, 70 grammes of glycerol with 20 grammes of lone glycol, they found that was even more effective than IV glucose and insulin, and more effective than just crack corn orally as well. And when this is time critical treatment, we want the fastest option to elevate the plasma and CSF glucose concentration, protect the brain, protect the CLS, correct the hypoglycemia as quickly as possible.
Some farmers, they'll still be using oral glucose powders where they're mixing in a sachet into some water and pouring it in, in, you know, or drenching it into the sheep. In principle, that sounds like a good idea, but the problem is that all glucose powder is just fermented by the ruminal flora. It doesn't penetrate the rumen matte, and it isn't rapidly absorbed, so it doesn't rapidly increase the plasma glucose concentration.
You need a glucose precursor to have that effect. So when we know we need to provide glucose precursors. Then we need to think about step 2.
We need to correct the dehydration and the electrolyte deficits. Bovine pregnancy toxaemia is widely recognised as a dehydrating condition. The earliest reference I found was a 1950s paper from from math, so the precursor to Deri APHA saying use twin lamb disease needed all fluids because it was dehydrating.
And they're dehydrated for lots of reasons. Ketones, if we think about actually what they are and how they work. Well, they're osmotic diuretics.
They have a diuretic effect in the kidney. We know also. There often is inhabitants in a pregnancy toxaemia, and if you don't.
Have feed coming in, you don't have the energy coming in, then that limits the absorption of water across the room of the wall. Often these present with diarrhoea as well, which again, we all know is increased loss of fluids from the intestine. If it's an automatic diarrhoea, then it's really drawing even more water out as well.
And If you tested, these ewes have elevated cortisol, so they've got reduced ADH production, antidiuretic hormone vasopressin, and that increases the diuresis further. The literature shows, and if you test these used penicide, well they've got a sodium and potassium deficit as well. The hyperkalema Deficits are shown to be as large as 1.0 millimole per litre, which is 30% of total blood of potassium.
Survival in all species. Affected by pregnancy toxaemia, it's been shown that survival rates increase the higher the potassium concentration is. So potassium directly correlates with survival.
1 in 4 of these have a concurrent hypocalcemia as well, and the hypocalcemia often facilitates the development of the clinical signs. It can make them worse. Remember again, we know these ewes become acidotic, we know they lose sodium and potassium.
And that can then develop a ketoacidosis, which will then cause respiratory distress, possibly diphsia. That can make the CNS signs worse. We then build to dehydration, euremia, and death, and this is where we might see acidosis or uremia on postmortem with those autilized lambs, as is described.
By Neil Tarderson in the literature. And in multiple studies, it's been shown that survivors have a higher sodium and potassium concentration than non-survivors. As I mentioned, we know this potassium deficit can be as much as 25 to 30% of total potassium, and one study showed, Clinical signs being correlating with those with the greater deficit, subclinical 0.8 to 1.2.
So that correlation, it's in human literature, it's in ovine research, it's in research from other species as well, and we're not talking about the importance of correcting the potassium losses enough, so we need to pick products that provide glucose precursors can help correct the dehydration and provide the right electrolytes. But in the worst cases, that's still not enough. We need to consider removing the energy drain.
It's a difficult conversation. We need to think about how we approach this with the farmer. We need to understand.
What's driving the farmer, what, what, what's more important for them, whether that's economics, whether it's genetics, we need to understand, we need to have that conversation, understand the farm, understand the system. Because if we have to remove the energy drain, we have to decide whether the focus is on. Optimising lamp survival or whether it's optimising optimising use survival.
In one study, once advanced stage 2 signs were observed, then the survival rate falls as low as 30%, and this is why educating farmers to pick out stage 1 signs and, Having the right products on farm is so important because the success and the survival rates of treating a stage 1 are so much greater than treating a stage 2. The best survival chance for the ewes is the rapid removal of the lambs as the cause of that energy glucose strain, and that's an emergency caesarean section. But that means it might be pre-term, survival of the lambs could be poor, and if it's really premature, then we know the survival rates go down as well.
The best option for the lambs would be to maintain them as long as possible in utero, deliver them as close to time as possible. We can also give steroids prior to caesarean section to aid with the maturation of the foetal lungs before we then induce. A number of protocols.
For inducement and a number of protocols for optimising lamb survival, the one that I'd advocate for, the one that I use and that's well described in the literature. Is this one here? Best done after day 138, day 139 of gestation, successes have been reported from day 135.
On day 135, 16 ms. Dexamethasone IM repeated BID until part tuition achieved. Using this protocol, Zolorreal found 75% survival rates compared with lambs born at term to caesarean settling.
We can add declorostenol. 0.375 Migs should be about right for effect.
It's important to note the steroids don't help treat the urine pregnancy to toxaemia. As you'll remember earlier we touched on the fact these ewes already have a high cortisol. But it, it's an important metropolitan disorder for a number of reasons, and part of it is because of the flock level impact.
So if there's one clinical case. As much as 40% of the flock could be subclinically affected. And these are the ones that aren't gonna be fully recumbent, they won't progress to a stage two.
They might not be picked out by the farmer, but they're still affecting the productivity and profitability of the farm. Increased lamb deaths. Reduce cluster and quality, reduce cost and production, if they're doing.
Brooks testing refractometry, they're gonna see the difference. They'll probably have more abortions, it could be unexplained abortions, and this is because the youths are saving themselves, getting rid of the glucose strain. If the lambs are born alive, well they're gonna probably have lower birth rates and they're gonna have a poor daily life weight gain.
If we have clinical cases, We're definitely gonna have increased lamb deaths. It's been shown to be correlated with an increased incidence of dystopia. Increased risk of metritis.
As with the Colostrum issues that we'll see, we'll also see reduced milk quality in production. That makes the daily life weight gain of the lambs even worse. More likely to compromise the immune system have increased mastitis.
If you haven't advanced Stage two, that actually it's as much as a 25% increase in that metritis, and we know from other literature and other presentations matritis in you is often underdiagnosed and undertreated. So that will further cause more losses within the flock. Often hand in hand, we have to consider another metabolic disorder, hypercalcemia.
We know this one is often misdiagnosed, and we know it's often mistreated. And we should pay a lot more attention to it as a condition. This case, as set out by Phil Scott in his 2013 paper, is a great example of why we should pay more attention.
You presented him recumbency. The farmer deduced to lamb disease cos it's down a heap before lambing, so that was their, their belief. They gave all propylene glycol.
There was no response, so the vets were involved. Blood sampling was carried out, a diagnosis of clinical hypercalcemia was determined. Treated with intravenous calcium.
And 5 minutes later, rapid response. The ewe was standing, eating, and urinating. And because of how these present, we know that they are often confused for ovine pregnancy toxaemia, or they're confused for pneumonias, respiratory diseases.
This can be a big cause of inappropriate or irresponsible antibiotic use because they're misdiagnosed as respiratory diseases, or they can be mistreated, thought of as OPTs. Just give them profe glycol, and they won't respond and they will die very quickly if they get the wrong treatment. So I was with Over on pregnancy toxaemia, hypercalcemia in sheep, we tend to see it in the pre-parterian period.
And this is the difference compared with dairy cattle where obviously we'll be thinking milk fever, postpartum paresis. Similarity though is that we do tend to see this in older uses, generally use over 3 years old. National flock prevalence, 0.4%.
But what's concerning is of that number of the 0.4%. Only 3% receive veterinary involvement.
So this is another condition where educating our clients on nutrition, educating our clients on diagnosis, management, intervention, if they do get cases, is so important because we're only gonna see about 3% of these cases as vets. The other 97% are gonna be managed on farm by the farmers or the farm staff. Driven by increased demands.
3 to 4 weeks before punctuation, the foetal bone starts to calcify. They're gonna be starting to prepare for calcium-rich colostin production, and remember, 70 to 75% of the growth occurs in the last six weeks. But there's also a dietary component.
We know if you are unable to absorb enough dietary calcium to correct the deficiency in the circulating pool, then they're gonna immobilise calcium from the bone pool. That drives the weakness. Potentially drives the recumbency.
And it takes at least 24 hours to mobilise calcium from the bone pool. So that can cause a transient hypercalcemia, but we know quite often we don't get transient, we get a long-lasting or fatal hypercalcemia as well. We have to be careful if we're feeding fodder beet tops or ryegrass.
They contain large amounts of oxalates and these bind calcium in the diet. Russian formulation errors, we know this can be a big cause, management, human error. Decab diets, they've been found not to reduce the risk of hypercalcemia in use.
We know also if people are feeding too much phosphorus, it risks increasing the hypercalcemia by reducing the synthesis of activated vitamin D3 at the kidney. Why is that important? Well, if we are deficient in D3, then that will further reduce.
Absorption of calcium across the gastrointestinal tract, we need, The activated vitamin D3, the Calcitron, for intestinal transcellular, and also now we know for power cellular transport of calcium in the intestine. If we have insufficient D3, it limits the absorption of calcium across the intestinal lumen. To only 10 to 15% of what is normal, that's been shown in ruminants in humans and in mice as well.
So the other bit that we absolutely have to talk about, which unfortunately seems to be becoming more common. Is stress induced hypercalcemia and more and more of this now. Is due to heep worrying by dogs or dog attacks.
It is still caused by moving pasture or rapid weather changes causing stress. But it's really important that we Remind our farmers, but also as a whole sector, we're doing more to educate the public about the impact of sheep worrying by dogs, it's not just about, Dog bites or, you know, fatalities as a result of a dog bite or a dog attack. It's about the stress, running them round the field, that's how the sheep worrying by dogs as well.
And the latest data from the National Sheep Association shows that in the last 12 months, 70% of farmers had an incident of sheep worrying by dogs or a dog attack on their farm in the last 12 months. And these stress events, they redistribute calcium and magnesium in the body. That reduces the serum calcium concentration.
Dog attacks in particular, they can increase the respiratory rate, causing hyperventilation, that causes a respiratory alkalosis, and increased pH and that increases, The calcium in the blood that's bound to protein, so that decreases the ionised or the free calcium that's available, causing the hypercalcemia and the low serum calcium on test. But both of these two metabolic disorders, the hypercalcemia and the ovine pregnancy toxaemia, well they can be quite similar when they present. Through the untrained eye.
And remember that case from Phil Scott, where he describes the misdiagnosis of clinical hypercalcemia, the confusion with ovine pregnancy toxaemia. It's Written in lots of the literature, lots of people comment on the fact that farmers and vets commonly misdiagnose hypercalcemia, as they run pregnancy, toxaemia, respiratory disease, and even Listeriosis. In one recent study, approximately 60% of farmers misdiagnosed hypercalcemia, and that caused thee to die as a result of an incorrect diagnosis and or inappropriate treatment.
Our awareness of our advice that we give and our treatment protocols for ovine hypercalcemia need to improve as a sector. Because there are lots of similarities between clinical hypercalcemia and ovine pregnancy toxaemia. You are gonna see ruinalatomy.
You are gonna see a reduced abdominal tone. And both of these will progress to become recumbent. But luckily for us, while there are some key similarities.
There are many more differences. The big one is the onset and the speed of the progression of the disease, and this is why we have to get the diagnosis right, because if we get it wrong, we don't necessarily have time to go back for another diagnosis and fix it. So with your hypercalcemia, clinical signs within 12 hours, coma and death within 24 hours.
OPT a longer progression, clinical signs within 48 hours, stage 2 designs. Develop over a number of days. As in other species, clinical hypercalcemia and heep presents with hypothermia.
We don't get that with OPT. Goes without saying Beta hydroxybutyrate concentrations, ketone concentrations in the blood. Increased in A1 pregnancy to toxaemia, 1.1 to 2.9 mil per litre subclinical, greater than 3.0 mil per litre for clinical.
With a clinical hypercalcemia, a true clinical hypercalcemia. The BHP concentration will be below 0.6, it will be in the normal reference range.
And then conversely, well, the clinical hypercalcemia prevents with low blood calcium concentration, less than 2.0 milli per litre clinical, 2.0 to 2.8 for subclinical.
Whereas a true OPT presents normal calcium concentrations between 2.88 and 3.2 milli per litre.
We're gonna see some of the signs that we'd see in a clinical hypercalcemia in cattle or milk fever in our sheep too. We'll see an elevated respiratory rate, that's where the competing with respiratory disease comes in. We'll see that outstretched neck.
We'll probably see some constipation, we might see a distended rectum. We'll see a reduced or absent pupillary light reflex, and we're gonna see that rapid progression in reduction of demeanour, depression, coma death. In a true ovine pregnancy toxaemia, these are generally gonna be within normal reference ranges these last criteria.
But remember, there is 20 25% of over pregnancy toxemias that will be compounded with a concurrent hypercalcemia. So to treat a true hypercalcemia in sheep. We need to give calcium But what we now know, what we've learned in recent years, is not all roots of supplementing calcium are equal.
It's been shown Subcutaneous calcium is not the most effective way of supplementing calcium. We used to have a licenced subcutaneous calcium preparation, it's not on the market anymore. We've learnt a lot more about supplementing calcium, we've learnt better ways to do it.
And actually, because of the changes in products that are on the market, we've been able to bring clients on the journey with us to using new and actually, Better absorbed ways of providing calcium as well. Intravenous calcium obviously is gonna provide a rapid increase in serum calcium concentration, but we also know this now has a short-lived effect. Because we give a rapid increase, and it lasts for a few hours, and that doesn't increase the mobilisation of calcium within the body.
So we get in a deer and a rebound hyper I've seen it. If we're gonna give it, we want to give it slow IV, 20 to 40 mLs of a 40% calcium b gluconate solution. But to avoid that rebound hypercalcemia than the deer, we wanna follow that IV calcium.
With oral calcium for a sustained effect. And preventing the deer. We know oral calcium has a longer and more sustained effect.
We also know it's easier to administer on farm as well. Lots of sheep farmers, lots of clients. Aren't trained or don't want to give intravenous calcium, but they are all capable of providing oral calcium.
It's easy to administer on farm. Since the removal of the 20% calcium boo gluconate products in 2019 that could go under the skin, lots of farmers have moved to giving all. In my experience, it's well tolerated by the ewes.
It's easy for farmers to. To do, they can't put it perivascular, like if they're trying to get an IV and they get it wrong, they can't cause damage and they can have a good effect with sustained and long-lasting elevation of that calcium concentration. Should we give anything else?
We absolutely could. For the last 30 years, we've known that you with a prolonged hypercalcemia, so hypercalcemia that lasts more than 24 hours, they're also dehydrated. Evidenced here in this study by the change or the increase in packed cell volume as a measure of dehydration.
And the authors of the same paper that demonstrated this, well, they showed that fluid therapy with sodium and potassium would also be beneficial for keeping. The fluids that were provided. In the correct place, not losing them into the cells, keeping them in the extracellular fluid, increasing the circulating volume.
So we could give oral fluid therapy, or if we're on the farm, we could give intravenous fluid therapy. And remember 97% of these hypercalcemia don't receive veterinary attention, so we need to educate clients in how to provide safe and effective fluid therapy. There's a video that we can refer clients to to show them that we can train our colleagues with as well.
But we need to be having the conversation, looking at protocols ahead of the landing time, if we're doing bloods. Before lambing to check energy status, check nutrition, then it's a really good chance to review these protocols, talk about what we're gonna do if we get problems, talk about how we're gonna prevent them as well. And then The 3rd of the big 3, well, that would be hypermagnemia or staggers.
And this one Nearly always presents after lambing. Often it occurs after first turnout within the 1st 6 weeks of lactation. Because that's when we get heat lactation.
Peak milk production about 6 weeks into lactation. And It's important to remember, particularly if we are maybe mainly dealing with, with cattle in our, in our practise, and we're not doing that much sheep work, we're seeing most of our sheep work just in the periparter period. Well, it's important to remember sheep's milk has a much greater concentration of calcium, magnesium and phosphorus in it than cow's milk.
So at peak lactation, they are losing a lot more magnesium than, say, your average cow would be. They need 7 grammes of magnesium intake peru per day. They can't produce their own.
They're entirely reliant on absorbing magnesium out of the rumen, so from the diet to meet these requirements. And we know if we turn out, we get good rain, we get a nice growth of lush grass. We think that would be good, lots of food available, lots of grass available for grazing.
Lush grass grows really quickly, it's really high in. Nitrogen and potassium, and these inhibit the absorption of magnesium across the rumen. Also, lush grass is normally rapid growth, so it doesn't have time to build up appropriate quantities of magnesium.
And if we're using high in nitrogen or high in potassium fertiliser, well that can increase the risk as well for the same reasons. So if we get a case of hypermagnamia, a case of staggers, how are we diagnosing? We've got some fairly characteristic clinical signs.
We see a hyperesthesia. We'll see ataxia and this will rapidly develop to collapse. Oushotonus Seizure, muscle fasciculations, and these will also often present as sudden deaths.
So if we are called to a sudden death, we need to take a history. We want to try and look at the grass around the carcass as well. Have there been evidence of lots of thrashing, lots of paddling?
Is it in an opposotonous type position with that net thrown back? Did the farmer see seizures or muscle fasciculations before it died, if they saw it alive? If we get it alive, then we want to test the magnesium in the blood.
If it's below 0.6. And that's gonna age your diagnosis.
But as I say, lots of these we are gonna find that we are gonna see them as sudden deaths, and we're gonna want to do a postmortem. So it's important that we refresh our sample connection skills as well. Because we want to test the aqueous humour.
And we need to test that aqueous humour within 24 hours of death. If it's below 0.33 mm per litre, again, that can be indicative of a hypomagnesaemia.
Make sure when you collect your sample, you're not disturbing the iris or getting any contamination. We just want pure aqueous humour. A history of nutrition, of turnout, of the grass growth, any fertilisers used, anything that the farmers saw if we are called to a dead you, it's gonna be important to build that clinical pit too.
If we're called before the sudden death though, we're called to alive, then we want to think about treatments. We want to provide 20 mL per 70 kilogrammes of a warm, calcium boring gluconate with magnesium product intravenously. And at the same time, we want to put 50 mL per 75 kilogrammes of a 25% magnesium solution under the skin.
Make sure that we get this the right way round. We put a large bolus of magnesium solution IV, we will, of course, be more than likely to cause a fatality. But in reality, most of these are found dead.
So it's about what we can learn and what we can do to prevent any other losses. So if we find one case and we diagnose. A hyperglycemia, whether it's on the aqueous humur, whether it's on postmortem, whether it's on the history or signs that the farmers saw, then we need to trigger preventative action rapidly.
We can think about water supplementation. We could dust the area with concentrates. An intraruinal bonus is a good option, but remember that's only a short term fix.
A ruminal bonus only lasts for 3 to 4 weeks. We could drench with a magnesium solution, but again, it's probably not a long-lasting fix. We want to add hay to the ration because that increases acceleration and that reduces the ruminal.
Potassium sodium ratio. And we want to just review which fertilisers we're using. If we're using ones that are really high in potassium or nitrogen, can we use anything else?
Can we move the ewes onto another field if they've just applied fertiliser and put them onto a field that's had a lot of fertiliser put on? Can we move them to another field to reduce the risk? We need to look at the management.
And that's a key part of all of these. Yes, they are clinical conditions, yes, we need to think about the individual affected use, but we need to also think about the wider flock level advice we're giving in terms of prevention, treatment and management. We know they often originate from nutritional issues.
We need to remember when we think about a pregnancy toxaemia, the financial losses, the impact on the flock. Well, it's not just about you mortality. Clinical and subclinical disease has sizable other impact on you health and lamb production.
Remember, colostruum quality, daily life weight gain, milk quality, potentially more abortions. We do not have good reliable. Proven hen side diagnostics that can allow for a rapid definitive diagnosis of over pregnancy toxaemia.
But we do know Oine pregnancy toxaemia is often confused with hypercalcemia. Pract protectionists need to have a good working knowledge of the similarities and the differences when it comes to clinical signs. Remember PLR presence of constipation and presence of hypothermia, or they'd be some of the key differentiators.
This really will feed into part two of this two-part lecture series, but we can use pre-lambing visits, strategic advice visits, and metabolic profiling to discuss the risks early, educate clients on the management and prevention of periareric metabolic disorders, and reduce the prevalence within the flock. We need to partner with our, our sheep producers and not just be called out as the person who sees the sick sheep or the person who does a lambing of caesarean section. We need to be a partner in the business, and we need to be able to give advice ahead of the time and work with supporting our farmers and building that vet farmer relationship.
So that's what part two of this two part series will cover. Part two, we'll think about in the run up to lambing in the peri-art 2 period, what can we do for housing, nutrition. How can we optimise oculum quality, and is there anything we can do to reduce, Vaginal prolapses in sheep as another common cause of losses or economic impact.
So relevant to this lecture in the metabolic disorders. Suggested further reading and some of the references, drawing from what we've now learnt in the last, particularly the last 5 years actually, is to massively build out this evidence base and increase our understanding of these conditions, the prevention, treatment and management. Further information and more links to those publications and the QR code.
And we'll see you for part 2.