All right. Hi. My name is Doctor Kelsey Walker, and today I am presenting colic and South American Camelets and how we can manage these as practitioners.
I'm going to be focusing on the two domestic species from South America. So, the, the llamas and alpacas. There are two more non-domesticated species, the vicunas and guanaos.
And a lot of what I'm gonna talk about today can be extrapolated and used for those two species, but we'll be focusing on the two domestic species that you are much more likely to actually see in practise. So, our learning objectives for today, I'm going to go over the definition of colic, why the colic and why we see those clinical signs and pain, as well as some of the more common etiologies. I'll be talking about clinical signs in colic, in alpacas and llamas, they have more subtle signs than what we classically are used to seeing in a lot of our other species.
And then I'm going to discuss some of the diagnostic workup that you might expect on the alpaca or llama, as well as some specific findings that you can see with a couple of these specific diseases. And when a diagnostic workup might lead you to think that you might want to do a surgical intervention versus medical. I'll talk about the basics of medical mal management for colic in these species.
And then when do we decide to go to surgery, how do we push for that, and then some of the basics of how I'm going to approach the abdomen or which organ system that I would like to, or which organ I would like to reach. Going to briefly go over just a little bit of anatomy on these species cause it's a little different. They have a gastrointestinal tract that is going to be closer to a ruminant or a cow than it is to a horse.
They have pretty complete bacterial fermentation in their four stomachs. And it is divided into three compartments that are conveniently called compartment 12, and 3. Compartment one is somewhat analogous to the rumen and reticulum.
But unlike cattle that have a really defined fluid layer and fibre mat, they tend to have a more homogeneous mixture going on. They also tend to have a few more contractions over 2 minutes, a little bit more frequent than, than a cow does. C2 is similar to the Omasum, but not exactly the same.
And then the C3 is somewhat like the limasum and the kind of caudal 20% or caudal fifth. The first cranial 4/5 of C3 still has quite a bit of that bacterial fermentation going on. So that last fifth is going to be that more true stomach where the pH is going to drop and it's going to be lined with more of those gastric glands.
C3 goes into the proximal duodenum. The diameter of that duodenum is gonna be about the same when it first starts. And then it will decrease in diameter as it goes throughout the length of the small intestine.
And it will reach a maximum diameter of only about 1 centimetre for adult alpacas, and then 2 centimetres for adult llamas. It will not normally be that dilated. It is usually only when there is ingesta actively passing through or if it is dilated due to an impaction or fluid that is backing up.
It does have the proximal duodenum or cranial duodenum does have this really prominent M-shaped loop. So the combination of those frequent turns in addition to the decreasing diameter causes this to be an area where we tend to get gastric impactions and where we tend to get our bazaars that get stuck. The cecum is fairly small.
It is going to only be 7 to 10 centimetres long in alpacas, and then about twice as long in llamas, which fits cause llamas are often about twice the size overall as alpacas. And then it goes into the spiral colon. And the spiral colon does 5 loops kind of concentrically, and then does a hairpin turn called the pelvic flexure, and then loops back the other direction and where it goes into the rectum.
The spiral colon, All the loops themselves are pretty closely adhered to each other, kind of in this big ball. But then it is extended from the mesenteric root by pretty, by a pretty long tree. That has an advantage.
For us surgically and that we're able to really pull the spiral colon out of the intestine, exteriorize it, out of the abdomen fairly easily. The downside is because it's so long, it is more prone to being able to wrap around itself or wrap around other structures inside the abdomen. I have a couple of pictures here, just so you guys can see a 3D view of this.
Similar to a cow or a sheep or goat, the entire left side of the abdomen tends to be taken up by the gastrointestinal tract. So if I were looking inside the left side of an alpaca's abdomen, this is an alpaca's C1 here. I'd be able to see mostly C1 with both the cranial and caudal sacs here represented by numbers 1 and 2.
And then C3, I'm kind of seeing down going along ventrum towards the caudal part of the animal, if they were intact. Numbers 3 and 4 here are the beginnings of the circulations that are present in C1. We'll be able to see those more extensively on the right side of the abdomen.
So here you can see in the middle, those big circulations represented by 2. C2, compartment 2 is a little bit more dorsal than we expect for if it were going to be similar to the Omasum. It tends to be a little higher in the abdomen.
And then C3 is this very long, almost tubular compartment. And again, this portion that would be towards the animal's head on the right of the screen is going to be more fermentative versus when it's going down to the lower left of the screen where we see DA where that is going to be the dorsal or the cranial duodenum. You can almost visualise the M if you really squint just right, the M in that cranial duodenum that is appearing.
The 4, kind of that black outline in the middle, that would be where the omentum would be attached. The omentum has been removed for the purposes of this picture. So just a little overview about colic itself.
The major mechanism why the animal has colic or abdominal pain, it's gonna be really, really similar to pretty much all the other mammalian species that we see colic commonly in. It just has to do with the stretch receptors that are going to be activated, and these can occur both in the mesentery, in some of the visceral ligaments, and in some of our organ capsules such as our kidneys or our liver. Muscle spasms can cause some pretty sharp abdominal pain, and then just inflammation, whether that's in a viscera, in a solid organ, or just throughout the entire abdomen with a peritonitis.
And then ischemic lesions, all of those can cause abdominal pain or colic. Due to their anatomy and physiology, gas colic is relatively uncommon in adult camelids. They are able to regurgitate excess fluid quite nicely.
They have that nice muscular oesophagus that allows them to bring up a cud. This also allows them to regurgitate. It allows them to get the gas out from all that for stomach fermentation.
They have less hindgut fermentation, which causes less gas colic further down the GI tract. Although juvenile animals that are drinking milk can get a form of gas colic, kind of called milk colic. It tends to be pretty profound colic for a short period of time and then it resolves as it works its way through the system.
For common etiologies of colic, I've kind of divided it here into medical versus surgical. The items that are bolded are items that are more common based off of retrospective studies on alpaca and llama colic. And I'm also gonna focus on a couple of diseases where I'm going to talk about some specific treatments that might be out of the, the normal treatment options that we would choose.
Emeria macuaniensis, I will focus on briefly. For the enteritises, there are viral enteritises that can occur. Rotavirus and coronavirus are common.
There are other parasitic infections such as Tricurus, and then there's case reports of impactions from tapeworms and juvenile alpacas. Bacterial enteritis can occur. It's can be due to, most commonly clostridial enteritis, but it can also be due to salmonella.
These are usually secondary to other underlying processes. I have gastric impaction here with a little scar. Depending on the severity of the impaction, it can be managed medically, but if it's extensive enough or if the concretion has actually turned into a bazaar that won't be able to be passed, this can become a surgical lesion.
Salaframine poisoning is a regional and seasonal event, but it is a known cause of colic. These are often seen with lots of hypersalivation or slobbers and other sled signs, generally self-limiting, fortunately. I'm gonna touch on compartment 3 and duodenal ulcers just briefly.
As we'll discuss, it's not something that we know is a primary cause of colic but can occur with secondary disease. It'll, they're difficult to tell if they're primary or secondary. For the surgical lesions, I have these in order of frequency based off of one retrospective study where distal obstructions were more common than the proximal obstructions.
And then there was a few reports of ruptured viscous, septic peritonitis, and Necrotizing neuritis. Interestingly, unlike ruminants, where we think of displaced abemasums, there are no current reports of C3 displacements. So that is not one of our known causes of surgical obstructions.
There are, of course, some non-gastrointestinal. Diseases that can cause abdominal pain. Most commonly, like your genital system, we think of urinary tract obstruction.
And then these species have uterine torsions, relatively common compared to some of our other species. Somewhat anecdotally, of the, I've had several alpacas that have presented to me for dystociia that the majority of them turned out to not be pregnant, and they had gastrointestinal colic, and then a couple of them had a, a uterine torsion instead. The last kind of major organ system that we think of that's contained in an organ would be the, the liver itself.
And that can be due to several hepatopathy such as lipids, lipidosis and hepatitis. They don't have a lot of incidence of liver lobe or splenic torsions. It's very, very rare.
And then you can have colic associated with just a generalised peritonitis, not anything that's necessarily associated with an individual organ. I'm going to touch here, like I said, on compartmental ulcers. These are often subclinical.
A lot of them are incidental lesions found on postmortem necropsy exams. So how common these really are is really difficult to determine. And a lot of times, it's hard to tell or almost impossible to tell, was the ulcer the primary cause of the colic, or were they secondary to another disease process?
The aetiology is inconsistent. Specific historical factors have been found, although not every animal diagnosed with this would have one of these factors. Most of it is a management thing, similar to a lot of hor horse ulcers.
We think that as management. So, harassment from a dominant camelet can cause these, recent transport with or without a delivery of rea, just delivery of crea by itself, grazing, lush spring pasture, and then I've bolded some causes that you might be seeing in Hospital. So when we talk about prevention, we might want to talk about preventing ulcers.
So transport enteritis, septicaemia, GI foreign bodies such as bizarre's, or bowel ischemia. So these cases, we might consider ulcers as a comorbidity. Diagnosis is really difficult pre-mortem unless the ulcer becomes so extensive that it perforates.
Unfortunately, once it perforates, the prognosis is grave. It is very, very difficult to treat these effectively. So we often, if we're going to treat these, we have to do it as a preventative measure or kind of empirically.
Because we don't know the underlying causes and it's not consistent, treatment can be a little bit controversial. I generally, if I have an animal that's in the hospital, an alpaca or a llama, that's going to be there for stress or for surgery, I go ahead and start them on treatment just because I know this is a known comorbidity, but that is somewhat clinician-dependent. There is not a lot of drugs that are successful in raising the C3PH.
The only ones that we have are required to be given either IV or subQ. Pantoprazole is effective. You can give 1 mg per kg IV and then double the dose of giving subQ.
This can be done every 24 hours. Omeprazole high dose IV is effective as well. Other medications we have are either not recommended or are known to be ineffective.
So cimetidine, ranitidine, those are known to be ineffective. Oral omeprazole is ineffective. Sacralfate, high dose has been attempted, but it requires a lot of it and is not thought to really be, there's not any demonstrated that it is efficacious.
Misoprostol is effective at raising the C3PH, but it has an unacceptably high rate of adverse reactions, including collapse and death. So we don't generally recommend misoprostol for our South American camelids. Emeria macuaniensis or EMA is also sometimes called just a large coccidia.
There is a lot written on EMA, so I'm not gonna go into it in a great deal of detail here, but I would be remiss to not at least briefly discuss it as a cause of colic. And it can cause signs anywhere from being very subclinical to intermittent low-level pain in colic to an animal with chronic ill thrift. And hypoproonemia all the way to an animal that acutely collapses, has peritonitis, maybe with very, very minimal previous signs.
This particular organism, it has a really long pre-patent period of anywhere from 32 to 43 days. And the O cyst is substantially larger than the typical limeria. This can make it difficult to sometimes diagnose with a faecal float.
You have to have a really high specific gravity faecal floatation solution. And then you can have colic signs without having any evidence of the O cyst just yet. Or when they have those intermittent shedding, you can have signs even with those not being present.
Due to this, a lot of times we treat for immeria or EMEC somewhat presumptively or just empirically based on the clinical signs fit. I will talk about a couple of other diagnostics that can make immeria a higher differential. But in general, we treat these quite, quite frequently without having a definitive diagnosis.
Pennazaril and Toltazaril are effective against multiple life stages of the parasite. They still have to be given for several days in a row. Amprolium.
Needs to be given for 5 days in a row. The downside of Amprolium is it's only effective against the juvenile forms. And so it's not necessarily going to decrease shedding of that parasite right away.
And then, lastly, the sulfa antimicrobials are ineffective. This is true for dimeria. It's also true for any antibacterial properties that you might want.
It's just does not reach blood therapeutic levels once the foresomach of that animal has really developed, which occurs within a few weeks of age that development starts to occur. All right. So clinical signs of colic.
I mentioned earlier on that clinical signs can be a lot more subtle. So, for a lot of what we see, our behaviour, what that animal is doing in front of us is often the first clinical sign and the most reliable indicator that what is going on with our animal is due to abdominal pain versus another type of disease. Younger animals, animals like 6 months of age or younger tend to be more demonstrative, and they'll have more of those kicking at the abdomen, rolling violently on the ground and thrashing.
Those things we think of with horses, for example. As they get older and become adults, they tend to be a lot more stoic. And the clinical signs can be very, very subtle.
They might be laying in cush with their legs kicked out to one side, or they're kicking them back and forth a little bit. They might be more restless, just getting up and down. They might be having, grinding their teeth or broxysm.
And for inexperienced clients, they might be missing that broxysm and thinking it's just chewing their cud. Normally, llamas and alpacas will sit in like the sphinx cat perfect cush with their head up in the air, kind of looking around. So abnormal head position with their head directly on the ground, their neck flat out, or with their head laying against their side, those can be abnormal.
It's not specific for colic, but usually that animal is pretty sick if they're doing that. Vocalising or abdominal straining can occur with more severe stages of colic. But it is important to remember that camelids can have very mild or subtle signs and still have a life-threatening obstructive lesion, especially if that lesion is more distal, farther away from the poor stomachs, that might be more subtle signs.
I have a couple of pictures here. So this animal on the left looks pretty calm, like he's resting and not having any major signs. But you can look at his back legs, and they're ever so slightly kicked to the side.
This would be an animal that we'd wanna keep a closer eye on and see if clinical signs progress. Or maybe we need to do some further workup and evaluation. Lamas and alpacas can on occasion lay in lateral or roll, kind of dust bathe.
But you can tell with just some observation on this animal on the right that while he's on his side, he's been doing this for a while because he's disrupted all that bedding around him. So this could be an animal that maybe is in the hospital and you're walking by and kind of looking at it and you just have that thought like hmm maybe I need to look at that animal a little bit more closely or maybe I need to, you know, discuss with my clients so they recognise these symptoms at home. The hands-on physical exam, a lot of it is really variable.
So, the temperature, heart rate, and respiratory rate can be high, low, or normal. And any changes can be non-specific for both the underlying disease process and then how severe that disease is. Dehydration and depression.
These tend to get worse the closer the lesion is to the pylorus, the farther or out it is. And the more complete the obstruction, again, the worse dehydration, depression. And then if any condition goes on long enough, we can have clinical signs.
Anorexia, lack of faeces, and gastric hypomotility are really common with a lot of diseases that occur, so they're non-specific. Conversely, if you have an alpaca or llama that is appetent, has normal faeces, and is ruminating, that makes it less likely that it is a gastrointestinal condition or it's something very, very mild in the gastrointestinal tract, something transient. But you can't 100% rule out that you don't have like a really early stage of more severe disease.
So we don't just wanna rule out keeping a close eye on that animal if there is something else going on, some historical reason why they need to be looking at them. Like with cattle and sheep and goats and most of our species, faeces and defecation habits are really useful. They can help in this case, guide us towards maybe what type of gastrointestinal lesion do I have.
Obstructions, and this will depend a little bit on if it's a partial obstruction versus complete. But they start with more of those normal faeces, and then it goes to a dry or mucus-covered faeces, and it may progress to no defecation at all. Entrapments, we can have small amounts of normal or blood-tinged faeces.
And then strangulations, necrotic enteritis, and peritonitis. Those can start with diarrhoea that tapers off. Although those tend to be so, such severe lesions that we might not even really be noticing this diarrhoea before we're seeing, hey, my animal is down, is really depressed.
So this might be a secondary finding. Imuria or EMA can have kind of a characteristic finding with defecation where you've got this consistent passage of small amounts of diarrhoea with some ongoing colic signs. The diarrhoea doesn't really increase or decrease.
It's just kind of very, very consistent over time. If we have continued profuse diarrhoea or normal faeces, so the normal amounts of faeces over time, those are rare with surgical GI lesions, but we can have inflammatory lesions that will cause continued profuse diarrhoea. So it's not ruling out gastrointestinal lesions as a whole.
It's just less likely to be surgical. If the lesion is really far cranial, so right in C3 or going into the proximal duodenum, there are some more specific signs that we can see. They are mostly associated with fluid backing up into the four stomachs.
So the stomach itself, that's C1, C2, as we saw earlier, is a very, very large fat. So it can start to distend and cause quite the pot-bellied appearance. If the animal's in full fleece, it can be difficult to appreciate that pot-bellied appearance where you actually have to put your hands on the animal.
As one of my mentors used to say, you can't trust the fluff. So you have to really kind of feel. If they're sheared, of course, it's a lot easier to appreciate.
These animals can become profoundly dehydrated and profoundly depressed. And then if the fluid backs up far enough, the fluid can back into the cardiac where they're starting to have spontaneous regurgitation or vomiting that we're seeing. There are a few other conditions, some of which are more normal, such as pregnancy, for example, where we can have some of that pot-bellied appearance.
These should not cause that regurgitation or vomiting. They can include advanced pregnancy, effusive. Peritonitis, some of the enteritises.
And then if they have gotten their head caught in a fence, and they have venous congestion, for example, secondary to strangulation, they can have some of that. They're not eruptating appropriately. They can have some of that pot-bellied look.
For diagnostics, some of these are gonna be just general good information to have and they're not real specific. So for example, the complete blood count, we're looking at leucograms and differential counts are gonna be frequently abnormal with a lot of disease processes in our South American camelids. You can have changes due to any disease that can be camouflaged by stress neutrophilia.
So they might be a neutropenic, but you don't see that right on presentation to the hospital. So what is more helpful for us for an inflammatory or infectious lesion here is looking for signs of immature granulocytes or toxic changes. That's a little bit more specific for an infectious or inflammatory disease.
The red blood cell count in morphology is not specific to colic. This is good information to have if we're going to be going to surgery. Knowing if that animal's anaemic is very useful.
We can see some evidence of toxic change as well. And then fibrinogen can give us indication for inflammation. The serum or plasma biochemistry is gonna give us some good info.
The electrolytes, the chloride is gonna be the most important, electrolyte for diagnosing gastrointestinal causes of colic, especially for those really proximal lesions where we might be seeing a hypochloremia in our blood. Camelids tend to trend more towards hypernatremic as opposed to hyponatremic. And hypokalemia is pretty much universally seen in any condition that causes our alpacas and llamas to go off feed.
It's very, very common. If you see a hypochloremia and hyponatremia, but you don't have a concurrent metabolic alkalosis, that is very suggestive of EMAC. A lot of causes of disease in alpacas and llamas, especially gastrointestinal, can cause a hypoprotemia.
And we might need to supplement with plasma. So looking at a total protein is really helpful. It also gives us an idea of the albumin globulin ratio to determine do we have one that's preferentially lower than the other or not.
Other enzymes that we can look at are like renal and liver enzymes. They might be specific. A lot of times it just guides us towards looking for comorbidities, but they might be elevated by themselves, leading us to, do we have more of a renal injury, not gastrointestinal, or is it liver.
Creatinine tends to be more useful for renal, values than BUN just because of diet. These are also useful for overall prognosis. Lactate is helpful for evaluating perfusion status.
It will also be useful when we're comparing it to our abdominal fluid if we're doing an abdominocentesis to check for possibilities of ischemic lesions in the abdomen. For acid-base balance, metabolic alkalosis is more common, and even just ileus by itself. So if they're off feed, if they're just not feeling well, they're not eating very well, this can cause a mild metabolic alkalosis by itself, just from the sequestration of chloride into compartment 3.
Small intestinal obstructions can cause a profound metabolic alkalosis. And small intestinal entrapments and cecocholic obstructions can cause a mild metabolic alkalosis. But a lot of times, this is a secondary finding to other more severe clinical signs.
Metabolic acidosis is more commonly going to be associated with, we have a hyperlactatemia due to like inflammatory lesion, ischemia, or due to an obstructive lesion that has been there for a long period of time and that we are having hyperlactatemia. These tend to have more severe disease and overall a poorer prognosis. Rectal exam is a cornerstone of diagnosis in cattle and horses.
With colic, we get, it's feel quite a bit. It's often very useful. Unfortunately, due to the size of llamas and alpacas, it's a little bit limited.
So large adult llamas, we can do rectal exams or if you have a clinician or really small hands, you can do a lot more of these animals. The biggest concern here is you have to have really good restraint, both physical and potentially with chemical restraint. These guys tend to, whenever they have something they don't like, if they're standing, they tend to abruptly collapse.
And if they're sitting down or like pushed, they will sometimes just spring up into the air. So good restraint is important. There have been rectal tears and bladder ruptures reported from rectal exams.
In addition to the chemical restraint, we can also consider infusing lidocaine into the rectum to make them more comfortable. If you're able to perform a rectal exam, it is similar to cattle. So you've got compartment one taking up a good part of the left side of the abdomen.
You can palpate bladder and the female reproductive tracts. You should be able to feel the caudal pull of the left kidney. And then down in the right ventral abdomen, there really shouldn't be any distinctly palpable viscera.
If you can feel something that's distinctly palpable, it is likely going to be an impaction or an interception or dilated loops of bowel. So I can help you guide, do I need to go to surgery or not. Transabdominal ultrasonography has replaced the rectal exam, because it is easier to do and generally safer.
You can do transrectal. It just tends to not give you quite as much information cause you can't see as much and we generally do the transabdominal. This can be done with the animal standing or laying in a cush or on their side, depending on what their comfort is.
You can go into the flanks and see fairly well, but if they're in fleece, you either have to part the fleece to be able to see into the abdomen, or if you want to do a really complete exam that may require clipping or shearing. There's a lot of work that we need to do to establish some of the parameters of normal, what is versus abnormal. So thickness of the wall is still somewhat subjective, but it's going to be really helpful for determining, do I have free fluid in the abdomen?
Is it going to be in the viscera instead? Do I have two populations of bowel? You can't Really see it inside the lumen of the viscera, just like in other species, but it should help.
You can tell, do I have decent peristalsis. And then if peritoneal is visible at all, it should be very scant in a normal animal. If you have large amounts of peritoneal fluid, that should really direct you towards, I need to do an abdominocentesis.
There is something going on inside, inside that abdomen. Then Collecting an abdominocentesis is a slightly different position than we're used to in horses and in cattle. It's generally done in the right paralumbar region.
So this picture here on the right, the curved black line towards the right of the screen, it's gonna be the last rib. The red dot there is the abdominocentesis site. And then the black straight line is the internal, external abdominal oblique muscle attachment.
Doing this with the T cannula is recommended and similar to rectal exam, we need to have really good restraint during this procedure cause they tend to collapse even with a lidocaine block. They tend to collapse once you go through that, the peritoneum. I've included here some normal indices.
Normal peritoneal fluids should be clear and colourless to light yellow. Total protein should be less than or equal to 2.5 grammes per deciliter.
The nucleated cell count, the total count is more important than the percentages. So the nucleus cell count total should be less than or equal to 3000 cells per microliter. The reason that is more important is on studies of healthy alpacas and llamas, they found a huge variation in neutrophil percentage anywhere from 15 to 98% compared to other herbivores.
So the nuclear cell count total, again, is a lot more useful information for us. If there is a nucleid cell count of greater than 5000 cells per microliter in combination with a total protein of more than 3, this is suggestive of a surgical lesion. You can compare the lactate to the peripheral blood.
Lactate should be less than the peripheral blood. If it is greater, we need to start thinking about potential of ischemic lesions. The glucose of the abdominocentesis is generally not useful.
You, it is potentially helpful for peripheral for a couple of conditions, but the abdominocentesis value is generally not super diagnostic. Other diagnoses, diagnostics we can consider. For stomic fluid analysis is useful for a lot of conditions, but for determining why this animal is colicky is, is not super helpful with the exception of C1 chloride.
The normal pH just for your information, is 6.4 to 6.8.
It can be higher if they're not eating or if you have salivary contamination. The normal C1 chloride should be less than 30 mLivalents per litre. Once it starts getting above that, especially if it is getting above 40 mcs per litre, that is gonna be suggestive of a surgical obstructive lesion, especially a more proximal obstructive lesion.
Faecal floatation is helpful for diagnosing endoparasitic infections such as tricurrus and tapeworms. As I mentioned before with Imeria, EMA, it is a little bit less specific and a little bit harder to find. The faecal occult blood analysis, would seem like it would be useful for diagnosing ulcers.
Unfortunately, there's a large incidence of false positives and false negatives, so it's generally unrewarding. So we don't really do that very often. Plain film radiographs are not really helpful for a lot of our causes of colic that tends to be obscured by the large gas ingesta of C1.
So if we're going to want to do advanced imaging of the abdomen, we often reach for CT or computed tomography. This can help identify thickened bowel. And if we have masses or neoplasia, those have been reported in the abdomen.
Endoscopy is gonna be limited to esophageal lesions going into C1. We can't see anything past C1 and we cannot fast them long enough to be able to see past that. So endoscopy has pretty limited utilisation.
When we get to the actual management of colics, we've done our diagnostics based on clinical signs. We think that we have a colic sign. A lot of the medical management is Going to universal for a lot of diseases.
If my animal's dehydrated, I need to restore hydration. I want to restore electrolyte and acid-base disturbances, and then protein norms. Fluid therapy can be a little bit complicated in South American camelids.
The biggest problem is because of the high prevalence of hyperprotonmia, and it can be difficult to estimate how, how much of a deficit they have, it can be relatively easy to fluid overload them compared especially to our cattle or our equine species. If we're going to be using a lot of fluid therapy, we need to be looking at our patient, making sure we don't have signs of any edoema, making sure our lungs sound clear, and then monitoring for signs of edoema both systemically and externally prior to and then during our IV fluid administration. If we have indications for plasma, we might want to go ahead and utilise that prior to or in combination with fluid therapy.
I'll be discussing plasma just a little bit on the next slide. Amount is going to start with our bolus if they, we think that is indicated. It's going to be a relatively low bolus where we can go up to 5% of body weight in adults.
Although I often utilise a little bit more caution and start lower than that and then work my way up unless my patient is just very, very, his perfusion is just very poor. Neonates, you can go a little bit higher. So you can go up to maybe 10%.
Again, keeping a close eye on that animal to make sure that we don't have any signs of pulmonary edoema forming. Following the initial bolus, if it is indicated, we can follow that with a 2 mL per kg per hour for adults, up to 4 mL per kg per hour for our neonates. Generally, a polyionic buffered fluid is, is pretty, is generally adequate.
Hypertonic saline, these patients are generally small enough. We don't really have to reach for hypertonic saline very often unless they're just very down and out and it's kind of a last resort. We also have higher incidences of hypernatremia and stress camelids.
So you might wanna consider, do I want to give that much sodium and chloride to this patient unless I have a really good indication to do so. Plasma transfusions could be indicated if the blood albumin is less than 2 grammes per deciliter or your total protein is really low at less than 4 grammes per deciliter. There is commercially available llama plasma.
This is used with, for both alpacas and llamas. Generally, adverse reactions are, are pretty rare. We don't have a lot of problems with that, fortunately.
And the commercially available plasma is going to give you a dose range. It'll be 15 to 30 mLs per kg. We often start 20 mLs per kg like with horses.
And you can consider doing this. Do you do it as a bolus versus do I have an ongoing protein loss from an inflammatory bowel condition or maybe a CRI is gonna be more indicated. This can be an expensive endeavour, but for some of our animals, especially our really high dollar breeding animals, it is worth the investment.
Especially if we're gonna be considering, do we want to go to surgery. Pain management is important for colic. Pain by itself can cause ileus.
So if we can help reduce pain, reduce inflammation, we're more likely to get that animal eating again. They're more likely to have more normal gastric motility if that is like an, a mild impaction that maybe we're trying to get past. If there is a surgical lesion, just be aware.
Like with other species, it is possible that we can temporarily mask a surgical lesion if we really go gung ho with our pain management. So we want to be keeping a really close eye on those animals. Low dose flunixin melamine at 1.1 mg per kid, kind of the low end of the range, IV every 12 to 24 hours.
This is going to give some mild pain relief. It tends to not control anything beyond really mild colic. So we may have breakthrough pain that might lead us towards, do we need to look for other causes of more severe causes of our colic signs.
It is also useful for just reducing inflammation and then even lower doses of 0.5 to 1 mg per kg IVQ 12 hours can be useful for some of our causes of enterotoxemia. So that can give us an adjunctive therapy there.
If we need to reach for more aggressive pain management or post-op pain management, we can use lidocaine, similar to a horse as well as ketamine, 0.05 mg per kick per minute for the lidocaine, or ketamine up to 40 mcg per kg per minute, both of those as a CRI. That can be beneficial for, again, more aggressive pain management and for postoperative pain.
In general, we want to avoid reaching for the alpha-two adrenergic agents, at least for repeated dosing, especially for pain control. We do worry about the cardiovascular effects of these drugs. Antibiotics or antimicrobial therapy.
This is especially indicated if we have confirmation of a bacterial enteritis or if we are concerned for enterotoxemia, both of those would be reasons to reach for antimicrobials. If we had a severe neutropenia, we would want to reach for antimicrobials, for example, as well. And you can consider reaching for these if you're having to do abdominal surgery.
If you're having to enter or do, those kinds of things, we might wanna reach for antibiotics. We really very often do not have a definitive cause of bacterial enteritis. So, we generally reach for broad spectrum.
If clostridial enteritis is suspected, we reach for very, very high dose penicillins. So, clostridial enteritis would be an animal that is very, very acutely, very ill, very depressed, very dehydrated, has bloody faeces. Those would be things where we want to give a higher dose penicillin.
Penicillin is often combined with amino glycoides to help increase the spectrum. If we're going to be giving amino glycosides, we just need to consider a hydration status and maybe consider IV fluid supplementary therapy, even if my patient didn't start off really dehydrated. Especially if I'm going to be adding this to bantamine or fluexin that I'm already administering.
There is some argument for adding metronidazole, for increased anti anti anaerobic spectrum. If we're gonna be using metronidazole, just be aware of the legality of doing so, providing adequate withdrawal times. There are people who do eat their llamas and alpacas and consume those animals.
So we do want to make sure that we are following appropriate meat withdrawal. Setia sodium is useful, and it does have to be given more frequently at a higher dose than label indication for cattle. But it may not have really great distribution or sufficient distribution to the peritoneal cavity.
So when we're targeting a gastrointestinal lesion, this might not be the, the best antibiotic choice. We get to surgical management. I'm not going to go into a lot of the surgery itself.
Mostly, I'm gonna focus on the reasons why we might reach for surgery. That can be done based off of either clinical signs or based off diagnostics that can help support that decision. So on the clinical signs, we might see continuous or intractable pain, especially if this is after administering pain medications.
Or if there is a persistent low-grade pain that continues despite adequate supportive care. However, as I mentioned earlier with EMA, both of those can be seen even if we have a medical lesion in ours, for example, the EMAC is treated medically. This has led to some cases that have not gone to surgery as early as they should have because EMA was a known disease factor for that herd.
Conversely, is also there are going to be cases where you will go to surgery and you'll open up the animal and you will find those really extensive EMA lesions, and that animal didn't necessarily have a surgical lesion. But you wouldn't know that until you've gone in for a lot of those cases. Any animal that has not passed faeces for more than 24 hours, you really need to think about intestinal obstruction.
They should pass faeces multiple times a day. Or if the animal has not urinated for more than 6 to 8 hours, especially if they are receiving supplemental fluid therapy, needs to have its urinary tract evaluated for a urinary tract obstruction. Diagnostically, a hypochloremic, hypokalemic metabolic alkalosis can lead us to considering, do we have an obstructive lesion, especially if this is severe.
But as I also mentioned, that these are very subtle signs and we don't have other signs of colic, they're not uncommon for just a mild ileus from inappotence. An increased total cell count or an increased total protein or abdominocentesis can help guide us that this might be a surgical type of lesion. And then if that if that C1 chloride is greater than 40, we need to be considering especially a proximal obstruction that is likely surgical.
In general, this is true for all of our species that we see. Exploratory laparotomy is going to be much safer and much more likely to be successful if it is elected early in the disease course. If at all possible, we want to avoid using it as a last resort to establish a diagnosis.
It is definitely a diagnostic type of procedure. But if we want it to be therapeutic, it is helpful if we go earlier, especially if that animal is valuable to that client. Indicators of a less favourable prognosis for Calas with surgical lesions include a relatively low serum albumin of less than 3.5.
Increase serum creatinine, or if the duration of clinical signs have been quite prolonged. We can help with some of these by stabilising our patient with IV fluid, for example, to bring down azotemia, giving plasma if needed. But we don't want to do that at the expense of prolonging the disease to the point that it is no longer fixable.
For the surgical approach, there is, we can do this either as a ventral midline or as a flank celiotomy. Ventral midline is going to give the most access to the abdomen. And is generally the recommended approach.
The downside is the animal's gonna be on dorsal recumbency. So this really is done under general anaesthesia, ideally with a, either a orotracheal or a nasotracheal intubation to protect the airway. Flank celiotomy is almost always gonna be a right flank celiotomy unless you're specifically needing to get into compartment one or the spleen, or if you're doing a C-section, in which case, we would use left flank.
But the right flank will allow access to most of the gastrointestinal tract. Eventual midline can be used for an ovarectomy or nephrectomy, but if that is your sole purpose for going into the abdomen, if you know you have a hydronephrosis, for example, you could choose the side of the abdomen that is closer. Flank elliotomies can, in theory, be done under heavy sedation and a local block.
But it is a little bit more complicated. They tend to not be super cooperative, and they are not going to stay standing for these procedures. So that would need to be done with them in sternal or semi-sternal recumbency.
In general, flank celiotomies are also easier to do under general anaesthesia, although there is some increased risk associated. Post-operative management is going to really focus on a lot of our discussed for the medical management, where antimicrobials will come into play, that multimodal antimicrobial therapy, non-steroidal anti-inflammatory drugs, maybe lidocaine prophyla lidocaine CRI to help increase comfort, and then that ulcer prophylaxis. The reported complications are going to be the same as with other species, where we have incisional infections, herniations, peritonitis, and intestinal adhesions.
There is nothing that is unique to South American camelids there. Overall prognosis for colic. Is extremely variable.
So it's very difficult to give a client over the phone. My patient has colic, what is the prognosis if I bring it in? Or should I just Not bother with treating.
It depends on what is the underlying aetiology, what comorbidities are present, how long the disease present process has been going on. And they can have relatively mild signs at home and still be really severely affected. And alternatively, they can also have some very treatable diseases and still be very colicky.
So, it is difficult to determine prognosis without seeing the patient. So, overall review, colic is a relatively common condition of South American camelids. Clinical signs can be really subtle even with severe lesions.
Early intervention is key for improved outcomes. Medical management involves restoration of hydration, electrolyte acid-base, and protein norms, and then treatment of underlying disease, especially if we can find a specific underlying disease that we can treat. And it can be determined, difficult to determine when we want to surgically intervene.
Thank you all for your time.