Hi, so my name is Chloe Fay. I'm a VTS in emergency and critical care. I gained that in 2018.
I currently work in a referral hospital in Brighton. We do cardiorespiratory referrals, imaging referrals, and we have an out of hours service which I run. So we get a lot of medical cases because we have long-term inpatients, so.
We do see potter systemic chunks in our practise, so that's what we're gonna talk about today. So first, I wanna go through the pathophysiology. Some, it might be a little bit, like teaching you to suck eggs.
But I just wanna go through like liver pathophysiology and the function. So when we think about what's going wrong, in that liver, and how that's gonna then affect, it's function. So the lobe is made up of two main lobes.
The right lobe is much larger than the left, and then these lobes are subdivided into smaller lobules. Each lobule is made up of millions of cells called hepatocytes, and these are basic metabolic cells of the liver. So within these basic cells, the the function of, Metabolism of carbohydrates, protein, fat, thyroxine, which activates thyronine, bilirubin, insulin.
Medicine hormones so like prednisolone to prednisone to prednisolone, aldosterone and vitamins. So lots of different . Functions just from that one bullet point and it's responsible for a large portion of the metabolism of everything that that patient receives intravenously, orally.
Anything that's going on in that body is mainly metabolised by the liver. So if we don't have correct function of the liver, it's gonna start to affect this metabolism, and we'll talk about a little bit but we get these, byproducts that we don't want. It's also responsible for synthesis of plasma proteins, so things like albumin, clotting factors, so it creates fibrinogen, and also creates cholesterol, glucose, bile, amino acids, and urea, so.
All these are synthesised by the liver again if we have issues with our liver which we'll see in a systemic shunts. These are affected, so we might get hyperalbia anaemia, and we may get . Change to clotting practise, we may have coagulopathy, we have increased or decreased cholesterol again, increased or decreased glucose, as well as bile amino acids in your ear, which a buildup of those is gonna be bad for our patients, as we know.
So it also is responsible for storage of fat-soluble vitamins, so A, D, E, and K, as well as that, and glycogen. It regulates our blood sugar, so it's important in our patients, both those with diabetes and normally as well. And it's also responsible for the immunity, so the liver contains over half of the body's macrophages.
So we have a problem with the liver and we have a problem with our immunity, and we're gonna have an increased susceptibility to, infection. So the total blood flow is responsible for 80% of the total liver blood flow, so you can see. On this diagram, we got the portal vein going to the liver here, and then the hepatic veins taking blood back to the heart.
This portal vein takes blood from the spleen, the gastrointestinal tract, the pancreas, and delivers that blood along with those, Substances that we just talked about, so like protein, fat, thyroxine, and insulin, all those kind of things, I'm are gonna be taken to the liver in the bloodstream and by that or to be. And then metabolised by the liver and the. And blood and then taken back to the heart.
So hepatic growth and size are maintained by this normal portal blood flow, as well as hepatotrophic hormones, so things like insulin and glucagon. So those hormones, those tropic hormones, some of those are going to come from other organs via the portal vein. So again, it's gonna affect the growth and size of our liver.
So essentially what a portal systemic shunt is, is a diversion of this portal blood flow. So you can see on this diagram, and there's a little labelled thing here it says shunt, and basically just means that this blood supply from these organs is shunted back into the cardiovascular system that's going back towards the heart and it misses the liver completely. And this diversion of portal blood flow results in attribute of the liver.
And then further deteriorates your liver function that we've talked about. Because that blood from the abdominal organ should be drained by the portal vein into the liver. And instead, it's going into the systemic circulation by the shunt.
There's a couple of different types of shunts that we'll talk about, but essentially, what a shunt is, is just, it's moving any blood that should be going to the liver, away from the liver. So unfortunately, the toxins, proteins, and nutrients absorbed by the intestines and will bypass the liver, and they shunted into that systemic circulation. So we get a, a buildup of those toxins, those proteins, and those nutrients in the systemic circulation, which is obviously not good for our patient.
That's gonna start to have metabolic effects on our patients and which we'll talk about shortly. So we there's an abnormal connection between the portal vascular system and the systemic circulation. Vascular anomalies that divert blood from the, abdominal viscera to the heart.
So you can see through this one, on this diagram. It can happen inside or outside of the liver. The previous picture was an extra hepato, hepatic portosystemic shunt.
But you can get, these intrahepatic. So, on this diagram, this would be, this shunt here. Whereas ordinarily you'd get your normal blood flow through, the hepatic portal vein, and then back out through, the hepatic veins into the cornal caudal vena cava.
So basically they bypass the hepatics andoids which are pos which, you know, like beds that are then gonna do all this, these liver functions that we talked about, . It carries intestinal absorption products directed to systemic circulation, which is obviously not good for our patient. And so these extrahepatic or intrahepatic .
Autosystemic shunts are either going to be Acquired or congenital. For the most part, we're going to talk about congenital, because it's the most predominant patients that we see. You know, the young, they're maybe 6 months old, patients that we see that, maybe seizure after eating, have small stunted growth.
We'll talk about the clinical. And shortly, but these are the ones that we can most commonly see, acquired, again, we'll talk about, but basically these are the older potentially older patients, that have got acquired liver disease, and therefore they get these changes to the blood flow. So congenital and port systemic shunts, and they usually occur as single large vessels.
So, It's just that it's congenitally something has gone wrong, and there's a, a new, larger, single large vessel that diverts that blood away. Whereas acquired shunts are often numerous and they have small in size because, it's almost that they've adapted to the liver disease and, And created new pathways for that blood to flow. So common types of single congenital portovvascular anomalies include intrahepatic portokabal shunts, so patent dentist venosis, extrahepatic portokabal or portal asymous shunts.
So, intrahepatic, like I say, it's gonna be, within our liver. We have this, patent ductal spinosis, that diverts that blood from that portal vein. Extrahepatic portal carol, is gonna be, .
External, so often it's from around the gastric vein, the left gastric vein shunts to the caudal vena cava. And then the portal is yer shunts as well. So again, this is yus system, from the stomach, it's gonna be shunted and the cordal vena cava.
So the shunts may connect to the portal vein with the caudal mina cava directly, this is what we talk about like our port carl shunts, or extra hepatic portal shunts, . But they may originate from a portal tributary, such as the left gastric vein, and terminate on the emphrenic veins, so over by the ribs. In a small percentage of dogs, the pre-hepatic portal vein is also congenitally absent.
So it's not often that that isn't there, it's just that it's just been bypassed. So, I'm comparing congenital versus acquired in our systemic shunt, so, . Often our dogs or cats that have this congenital PSS are gonna have these multiple clinical signs that we're gonna talk to, that are related to hepatic encephalopathy.
I'm gonna talk a little bit about hepatic encephalopathy as well because basically due to the buildup of all these toxins, . And that we see this hepatic encephalopathy. As acquired PSS are almost, almost always multiple vessels, we don't always see these clinical signs that are related to hepatic encephalopathy, but we do get a, a hepatic hypertension, .
Which causes the vessels to come about. So portal hypertension is secondary to primary liver disease, so things like hepatic cirrhosis. And they, they create those acquire shunts.
The differentiation between single congenital and multiple acquired, is really important as a treatment and prognosis differ greatly. Again, we'll talk about this later on, . But basically the treatment for choice of congenit for congenital shunt is a partial complete surgical ligation of that vessel.
And so that single vessel that we talked about is ligated so then the blood can then flow through the portal vein. If we do this in an acquired sh, . Then these shunts have occurred because of portal hepatic hypertension, and portal hypertension.
So if we block off those pathways, that portal hypertension is only gonna get worse, so it can be fatal for those patients. And therefore, medical management is the only real option for those patients. So it's important to think about history, and look at our diagnostics when we, A differentiating between congenital and acquired.
PSS. So there's many predisposing factors and so as I mentioned, acquired shunt can occur in any breeder or age of animal. It's basically just down to whether there's liver disease in that patient, causing portal hypertension, .
Pure bred dogs seem to have a higher incidence, and this is more true in our congenital port systemic shunts. And for those with congenital, most most patients are diagnosed around 1 year of age, but those clinical signs can occur as early as 6 weeks or as late as 8 years of age, but often we're gonna see them between that 6 months to 1 year of age. Patients and these are the ones that we're gonna be suspicious of that congenital and porto systemic shunt.
So single extra hepatic shunts are typically congenital, and they tend to affect small and toy breeds such as Yorkshire terriers, pugs, Maltese, terriers, miniature schnauzers, shih-tzus, . I have seen it a lot in . Dash hands as well, often, they can be single up extra hepatic shunts, .
So, single intrahepatic shunts often affects larger breed dogs such as, standard schnauzers, poodles, Habernees, Irish wolfhounds, Australian cattle dogs, golden retrievers. Old English sheepdogs, and Labradors, these are less common, and more frequently, but anecdotally, I've seen them in schnauzers and poodles, out of all those breeds. Cats nearly always have these extra hepatic shunts, and that left gastric vein that we talked about is the most common one, the one that goes up to, .
Up to the front and then. So, hepatic encephalopathy is important to discuss because often with these congenital patients, this is what we're seeing the clinical signs of, this is why we're noticing that these patients potentially have, a problem. So let's just go over a little bit on pathophysiology.
So it's been recognising that animals with poor systemic shunts, things like end end stage liver disease, as well as congenital urea cycle enzyme deficiencies. So we're gonna be talking about PSS and also a little bit of end-stage liver disease because we think about the potential for acquired systemic shunts. So basically it's the accumulation of neurotoxins and the sim systemic circulation, which are normally extracted by the liver.
So you think about that liver and pathophysiology, and the pathophysiology of PSS is that those aren't being able to be metabolised by the liver. So the two most common causes are liver failure, so with significant reduction in the liver function or causes systemic shunts. So the major toxins are ammonia, and ammonia is derived from, the degradation of dietary or endogenous proteins and amino acids by bacteria in the gut.
So we get this ures, positive bacteria in the normal flora of the intestine which produces ammonia from urea. So in the liver, ammonia is transported by the portal circulation and transformed into urea. In patients with port systemic shunts, ammonia is distributed unchanged to the systemic circulation where it acts as a potent neurotoxin.
So it also increases the permeability of the blood vein barrier, and basically these can increase cerebral concentrations of inhibitory neurotransmitters. So it's really potent neurotoxin, but there isn't any correlation between, patient blood levels of ammonia and severative neurological signs. So it might suggest that these other toxins are just as important, in.
Hepatic encephalopathy. So we have Macartans, and these are a result of bacterial metabolism of methionine in the gut. So, methan lol is, the most toxic metabolite of meartan, and at a low dose, it acts synergistically with ammonia, and short chain fatty acids to, induce this, hepatic encephalopathy and coma.
So, I'm Tryptophan and aromatic amino acids. So, These, and the short chain fatty acids as well. So we get this metabolism of these dietary medium chain trigosloris, and they form these short chain fatty acids, .
So they alter brain energy metabolism, but they're less neurotoxic than the first two on this list. The concentration of circulating and, aromatic amino acids, so, . These increased during hepatic encephalopathy.
They induce a synthesis of weak neurotransmitters, as well as inhibitor, neurotransmitters. I'm So basically these induced neurological signs, tryptophan, which is one of the aromatic amino acids, and the most important one of the aromatic amino acids, is highly, Neurotoxic and it's a precursor of serotonin, which is a potent inhibitor. I So agaba aminobuyric acid, so GABA, is an inhibitory neurotransmitter that's found in increased concentrations of cerebral spinal fluids with hepatic encephalopathy.
So basically these GABA-like activity substances are produced in the bacteria by the GR tract, and then they dump binds to receptors, . And basically cause neurological signs. We may have false neurotransmitters as well, and basically all these, and other toxins that may be involved in pathogenesis of hepatic encephalopathy include phenols, bile salts, and this metal molecule.
I'm So these neurotoxins don't induce hepatic encephalopathy alone, but basically when we have ammonia plus all these other toxins, and they work synergistically and this is when we start to get neurotoxicity, and this hepatic encephalopathy. So clinical signs include depression, obviously got neurotoxins. So, it's gonna be a lot of neurological and central nervous system kind of signs.
So get may get dementia, some behaviour of patients may change and particularly, you know, they may be stuporous, or comatose, they may be head pressing. I'm, I'm a toxic, I'm You know, barking at walls, . They may have motor abnormalities.
They may have deficits, peripheral deficits, as well as things like muscle tremors, blindness, they may have aggression, and most commonly that we see, may have focal and generalised seizures, and grouped into this is all . Post-prandial seizures, and so after they eat they get this and they get seizures, and that's because of that increase in protein that's unable to be metabolised by by the liver and going into the systemic circulation. So let's talk a little bit about comorbidities.
So predisposing factors that may influence whether a patient gets port systemic shunts or that may make portosystemic shunts worse, diuretics, . Protein overload, obviously an obvious one, because our patients are unable to, have a functional liver that's gonna metabolise that. I'm protein.
I'm alkalosis, I'm Again, I need to change the metabolism. I'm Transfusion of stored red cells, so blood transfusions, it's gonna put more pressure and you know, they can't be metabolised by the liver and . Immunity is, I'm one of the liver's main functions.
I'm So if there's an immune reaction to transfusion, . Red cells. Hypoxia, hypovolemia, again, we're decreasing our, tissue delivery and to the liver, we're also, decreasing our, blood flow that can get to the liver.
Gastrointestinal haemorrhage again is gonna cause hypovolemia, to change the portal vein, . Volume infection, we talked about those ability with those macrophages in the liver and patients are gonna be more susceptible to infection. And therefore it's gonna, Increase the risk of any post systemic getting worse and that patient becoming sicker because of that infection as well.
Constipation, just because you get a backup of the proteins in the faeces. As well as increased cerebral sensitivity to sedative, analgesic, and anaesthetic agents, so we know that, that, livers not to be able to metabolise any drugs that we give, the patient as well as a, a normal patient, so it can induce coma in patients with broad systemic shunts, even when normal dosages are used, so we want to consider when we're using drugs. I'm what we're using.
I'm So, patients with postsic shunts have a long recovery time. Especially if things like benzo dietine. Barbiturate, phenothiazine have been used, and that's because those drugs have a longer half-life, because their detoxification requires normal liver function.
Yeah. So diagnostic tools are really important in our patients with systemic shunts and diagnosing whether. These patients have congenital acquired portal systemic shunts.
So the most consistent presenting signs in patients with poor systemic shunts include a small body stature, because we talked about that failure to grow because the liver's not growing, and it'll have a knock-on effect of everything else and that patient's not gonna grow, as well as that we might have weight loss. I'm We may have patients that show signs of hepatic encephalopathy that we've just discussed, . And .
An intolerance to various drugs, so we just talked about those drugs like diuretics, any analgesics, anaesthetics. We, you know, we might, see an intolerance to those drugs. Behaviour changes, we talked about those neurological changes, and cats often present with, tilism, so they drool a lot.
Anorexia, vomiting and diarrhoea, . And unresponsiveness to medical therapy and a common to like to common gastro gastrointestinal signs. So, you know, if we're treating patients for gastrointestinal signs and they're not responsive to that, it may point us towards poor systemic shunts.
I These patients are often anorexic and vomiting as well, just because that buildup of ammonia, we think about our patients that, like our renal patients that have that buildup of your ear, it makes them feel quite sick, and it's the same principle. So dogs may be polyphagic. And as well as that, we may get things like polyuria, hematuria, and dysuria, and often are associated with urate crystals and, patients with autosystemic shunts.
So it's important to take a thorough history and finding out how long the clinical signs have been going on for, and whether they're aggravated by medication, whether they're aggravated by meals, and we talked about those postcranial seizures. And the behaviour change as they progressively getting worse, more than it's same. I'm so.
Laboratory tools and We want to do a complete blood count and a blood smear. Often patients with important systemic shunts are gonna have microcytic normochromic anaemia. I'm So I'm It's important to also do like a blood smear as well to look at the blood cell, red blood cells to see if they're microcytic or if they're noachchromic.
I'm looking at platelets as well. I'm. And then the next ones that we're gonna look at are our biochemistry.
So. Alkaline phosphatase, so ALP and alanine amino transferase, so ALT are often usually mildly elevated. The increase in ALP is partially due to bone turnover in young animals, so, often we might see an ALP increase in our younger animals that we're seeing for congenital or systemic shunts anyway.
I'm You may have a bilirubin that's generally normal, as a, we're not talking about an obstruction to bile flow, . And only a small portion of the functional liver is necessary to conjugate free bilirubin. So although we've got that decreased blood flow, to the liver, there's not an obstruction, so hopefully your bilirubin would be normal.
Potentially if you've got an acquired shunt, this is where you might be different, you might have an obstruction and therefore you might have an increased bilirubin. Decrease BUN, so blood ura nitrogen, and that's secondary because we know that that conversion from ammonia to urea, . We don't have that with our stomach because we've just got ammonia circulating.
So, we've this is commonly found in about 64% of patients. Hypoglycemia, is a consistent finding, and this is because of this decrease in insulin metabolism by the liver, and therefore, there's also insufficient hepatic glyco glyco storage. So, this hyperglycemia comes as a result of that, .
Because it's just been used up by insulin, excessive insulin that's not been metabolised. I'm Hypo chlororemia, a mouthful, is present in about 65% of the cases, again, . I'm the Liver isn't metabolising that .
I'm I'm making cholesterol. So around protein and so specifically albumin levels are reduced in patients with quaystemic shunts, and that can be around 90% of dogs that we see with PSS will have a decreased albumin function. And that's because the hepatocytes are responsible for albumin synthesis, so, they're not getting the blood flow, they're not gonna synthesise the albumin.
And because of that decreased functional liver capacity and MPSS, albumin is decreased. If it's severe enough, we might see as SITS in our patients, . Hopefully this wouldn't be the case and potentially with our acquired ones we're gonna see this sooner because we've got other disease processes going on and potentially infection as well, .
And then I'm Urinalysis. So I'm looking at our urine for an ammonium poureate crystals, . So ammonium biourly or crystals are an important diagnostic finding, so they're in about 50 to 60% of patients with important systemic shunts, so it is a good adjunct, to add into your initial testing phase.
So liver function tests are important for their diagnosis, of for systemic shunts. There's a couple, so I brought myself fille, ammonia tolerance test, and bile acids are the ones most commonly used. I think in, general practise bile acids, tests are probably the ones that are most commonly used, and it is the only test that's dependent on portal systemic vascular flow.
So basically a plasma concentration of bile acid is dependent on, enterohepatic circulation, and so bile acid evaluation is as sensitive as that ammonia tolerance test for the detection of circulatory abnormalities. So, Serum bile acids are synthesised in the liver from cholesterol. Obviously we talked about, we might have a hypocholesterolemia.
So after conjugation with taurine, they're secreted into the bile and stored in the gallbladder. So during food intake, neurohormonal and hormonal practises such as, cholecystine, Stimulate the gallbladder contraction and excretion of bile acids into the small intestines, where they form my cells that enhance lipid emulsification and absorption. At least 95% of intestinal bile acids are actively reabsorbed in the ileum.
And then they're transported by portal blood back to the liver by the hepatic cycle. So obviously there's a, if there's a PSS then this . Intercept this.
I'm being, I'm this cycle. So plasma concentration of bile acid is dependent on this circulation, . And so we take a test, on a test before we do anything, generally after 12 hours of fasting, for a pre-pranial biascid concentration, and then what we do is we feed the animal a high protein meal, and then the serum biastic concentrations, are taken 2 hours after this meal.
So normal values for time. Fasting bi acids are less than 5, in dogs and less than 2 in cats. And then normal post-parential values are less than 15.5 in dogs and less than 10 in cats.
Serum biolatic concentrations can be elevated with cholecystasis, jaundice or post-systemic shunting, so we may see higher figures than those with acquired because we may already have, as well as a supported systemic shunting, we may have jaundice or cholecystasis as well, . But they're not significantly affected by dehydration, hypovolemia, and passive hepatic congestion, and though they may be affected by leukaemia or hemolysis. There's no special techniques for handling or storage with these, which what makes them, really useful in general practise.
Often you can get the snap test now, that you can do on the IE machines, or you can send them out, . So, really easy to do and Low impact on the patient, as long as we're monitoring them, . If they're really sensitive to high protein meals, you can do a low protein diet mixed with a few millilitres of corn oil, but I would just suggest that you do a high protein if you're unsure whether that dog's got PSS .
And then just monitor them. So, normal hepatic function is essential for conversion of ammonia to urea. We've talked about that.
Increased rest in ammonia concentration indicates that there's a decreased hepatic mass or shunting of portal blood. So that's why we do this ammonia tolerance test. So basically concentrations of blood ammonia are not, well correlated with, sorority of hepatic encephalopathy.
So it may be normal in, up to 20% of dogs with, a systemic shunts, especially after fasting. This test was developed to provide more accurate diagnosis of liver function. So basically you get another sample of base a heparinized baseline sample after 12 hour fast, and then ammonium chloride is administered orally by a stomach tube or a gelatin capsules, or as an enema, and then a second blood sample is obtained 30 minutes after, the ammonium chloride administration.
So they need to be transported on ice for immediate, plasma, separation and analysis, and then the normal values vary with the method of analysis, so it depends on what the lab's doing. Things like improper sample cooling, incomplete plasma separation, or delays in sample analysis are gonna give you falsely elevated values, because of this erythrocyte and plasma generation of ammonia, as it degenerates. If the patient has any vomiting, or if there's any diarrhoea after rectal menstruation, and these patients, need to have a retest.
So I would say the gold standard within general practise is our bile acid stimulation test. I'm The next steps that we're probably gonna take in general practise are radiography and ostenography, . And basically there is a gold standard of perectal portal yippy, which is a non-invasive techniques and looks at the portal system, the portal circulation, basically like an enema and then you plus .
Like a a catheter, a paediatric feeding tube through the colon. And then record through a Gala camera after injection, and for 3 minutes, . But within practise, we're gonna be looking towards our radiography and ultrasonography to help us diagnose.
So on our radiographs, we're gonna have, abdominal radiographs that are gonna reveal a generalised decrease in contrast, and that's because of a decrease in the abdominal fat. You may well see the shunts and Clearly because you have this decrease in abdominal fat, but often the liver is common like commonly reduced so atrophy and your kidneys are enlarged because they're taking on a lot of the work of the liver. Ultrasound is really sensitive for intrahepatic shunts, so 92% sensitive and 98% specific, .
So basically with a combination of a small liver, large kidneys, and then potential those uroliths that we talked about, let's say ammonioureate and neuralys may be present, especially in those with congenital or systemic shunts. You can also look at the portal vein aorta, and portal vein coral vena cava ratio. They're much smaller and those with extrapatic or systemic shunts and again for the more more .
Experienced diagnostic image, they'll be able to identify those shunts on a. On ultrasound, you can see it's portal vein, the cordo vena cava, and there's the shunt that's taking that to the cordo vena cava. So we just talked about this, gold standard, and also they'll do this in referral centres.
So basically on a normal dog, the liver uptake of this radioisotope is higher than the uptake by the heart, but then when there's a postsystemic shunt present, the uptake by the heart is higher, and earlier than the uptake by the liver. I'm So I sent a shunt fraction, and so I'll give you an idea of the significance of the shunt. So normal dogs have a shunt fraction, of less than 10% often while dogs with poor systemic shunts have a shunt fraction of over 50% often.
So let's move to treatment. Medical treatment, I'm, we're mainly talking about our preoperative medical treatment, but obviously we're talking about our, Acquired, post-systemic shunts, and this is gonna be our long term treatment as well. But basically they're used to decrease these acute signs of hepatic encephalopathy, socoma, seizure, abnormal behaviour, which are gonna create a better condition for our patients to have an an anaesthetic and a surgery, .
So the goal of medical treatment is to reduce the production of ammonium, and it's absorption from the intestine, so trying to get as much of that ammonium out as possible because we know that, working with those other toxins, that's the thing, you know, if they all, there's a lot of ammonia and then there's those toxins on top, they work synergistically to cause this hepatic encephalopathy. So patients present with seizures or coma are gonna require emergency treatment, and often this is gonna be fluid therapy. I'm.
Potentially a aidine enema, neomycin or metronidazole, so metronidazole at 7.5 makes the cake 3 times a day, and then oral lactulose, when we have the ability to give, oral administration, . So dehydration should be treated aggressively, as azotemia can aggravate the encephalopathy state by increasing intestinal production of ammonia.
So we know that that aotemia is gonna be circulating in your ear which then is converted in the guts to ammonia, so there's gonna be even higher amounts of ammonia. So correcting that as soon as possible, but obviously being mindful that dehydration happens over a long period of time so you might be doing it over 12 hours, 16 hours, and we just get them on a dehydration plan. I'm Using replacement fluids such as 0.5 .
Sodium chloride with a 2.5% dextrose is recommended. It's a hypertonic, .
Say one, I'm. And that's because animals with liver disease we know tend to become hypoglycemic and they also retain sodium, so we don't want to add any more sodium in there, and. And we want to make sure that those patients get enough glucose, because, they're constantly using up that glucose.
Obviously if those patients come in and they have electrolyte imbalances, and they have metabolic, disturbances, we want to replace those first, so we might be using more balanced electrolyte solutions such as, Homans to begin with, so, replace deficits and then put them on those replacement like maintenance fluid of hypotonic saline and dextrose. So benzodiazepines, barbiturates, I'm. Should we use a caution for patients with seizures, because we know that we've got an increase of drug sensitivity, so, .
We can use them in an emergency situation, just be mindful that we use lower doses, . But we might use things like . Or Keppra, so, le seriter again under the mouthful, .
Yeah, so you might be using like things like Keppra rather than benzodia, peanut barbiturates, long term for these patients, because . The patients respond a little bit back to these. Manitol can be used to reduce that intracranial pressure, particularly the patients that are gonna be seizuring, we wanna, control that, intracranial pressure as much as possible, and the way we're gonna do that is for our blood flow, .
Cerebral blood flow. So you can use a 0.5 makes to kick IB, .
But I say these in patients that are like seizuring quite badly and and showing really bad neurological signs and So we also want to stop our oral intake of food for 24 to 48 hours, . And this is just an issue for our in preparation for our surgery and we don't want to be adding more protein to these patients. Obviously that's not an appropriate .
Not appropriate for our patients that are going on long-term medical therapy like our required ones, and in which case we wanna give these patients a protein restricted diet, and this is gonna help to reduce the amount of, ammonia in the intestine. So the ideal diet should be highly digestible, so we want to make sure little residue is possible. Which is a colonic bacteria.
We want it to contain high biological value protein. So high levels of branch chain amino acids, and arginine and low levels of those aromatic amino acids and methanine, and then have a highly digestible carbohydrates the primary source of calories. So the protein content should only be about 14 to 17% of the dog and 350 to 35 of.
Cats. I'm So the protein restricted diet and the lactulose are often continued after surgery until that liver function improves. But then they can be weaned gradually weaned off from about 4 to 6 weeks after the surgery, .
And then bile acids, and your albumin evaluated are often 246, and 12 months after the surgery to make sure that the liver is functioning properly. Once you've had that surgery, that protein, that diet can slowly be increased once those bile acids are normal, . But in dogs with a mildly elevated bile acid, a normal albumin, it may be necessary to monitor the clinical response to diet change and see whether we can do that.
I'm So thinking about medical treatment in terms of pre-surgery, preoperatively most animals are gonna need those analgesic, so opiates are often used frequently, so use those with a very low dose, and again sedation with a low dose. Especially for those patients that are volo or abdominal pressing in the postoperative period that we'll talk about in a minute. So surgical treatment.
I'm, as I talked about this congenital, this is gonna be the only way that we can. Correct this and stop the patient from From getting hepatic encephalopathy, and it being fatal. So the liver.
Needs catastrophic substances from port to blood flow, and the deterioration of liver function can be expected if the shunted blood flow isn't, surgically corrected, . So, congenital patients, in one study, there was this, only 2 of 8 dogs had not received medical treatment and didn't receive surgical treatment were still alive at 6 months. So it's really important that we, either do the surgery or refer them out for surgery.
I'm So, The way that we do this is restoring the flow of hepatotrophic substances, the sinus sinusoidal my results in the substantial hepatic regeneration and reversal of functional impairment. So basically just reverses, the disease process, and often you don't see long lasting signs. So basically it involves a surgical attenuation, so narrowing or full ligation of the abnormal shunt vessel.
And the way we do this often is through these amyloid constrictor rings that you can see in this picture, . So basically have this metal outer ring that will sit around that vessel and inside this milk casing that slowly swirls and will occlude that vessel slowly until that vessel is fully occluded. You may use suture material, other things that you can do as well as intravenous injection of an embolus, of a special glue material, but I would say most commonly, amyloid constrictions are used, and they're easy to place, and they're reliable.
And also, . We can, View them on radiographs, and, and if we're going back in surgically, we can remove those, whereas, you know, these glue materials . So a bands are difficult to remove.
So partial ligation of the shunt is often carried out by partially losing the vessel to suture, which obviously we can as well. So postoperatively, these patients are at risk of seizuring, . If the I'm Between about 5 and 10% of small breed dogs develop seizures after shunt ligation.
It's not really known why, but they're not, the affected animals, don't often respond to fluids or dextrose or animals, . Seizures can be corrected with bottles of diazepam, blood glucose, and, and so if that's measured low then that needs to be corrected. If the patient continues to seizure, you can repeat the diazepam, and then place them on an infusion of propofol, and then weaned off, .
Cats can betries with oral las and demycin as well when they're conscious, but the prognosis is quite poor for those with postoperative seizures, and they might still have a neurological problems they may still have like long lasting effects of . Of that hepatic encephalopathy. So hypothermia, and hypoglycemia, again, we want to correct those, hypothermia, and that patients at risk of, shaking, abdominal tension, and we're just gonna put pressure on that ligation or am constrictor, .
It's important to look for systemic blood pressure and we want to make sure that these patients don't have hypovolemic shock, . Because we're gonna be reducing that blood flow to the liver, which obviously we're trying to correct. Pain, again, we're going to get this, potentially.
I'm abdominal tensing, I'm And therefore, all these things would kind of increase portal pressure, and, . Damage our surgical site. Again, increase that intraabdominal pressure to bandages on the abdomen, as well as fluid balance and signs of portal systemic portal hypertension, the sharp pain, and abdominal abdominal distension altogether are going to be signs for our portal hypertension, which we are trying to avoid.
So treat postoperative total hypertension, it's using our fluids, systemic antibiotics, and if it's unresponsive to fluids and systemic antibiotics, and pain relief. And potentially we need to be considering immediate surgery to remove that ligature or that constrictor because otherwise we're gonna get an extreme case of portal hypertension as a result, hyper the hepatic encephalopathy as well. So talking about, a protein restricted diet that we're gonna be continuing after surgery, with that lactulose, and then wean in 4 to 6 weeks afterwards, once we've evaluated our bile acids, and albumin.
I'm Just as a side note, there is a concern around older dogs, those are 5 years or older that have congenital or systemic shunts and clinical and normal and don't have, you know, minimal changes on the biochemistry, and liver. They often don't suggest doing surgery in those, just because it can, . Cause the problem to be worse.
I But this whole area is a bit controversial with whether you do corrective surgery or not. So we talked about the post ligation, seizures, and make sure the patient is in hypoglycemic before we start treating them with seizure medication. And then In general, cats with congenital post-systemic shows do seem to have more postoperative problems than dogs, .
So, as well as that doctors with intriotic shunts have worse prognosis, and often because it's much more technical to perform the surgery, . So often if it's in the intrahepatic shunt, I would definitely refer those, because they can place, the shunt, the coils in the shunt with, intravenous catheters using the fluoroscopy, in a much safer way to correct that problem. I'm So I think that is everything.
If there's any questions, we'll be more than happy to answer them, and you can either ask them and I'll get some of them or you can email me at chloe@nehyphen priority.com.