Hi, my name's Sophie Chedzoy, formerly known as Sophie McMurr. I'm a registered veterinary nurse and a veterinary technician specialist in small animal internal medicine. And I'm here to talk to you about jaundice today, jaundice mainly in dogs, which is quite a broad subject, so I'm going to focus mainly on the areas which are most beneficial to us as RBNs.
So we'll start off talking about the anatomy and physiology of the liver. The liver has a multitude of different biological functions, so it's really important that we understand the physiology of how the liver works so that we can help treat our patients later on and look out for certain signs that we may be aware of if we understand how the liver works effectively. So the liver sits next to the stomach and it's just caudal to the diaphragm and it's strategically placed between the vessels that drain the gastrointestinal tract and the circulation of the rest of the body, and that's so that as our food and our nutrients enter the gastrointestinal tract, they can enter the bloodstream, go to the liver to metabolise any of those important nutrients, excrete any.
Any toxins before it's taken to the rest of the circulation in the rest of the body. Now there are many, many different roles that the liver plays within the body. Some of those are the storage of minerals and vitamins, excretion of toxins that may be harmful to the patient.
It does play a part in digestion. And it produces many different things, so some of those include plasma proteins, coagulation factors, and cholesterol, and it also metabolises endocrine hormones, carbohydrates, lipids, and proteins. So there was a study to give you an idea on how well this this organ, the liver, can regenerate.
There was a study performed in rats, and they had lost around 70% of their liver, and it took about 5 to 7 days for the liver to restore back to its original size. So it has an absolutely incredible regeneration capacity. Now there are some factors that will impair this function and they can be certain liver diseases, so if there's fibrosis present, inflammation or any viral infections, they will affect the function of the ability to impair itself.
To repair itself And Clinical signs often don't appear with liver disease until it's relatively end stage, so sometimes we can lose up to 70% or 75% in some cases before we start to see any clinical signs. Now the liver is made up of hepatocytes, thousands of hepatocytes, hepato meaning liver and cytes meaning cells, so simply just liver cells. And it plays an important part in our bile production and how bile moves throughout the liver so that it can get to the gastrointestinal tract effectively.
So between all of these hepatocytes, we have bile caniculi, and they're located just between each of the hepatocytes themselves, and this just helps the bile drain into that common bile duct before it exits the liver and empties into the common bile duct. Once it's in the common bile duct, this then enters into the duodenum once the patient eats, and the bile is used for lipid digestion. The regulation of our blood glucose takes part in the liver, so glucose is absorbed via the small intestine, and then it's metabolised as energy in the form of ATP.
And if we have more glucose than what we need, we can also store it as its storage form called glycogen within the liver itself. The liver plays an important role in protein synthesis, albumin being the largest protein within the vascular system, and albumin plays a really vital role in maintaining an osmotic pressure within the body, and that just creates the oncotic pull into the intravascular space, and it just keeps the fluid within that intravascular space and prevents it from leaking out. Now with liver disease, we can start to see a reduction in our albumin production.
And when you start to see hypoalbuminemia, you may start to see signs that that oncotic pull is reducing, and those signs would include third space disease, so things like ascites, pleural or pericardial effusion may start to occur, and that's simply just because of the reduction in albumin and some of the other proteins that we may see start to reduce with liver disease. And it also synthesises and produces coagulation factors. So this is an absolutely vital point to remember because if your patient is going to theatre, for example, to have liver biopsies, we need to remember about our coagulation factors.
We need to check them prior to going to surgery, and we need to take the necessary actions and precautions in case there is an issue. Before we go ahead to theatre, but we'll talk about that in a little bit more depth later on. Now I've listed some of the most common liver diseases, but there certainly isn't a full list.
So there are many other different conditions as well. So we have idiopathic chronic hepatitis, which is the most common liver disease that we see in dogs. And then we have cholangitis, which is an inflammatory disease and it's one of the most common diseases that we see in cats.
But then there's also portosystemic shunts which we see relatively commonly, and there can be two different types. There's congenital or acquired shunts. Congenital just meaning that it's there from birth, and an acquired shunt is often that can be secondary to another disease.
So if you have liver disease, for example, and you get some fibrosis of the hepatic tissue. Then the blood flow through the liver may be altered, so in order to try to regulate the blood flow, you can start to branch off with little acquired shunts, and this will just help help the blood flow through the liver, so you can get acquired shunts usually in the older patients and with more chronic disease. We can also see hepatic lipidosis, which is most, the most common, but one of the most common conditions in cats seen in the US, the UK and in Europe.
And then we have copper storage disease, which, although this can happen in many different breeds, both dog and cat, we can see this in Labradors, Dobermans, the cats tend to be some of the Orientals like Siamese, but there is only one genetic . Genetic breed that is linked with copper storage disease, and that's the Bedlington terrier. And they carry a gene called the COMD1 gene, and this just makes them more susceptible to developing copper storage disease.
And if you have a Bedlington terrier which is starting to show signs of copper storage disease or liver disease, it can occur in patients younger than one year old, so quite young. And then we may also see hepatic tumours as well. When it comes to the clinical signs of liver disease, these can vary massively depending on what the liver disease is, but often they're very non-specific.
So this can make the diagnosis quite challenging for liver disease. So we need to look at a multifactorial approach to look at all of the different factors rather than just looking at one specific thing like a blood result. So we need to look at the patient's signalment, the age, their breed, what current what common conditions are they likely to to develop.
Look at the patient's history and the physical exam. Are they already showing any clinical signs? Are they jaundice?
Are they, do they have PUPD? Look at the biochemistry and the haematology, so our blood results can tell us quite a lot, and then we need to combine that with diagnostic imaging. And if we still believe that liver disease is high on the list, we may need to do some liver sampling as well, and we'll delve deeper into all of these as we go along.
So as I mentioned before, the clinical signs of many different liver diseases are very non-specific, so vomiting and diarrhoea, which we see with so many different medicine, patients, anorexia, lethargy, PUPD. Now ascites we may see with some patients, particularly in end stage liver disease, but again, ascites can be a sign of many other different diseases, so it's non-specific. We could also see hepatic encephalopathy, which we'll talk about in a moment, and we may start to see jaundice.
And you may look at these two and think, ah well they're more specific to liver, but they're not really because you can see jaundice for many different reasons. You can see it because of increased hemolysis with your patients such as your. IMHA patients, so yes, they're slightly more indicative of liver disease, but they're not specific.
So again, this patient who presents with all of these signs does not scream liver disease to me. It can. It could be a multitude of different medical conditions, so that's why we need to look at a multi-factorual approach.
Now, I've just mentioned hepatic encephalopathy, so I'll talk a little bit about what this is before we go on to the other clinical signs. So this is dysfunction of the brain caused secondary to liver dysfunction. So When we eat, food enters the gastrointestinal tract, and a lot of different toxins are derived from our food, and those toxins are derived by the liver.
Now, one of those toxins, the most important toxin, is ammonia. Ammonia, when it enters the bloodstream, it's a waste product that needs to be converted so that it's a safer form and then it's excreted. So ammonia is converted by the liver into urea, which we see all the time.
Now there's two different types, so you can have acute, which is often accompanied with hepatic failure, so very end stage liver disease, and often if they're bad enough to be in liver disease, which is a which is causing acute hepatic encephalopathy, this carries a very, very poor prognosis, and usually they will die within a few days. Whereas the more chronic form is the one that we more commonly see, and this carries a better prognosis. As long as the disease that's causing it can be treated.
And this may be seen with feline lipidosis, or more commonly it can be seen with portosystemic shunts. And the reason we see it with portosystemic shunts is shunts are a vascular anomaly. So rather than the portal, the blood coming from the gastrointestinal tract to the liver to metabolise the the toxins before it goes to the body, the vascular anomaly.
Takes the, it shunts the blood away and around the liver, so rather than taking it to the liver, it just shunts past, so it bypasses that liver, so all of these toxins remain in the bloodstream, and that's why we will see a higher ammonia with portosystemic shunt patients and a lower urea. So hepatic encephalopathy can sometimes accompany a portosystemic shunt. Now the signs that you may look out for for hepatic encephalopathy are apathy, so this just means a lack of motivation, listlessness, maybe a reduction in their mental alertness.
And then some of the more severe signs are ataxia, so a wobbly gait, circling, head pressing on inanimous objects, so maybe quite commonly you can see the patient's head pressing in the corner of the kennel or against the door, the wall, they can often stare into space and seem quite neurological. Salivation often comes along with this, and they can also become comatose if it gets bad enough. Now less commonly we can see seizures, but this is not very commonly seen, so I won't delve into that too much.
Now, if you have a patient, which you need to test the ammonia on, we do need to be very, very careful when we're, handling these samples, and it's vital that we follow all of these rules so that we can make sure we get an accurate diagnosis for these these patients. Now it needs to be a fasted sample in a lithium heparin tube only. Now I tend to keep some of the tubes in the freezer just so that they're really cold.
And when you take the the blood, pop it into the tube, and it needs to be spun within 30 minutes. And when you get, when I get that tube out of the freezer, I sit it on ice, take it to the prep room where I'm gonna collect the blood, and straight away, once the blood's in that tube, sit it back on ice, ideally between two ice packs to transfer it back to the lab. And the reason for doing this is the ammonia will start to degrade and reduce as the sample hits room temperature.
So the longer the sample is sat, the lower the ammonia level will be and the more inaccurate the level will be. So it's absolutely vital in order to get an accurate diagnosis for a patient with hepatic encephalopathy. Now an increase in our hepatic enzymes do not necessarily correlate with our liver function.
So our liver enzymes can tell us many different things, but unlike many of the other organs and the other diseases, they're not very specific, and they don't always tell us. About liver function, or they don't tell us about liver function at all. And around 70% of liver dysfunction can be present before any signs will appear.
So you could have a patient with 60% of liver dysfunction and your hepatic enzymes may be normal at this stage. So they do have their limitations. Usually when you're doing bloods and you find an elevation in your liver enzymes, this usually is the first finding that makes you suspicious of er hepatic disease.
Because of those non-specific clinical signs, we may well see an increase in our liver enzymes, and that may ring alarm bells for liver disease. But there's many different tests that we can look at to assess liver function alongside these so that we can get a more broader description of what's going on. Now some of the more common liver enzymes are, we've got ALT and AST and if these are raised that can indicate hepatocellular damage.
We also have ALP and GGT which can indicate liver disease, and it's important when we look at liver enzymes that we look at them in correlation to, other things as well, so that we can try and pinpoint, is it liver, is it cholestasis, is it. Another disease such as Cushing's disease can cause your ALP to increase. So it's really important that we don't just take one liver enzyme and run with it.
We need to look at what it correlates with so that we can get a more accurate approach. And the the enzymes don't indicate an altered liver function, so you could have sky high ALT and maybe this patient has been in a road traffic accident a few days ago. It's had an acute trauma, a blunt trauma to the abdomen, which has destroyed some of the liver cells.
So hepatocellular damage, liver cell damage. The ALT could be through the roof, but that doesn't mean that our liver isn't functioning, and it doesn't mean that we have liver disease necessarily, and it also doesn't mean that it won't regenerate. So it's important to look at these enzymes, but it's also important to be aware of the limitations that they have and that they are not specific to liver disease necessarily.
Now when we look at some of our other blood work, we can look at our biochemistry. And we mentioned earlier that albumin is one of the proteins, the largest protein that is produced and synthesised by the liver. So if we have liver dysfunction, hypoalbuminemia, so a low albumin level, may be seen.
But you may not see this until we have around 70% liver functional loss. And I mentioned about ammonia being increased because either the liver is not functioning properly, so it's not converting the ammonia effectively, or if we have a shunt, it's bypassing the liver, so it's not converting the ammonia into urea. So that's why we may see an increase in our ammonia, which is a waste product, and a decrease in our urea.
We may also see reduction in our cholesterol and also in our glucose. So the liver plays an important role in the use of energy and the storage of glucose, but again, we may not see a hypoglycemia until we have around 75% hepatic loss. We may increase our bilirubin and bile acids, and we'll talk about those in more depth in a moment, and we could also see hypokalemia, so a reduction in our potassium value.
And this could also be because of the the vomiting, the diarrhoea, so we have an increased loss of potassium and a decreased intake if the patient is anorexic or hyporexic. Now If we have an increase in our cholesterol, that could indicate hepatobiliary disease. Whereas if it's decreased, it could indicate end stage liver disease.
So it depends whether it's high or low as to what could be the cause. And then we can look at our haematology, so we may see anaemia. So often with chronic diseases, we can see an anaemia of chronic disease, and this can be for many different diseases, whether it be liver, renal disease, many different things, diabetes.
And It can just be a cause of bone marrow suppression just from the chronic disease and the chronic effects that it has on the body. We may well see a decreased platelet count and a reduction in our coagulation factors, and the coagulation factors are because we know that they are produced in the liver, so it's just not producing them effectively. We may see an increase in our APTT, which is a coagulation factor, which means it's prolonged, and we may be at more a higher risk of bleeding.
And if we have a patient that is going to surgery to have a portosystemic shunt corrected, We may have more pronounced coagulation abnormalities in the immediate post-op period, so that's a really important take home message if you do have a portosystemic shunt surgical patient at your hospital. So I've mentioned a few times that an increase in our liver enzymes doesn't necessarily tell us anything about the liver function, and that's why we can look at liver function tests. So some of those are bile acids, so your bile acid stimulation test and bilirubin, and these can both tell us about liver function more specifically.
And the other substances produced by the liver are less sensitive than bile acids and bilirubin. And they also may only become abnormal once we have around 70% of liver tissue which is damaged, whereas your bile acids and bilirubin will give you indications much earlier on. And we can have liver damage or liver disease without it affecting the liver function, so it's really important to do a bile acid stimulation test and look at bilirubin alongside those other liver blood tests rather than instead of.
And Also clotting times, we've mentioned they may be elevated with liver disease, which means that our clotting is delayed, so we may not be as fast at clotting or we may not be able to clot as effectively as we should be able to. So for that reason, we should be screening for coagulopathies prior to any liver biopsy or any FNAs or any surgery that the patient may undergo. Now, bilirubin is derived from the breakdown of haemoglobin and in red blood cells, and this happens in the spleen.
It's then metabolised and conjugated by the liver and becomes part of bile. So once it enters the gastrointestinal tract, it's excreted via the faecal root or it's absorbed back into the circulation and it's then excreted renally later on. Now, if you have high levels of bilirubin in the bloodstream, this can cause the patient to become jaundiced.
And An increased bilirubin level may be elevated with a few different things. So hepatocellular dysfunction, so, dysfunction of our liver cells, and that's because if you look at step two. The bilirubin is metabolised and conjugated by the liver, so if we have dysfunction, it may not be able to be metabolised and therefore it will start to build up in the circulation.
We can have bile duct damage or obstruction. Because if we have an obstruction there or something is damaged, we'll again get a backup of of bilirubin in that biliary tract and within the liver itself because it just can't excrete it, it can't get rid of that that bile and the bilirubin. So we'll start to see jaundice appear.
But it can also be something completely unrelated to the bile, the biliary, system or the liver, and that could be excess red blood cell destruction. So the likes of your IMHA patients who have an increase in red blood cell destruction. So therefore the haemoglobin is released out of the red blood cells as they're destroyed at an increased level, and your patient will become very jaundiced with this.
So diagnostic imaging makes up a really important part of our diagnosis for liver patients and there are a few different tools available depending on what you have access to in your clinic and also who you have access to in your clinic. So for example, an ultrasound does require the skills of an experienced ultrasonographer. Ultrasound is ideal for many different reasons, and one of these is looking at the ecogenicity of the liver itself.
So is it bright? Is it darker than usual? Is it patchy or nodular?
What is the liver size like? Is it small in size, like your portosystemic shunt patients, your congenital shunt patients, and what does the structure look like? You can also look at the biliary system, so all the bile duct, the common bile duct, the gallbladder itself, and the vascular structures.
So we also have Doppler blood flow on ultrasounds, which is really handy because you can put a Doppler blood Doppler blood flow over one of the vessels to check the blood flow, check it's going in the correct direction. And also check some of the vessels are in the correct anatomical location, such as your port of systemic shunt. Now it does have its limitations and the liver may appear sonographically normal even in the presence of norm of severe disease.
And just because you don't find a portosystemic shunt on ultrasound, it doesn't mean that it's not there. So it does have its pros and cons. It is really useful for looking at things like free abdominal fluid, and we can use it to guide our needle if we want to take an FNA fine needle aspirate of the liver or of any organs, or maybe if we've found a mass.
We can also use it to guide our true cut needles if you want a slightly bigger biopsy of any of the organs. So it is a really handy tool. But it just has its limitations that we need to be aware of, as do many of the diagnostic aids.
Radiography is quite handy at looking for hepatomegaly, so an enlarged liver that we can see on the X-ray, and you can measure that. CT is really useful and we can use this to assess liver size, we can find liver masses, and we can also look for portosystemic shunts and vascular anomalies. Now, CT has been shown to be 5.5 times more likely to correctly determine the presence or the absence of a congenital port or systemic shunt than ultrasound.
And you can also use contrast mediums for with your CT. So it just increases the sensitivity of this test, so that's really useful. MRI has also been shown to be very good at detecting potosystemic shunts, however, CT seems to be more favourable because it's quicker and it's cheaper with very similar outcome, very similar images.
So CT tends to be the gold standard modality of choice. And then quite often we go ahead and do, we need liver biopsies to get histopathology of the liver to get a definitive diagnosis. Now a liver biopsy is a diagnostic procedure and it's certainly not a benign one, so it does come along with its it's high risks.
Patients with clinical or biochemical evidence of liver disease, most of them, may go on to have liver biopsies. And there are a few different ways of collecting liver biopsies. So you can do, as we've mentioned, ultrasound guided FNAs.
And the beauty of this is they can be done under sedation, maybe just with an opioid on board if they're relatively sick. And They're relatively painless, so if they've got an opioid on board, that tends to be adequate for those patients. But if not, you can give a low dose alpha 2 agonist if you need to, depending on how the patient is and how how awake they are.
You can also do ultrasound guided Tru-Cut needle biopsies. This also requires sedation or a general anaesthetic because they need to be kept absolutely still. And especially because of the liver is very vascular, we don't want the patient to move while there's a true cut needle inside its liver and it's also very close to the diaphragm too, so we do need them to be very still with a decent sedation or a general anaesthetic.
But some patients, some conditions can only be diagnosed with histopathology, so they may need to go to theatre rather than having an FNA or a true cut. So depending what practise you work in, this, these can be performed under GA laparoscopically. So with keyhole surgery, And if you don't have those facilities, you can also do an X lap to open up the patient's abdomen, have a look, and take some biopsies that way.
And either way is adequate. Now before we delve into doing liver biopsies or repairing ports or systemic shunts, we need to Talk about our anaesthetic considerations because there are many with liver patients. And the liver has many different metabolic functions, so we need to bear that in mind when we're going to give certain drugs to these patients because they need to be able to metabolise those effectively and excrete them out of the body.
Now every patient should have a pre-anesthetic assessment. We need to assess liver function rather than just our biochemical parameters. So we need to know if the function is affected in these patients in order to tailor our anaesthetic drug plan.
And remember when you perform this pre-anesthetic assessment that if you see clinical signs such as your vomiting, diarrhoea, PUPD, any of the hepatic encephalopathy signs, anything that we mentioned earlier, if clinical signs are present. They're more the patient is more likely to have a severe dysfunction of the liver, so we said we don't tend to see clinical signs unless around 70% or more of liver function is affected. So the patients who do have the clinical signs are more likely to be the the more severely diseased patients.
And You can also look at your body condition score, so. Often if you do see a really small patient who looks like they're failing to thrive, we often say is it er the runt or a shunt, because they're quite small, they fail to thrive, and they're often quite thin as well. So if you do have a congenital port of systemic shunts, look at the patient's body, look at their bodily condition, look at the fat content and also the muscle as well.
And We need to make sure that we are preparing these patients prior to GA because that's absolutely essential to give them the best fighting chance to survive the GA and also to survive the surgery or whatever procedure they're undergoing. So if you have liver disease, which is quite severe, it can cause volume depletion. And this is because.
There's a decrease in the total vascular resistance and there's vasodilation in the area of the liver itself and the surrounding vessels. So before we go ahead to anaesthetize anything, we want to correct our fluid imbalances and we should be using fluid therapy to just correct any imbalances that we can see. And you can use your blood work to guide you on this, so run a PCV and a total protein to see where our proteins are sat.
Are they reduced because of our albumin levels are, are reduced. Is our PCV increased, which may indicate . A dehydration, but remember we can also have a chronic anaemia as well, which don't tend to be quite severe, they're often relatively mild, but we need to look at blood work and see how we can use it to guide us on what things we can correct before we go ahead to anaesthetize the patients.
And we need to pay particular attention to hypoproteinemia, so low protein levels, because remember that oncotic pull within the vascular system, that's absolutely vital to maintain blood pressure. Hypoglycemia, so especially if you do have a an end stage liver patient who may well have a hypoglycemia, it's relatively mild, usually unless they're quite severe with their disease stage or a portosystemic shunt, because these tend to be young, small patients. So hypoglycemia is definitely something we need to monitor, not just in the preoperative, .
Stage, but throughout the anaesthetic and also in the post-operative stage as well. We need to look at are there any anemias present and are they severe enough to need a transfusion. And hypokalemia, we have a patient who's likely to be anorexic or hyperexxic, so reduced appetite with potential ongoing losses, so vomiting and diarrhoea.
So if the patient is hypokalemic, where we have a reduction in our potassium value. Then we may need to supplement it so that we can . Just bring that back up to the normal levels because hypovolemia can be quite dangerous if it goes low enough if we're talking about 2 2.5, then we, we may well have hypokalemia affecting our respiratory muscles and causing a weakness of the respiratory muscles, so we do need to supplement it to get it back within the normal range, which is usually around 3.5 to 5.5.
And remember to reevaluate and recheck these bloods as well, because if you have a dehydrated patient, and then you pop them on fluids, their potassium looks absolutely normal, when you put them on fluids, you're promoting diuresis, and potassium and a lot of our electrolytes are renally excreted. So once you start to . Reperfuse these patients with fluid therapy, we're promoting diuresis, so we may well see an increase in our loss of those electrolytes.
So it's important to reassess, recheck your electrolytes afterwards and recheck any of these abnormalities afterwards as well to see if we now have an issue that we didn't have earlier on. And we mentioned that clotting factors can be an issue. So if we have a clotting issue, we can look at things like fresh frozen plasma because this contains clotting factors.
So we may need to give this before we anaesthetize the patient or take them to the theatre. Well, some clinicians like to give vitamin K. And you can administer this for 1 to 2 days prior to the procedure.
And the reason for that is vitamin K plays an important part in our coagulation cascade, so it will just help the patient with the normal clotting procedure. And if we do have a patient whose clotting factors are affected, we ideally should be blood typing prior to surgery so that if the worst were to happen and we were to have a haemorrhage, we know the patient's blood type, we've checked our blood supply and we know exactly what we're going to do. If you don't have the blood in, we need to know where we can source it immediately, ideally, the ideal scenario is you have one in the fridge in the practise.
Or if it's frozen plasma in the, in the freezer, depends on what blood product you're looking at. So if you don't have a practise where you can have the blood in, then at least have it prepared so that you know where you can quickly source it from a neighbouring practise or from the pet blood bank urgently, should you need to. And hepatocytes are particularly susceptible to hypoxia, so the goal of our anaesthesia is to maintain hepatic blood flow and oxygen delivery to those liver cells so that we can give our liver a fighting chance, and we don't want to cause any more disruption or detrimental side effects to the organ.
In order to prepare our patients for an anaesthetic, hepatic encephalopathy is something that we need to consider, and if it is present, we need to correct it, and this will just help. Stabilise the patient before we give any anaesthetic drugs, and it will also improve the mortality. So we give lactulose to reduce ammonia levels within the bloodstream, and it inhibits intestinal ammonia production and reabsorption.
So it changes the pH of the colon, meaning it's a colonic acidifier, and it has an osmotic laxative effect, so it draws that ammonia out. In patients who are conscious, you can give it orally, and it tends to be taken quite well, it's tolerated well, and this can, the dose can be 1 to 3 mL per 10 kg of body weight, and that can be repeated every 6 to 8 hours. If the patient is a little bit more recumbent or it has neurological signs or it's comatose, we don't want to give anything orally.
So in these cases it can go rectally. And first of all, we should give a warm water enema just to clear everything out and get maximum beneficial effects from that lactulose. So administer it rectally just with a.
A rectal catheter. And when the patient is anaesthetized, we need to look at our monitoring. So these patients, there are many different things that can contribute to hypo hypotension in these patients.
Particularly those with low protein levels, so your albumin level, hypoalbuminemia. If you have biliary disease or if you have a portosystemic shunt patient. Then hypotension needs to be high on your radar.
And if the patient has increased bile acids in the circulation, they can often be irritant to the endothelium, and this can affect our blood pressure, causing hypotension too. So if hypotension is present, we should treat it. Fluid therapy or positive ionotropes or vasopressors can work quite well, depending on what is most appropriate for your patient.
And when you have a patient with a congenital shunt, often they are very young juvenile patients. Quite often they're small breed dogs as well. So we need to look at thermoregulation for them, to monitoring our body temperature, our electrolytes as well, and particularly we need to pay particular attention to our blood glucose to make sure that they're not going to become hypoglycemic at any point during the preoperative.
Period during the surgery itself or also in the post-op period too. OK, so the post-op periods can be quite high risk depending on what the patient has had done. And there are some things that we can use to monitor these patients to make sure that we can improve their safety and keep them safe as much as we can.
So if the patients had liver biopsies, we want to regularly monitor for signs of haemorrhage. And we can do this by looking at at pulse rate and quality, so put your finger on the peripheral pulses ideally rather than the central ones like the femoral. So the carpal pulse or just near the tarsal joint.
So Assess the quality of those. Pulses, so are they bounding? Are they weak?
Is there a pulse for every beat, so listen alongside the heart rate with your stethoscope. This all of this gives you vital information on how the patient's circulation is performing. What's the respiratory rate?
Is it increased? Are they tachypic? Maybe because of haemorrhage going on that we're not aware of yet.
How do the mucous membranes seem? Are they pale? Are they tacky?
Capillary refill time. Some people really like this, some people don't. You may not see much of a change or you may see it decreased.
So it may be quite slow when you check the capillary refill time. And we should have been monitoring our arterial blood pressure throughout the whole of this surgery, so if you don't have a machine in your postoperative period, in your kennel area, bring that machine along with you if you can and monitor the blood pressure in the postoperative period. Or if you have a Doppler machine, they're really good as well, they're very accurate, so just pop a Doppler on there.
You can even, in the recumbent patient or if the patient's still quite sedate, you can tape the Doppler to the limb. And then you can just move it around to try and find that that pulse, which is easier than trying to relocate and put it on each time. And we tend to do that if we don't have a multi-parameter machine, you can also do that during the surgery as well, if it's a Doppler that you're using.
So just tape on the actual Doppler sensor to the limb and then just pop your thumb on and move it around underneath the tape, which tends to be, it works quite well. And if you do have a patient who is particularly high risk or one that you're worried about, and you think they are a higher risk of bleeding postoperatively, you could always schedule a second, post-operative ultrasound scan. So you could pop the probe on maybe 1 hour after, 4 hours after, depending on how the patient seems, or just.
Play it by ear and see if the patient worries you at all with any of those signs, you can pop the probe on at that point. But this can also be done after FNAs, after true cuts, it doesn't just have to be, it's not just surgical liver biopsies that carry the risk, they are all risky. And They all need monitoring for signs of haemorrhage, so you can absolutely do all of these for all of those different types of liver biopsies.
And if you do find any haemorrhage present, then you need to take the appropriate action. And if you have a patient in the post-operative period of a portosystemic shunt surgery, as we mentioned earlier, blood glucose is absolutely vital in these patients, they're small, they're young, monitor that glucose to prevent hypoglycemia. Hypotension has been shown to be more more commonly seen in the immediate post-operative periods for a report of systemic shunt surgery, so this is absolutely vital that we are able to monitor blood pressure in that post-op period.
And thermoregulation, so especially with young small patients or with cats, or with any patient really in your pre-operative periods when you've got them on the table, you're about to premedicate them, pop them on a hotdog, and give them a blanket. Do anything that you can to try and prevent them becoming hypothermic as much as possible. You can wrap their limbs in bubble wrap, there's many different things that you can do and prevention is definitely better than cure, because once the patient becomes hypothermic, it has a knock-on effect for many different things within the body, so if we can prevent hypothermia, that's, that's definitely the the preferred method of action.
OK, so that's all from me. I hope you've enjoyed it. A whistle stop tour on hepatic diseases, and I hope you found it useful.
Thank you very much.
