Bailey and Love Explained| Chapter 25: Nutrition and Fluid Therapy| Learn with podcasts

0:00 Welcome back to the deep dive, the place where we cut through the information noise, synthesize the densest research, and deliver the highest yield knowledge right to you. >> Today we are undertaking uh a really deep dive into one of the most foundational, I'd say life critical areas of surgical management, peroperative nutrition and fluid therapy. >> Yeah, absolutely critical. It sounds basic maybe, but the complexity underneath is huge. >> Oh, it is. This isn't just theoretical stuff. This is the absolute core of patient management. It's all dictated by how the body responds metabolically to stress, to illness. >> So for anyone listening, whether you're studying or practicing surgery, getting this chapter down cold, >> knowing when to step in, and crucially, how to intervene safely. Well, that's

0:45 the bedrock. It's how you prevent complications, how you ensure patients actually recover well. >> Our mission today is pretty clear. Then we're distilling this entire chunk of source material, really essential stuff for surgical practice, into concepts you can actually remember and use. >> Yeah. Making it digestible, memorable. We're talking about keeping patients metabolically stable when their bodies are under well extraordinary strain. >> And that strain, it often starts way before they even get to the operating theater, doesn't it? >> Absolutely. The source material makes that painfully clear. the underlying reasons people need surgery, major cancer, severe IBD, big trauma, these things frequently cause malnutrition before we even get involved. >> You look at figure 25.1 in the source. Yeah. Shows that impact, right? The wasting. >> It does. Profound muscle and fat

1:31 wasting. That's the result of long-term lack of calories, lack of protein. >> So, that's the starting point. The patient's already behind. >> Exactly. they're starting with a deficit and then the surgery itself, particularly big abdominal procedures, >> right? Those can really mess with the gut. >> They can temporarily or even permanently compromise the one thing they need most. >> The GI tract's ability to actually absorb food. >> So, if you combine that pre-existing malnutrition with not being able to eat properly posttop, >> recovery is severely compromised. It's a setup for failure, >> which means that old approach just sort of waiting for the patient to get better and start eating on their own. >> That's essentially malpractice these days. It's a failing approach. Yeah. >> So, the goalposts have shifted. It's not just about fixing the anatomy anymore.

2:17 >> No, it's about aggressively correcting those nutritional and fluid deficits and doing it early. There's this increased appreciation now for how vital nutritional status is. >> And that's driven changes in practice >> big time. We have better assessment tools now, much improved ways to deliver food both entrally and parentally, and the formulations themselves are safer, more balanced. >> So, the focus is really on catching and treating these deficiencies as soon as possible. >> That's the modern approach. Proactive early intervention # tag 2 physiological responses to nutritional impairment. >> Okay. Okay, so before we dive into fixing the problem, we really need to understand what breaks down metabolically when a patient is sick or or just starved, >> right? Let's start with the non-negotiable. The body's constant

3:04 critical need for glucose. >> That's priority number one. >> Unwavering priority. Tissues like the brain, red blood cells, white blood cells, the renal medulla, they have to have glucose. They're obligate consumers. >> So maintaining glucose homeostasis is key. eating or not, >> it has to be maintained. Hashtag tag tag tag a metabolic response to fasting or starvation. >> Let's take simple fasting first. Say the first 24 hours, the body's relatively calm metabolically speaking. Where does it get its fuel initially? >> It goes straight for the easy access stash stored carbohydrate. So insulin levels rot quickly. counterregulatory hormones, mostly glucagon, start to rise >> and that triggers >> glycogenolysis, breaking down stored glycogen in the liver and muscles into

3:51 glucose that can circulate. >> And there's a cycle involved here, often using lactate. >> Yeah. What's fascinating is the cyclical nature often involving lactate. It's the Corey cycle. >> Cakori cycle. Where where does that name come from? Is there a story there? >> Uh yeah, good question. It's a neat bit of history named after Gertie and Carl Corey, a husband and wife team who won the Nobel Prize. >> Oh wow. >> Yeah. They brilliantly figured out how lactate produced in muscles during activity or fasting travels through the blood back to the liver >> and gets converted back to glucose. >> Exactly. It's a really efficient way to recycle these energy substrates, keeping the brain fueled when food is scarce in the short term. >> But those glycogen stores, they don't last forever. >> Nope. They run out pretty quickly. Once you push past that first 24 hours, maybe towards 40 hours, that source is pretty

4:36 much depleted. So the body has to switch gears, start making fuel. >> That's the cue for gluconneioenesis, making new glucose from things that aren't carbohydrates. >> What are the building blocks for that? >> The main ingredients are amino acids, specifically glutamine and alanine, which get liberated from breaking down muscle protein along with lactate and also glycerol from fat breakdown. >> Okay. And this is where the muscle loss really starts to kick in, right? The body literally eating its own structure. >> Precisely. Catabolizing skeletal muscle becomes the default way to get those amino acid precursors. For an average adult, this can generate uh up to 75 grams of amino acids every day. >> All just to keep the glucose levels up for the brain. >> All directed towards that. Yes. >> But the body is incredibly adaptive. If starvation goes on longer, say past 48

5:23 hours, it shifts strategy again, doesn't it? To save that muscle. >> It makes a major metabolic pivot. This is the critical shift towards lipolysis, breaking down fat stores. Okay, >> so the fatty acids from fat get converted into ketone bodies. The glycerol backbone from the fat molecule can still be used for a bit of glucose production, but the main event is ketones. >> And tissues start using ketones instead of glucose. >> Most tissues adapt remarkably well. They start using ketones as their primary fuel, brain included to a large extent. Red cells still need glucose though. And the benefit is >> it dramatically reduces the body's dependence on glucose which means it significantly slows down the rate of muscle breakdown is trying to preserve protein >> and the overall energy expenditure drops too right summary box 25.1 shows that

6:09 >> yeah the resting energy expenditure or re can fall quite dramatically maybe from 2530 kilo all day down to 1520 >> the body's basically turning down the thermostat >> exactly partly by reducing the conversion of inactive thyroid hormone T4 to the active form form T3. It's a deep conservation effort, >> a survival mode, >> a remarkable survival mechanism. >> Yeah. >> But, and this is important even in this highly conserved state, the brain and those other essential tissues still need about 200 gram of glucose per day. That demand never fully goes away. >> So, conservation, yes, but still spending vital resources. >> Always #bar. Metabolic response to trauma and sepsis. Okay, that's simple starvation, relatively controlled, adaptive. But surgical patients, they're

6:54 rarely just simply starved. They've got trauma, sepsis, the fallout from big surgery, >> right? And the metabolic response here is completely different. Summary box 25.2 calls it the stress response. And well, it's a metabolic train wreck compared to quiet starvation. >> How so? What drives it? >> It's an inflammatory storm. The body needs to repair tissue, fight infection. So you get this early rapid surge of counterregulatory hormones, catakolamines like adrenaline, gluccocorticoids like cortisol, glucagon, growth hormone, >> and insulin >> and insulin too. But the body often becomes resistant to its effects, which we'll get to. Crucially, the energy requirements don't drop, they actually increase. >> Increase by how much? >> Sometimes spiking up to 40 kilo kills per day. The body needs fuel for tissue repair for all those hyperactive

7:40 inflammatory cells. Okay, so we've gone from conserving energy and starvation to just burning through everything in the stress response. >> Pretty much throwing gasoline on the fire is a good way to put it. And this is where the muscle loss becomes catastrophic. >> Why is it worse here? >> Those elevated stress hormones drive persistent aggressive breakdown of tissue protein. You get this severe sustained negative nitrogen balance. >> Just losing protein constantly. >> Constantly. And here's the key difference that really dictates how we manage these patients. >> Yeah. that adaptive shift to using ketones we saw in starvation. Yeah, it's often severely impaired or sometimes completely absent in severe trauma and sepsis. >> Ah, okay. So, that's the trap. If the body can't switch efficiently to using fat and ketones, >> it has no choice but to keep hammering

8:26 the muscle protein for gluconioenesis. >> Yeah. >> Even if you're pumping calories into the patient. >> Wow. That's a vicious cycle. >> It is. And it's made even worse by profound insulin resistance. This is often called the surgical factor. What causes that resistance? >> Stressors like pain, tissue damage, acidosis, they all trigger hormonal and inflammatory responses that make the cells resistant to insulin signal. >> And clinically we see that as high blood sugar, right? Hypoglycemia. >> Exactly. Even if glucose is available, it can't get into the peripheral tissues efficiently. >> Why not? What's the mechanism? >> It boils down to the failure of a specific protein, the glucose transporter called GLUT4. Normally insulin tells glut4 to move to the cell surface and let glucose in

9:12 especially into muscle cells. >> But in the stress state >> that signaling pathway is inhibited. Glut activation is reduced. So muscle cells effectively refuse the glucose >> which forces the liver to >> keep making more glucose by breaking down muscle protein because the body still perceives a need for glucose even though there's plenty around. >> So you're losing muscle and you've got high blood sugar damaging things like the immune system and wound healing. It's a double hit. A really damaging situation. >> And understanding this this whole metabolic picture, that's what's driven changes in how we care for surgical patients. >> Absolutely. It's led to a revolution. Really, modern interventions are specifically targeted at dampening this severe stress response. >> Things like the enhanced recovery after surgery, the ER protocols. >> Exactly. Things like giving

9:59 pre-operative high carbohydrate drinks. The idea is to load the system and improve insulin sensitivity before the stress hits. >> Makes sense. >> Prioritizing minimally invasive surgery to reduce the amount of tissue damage and inflammation and that aggressive focus on getting patients moving early mobilization. >> All aimed at minimizing that damaging insulin resistance, >> minimizing its impact, shortening its duration. It all ties back fundamentally to understanding this metabolic response to injury. >> Okay, the metabolic picture is clear and it can be pretty grim. But before we jump in with feeding tubes and IV lines, we need to know who actually needs help, right? >> Assessment first. >> Absolutely crucial. You don't want to feed aggressively if it's not needed or worse if it's dangerous. The source organizes this assessment really nicely

10:45 using the ABCD approach. >> ABCD. Okay. A is for >> anthropometry. Basically measuring the physical body to get an idea of its composition, its energy, and protein stores. # tag tag aan anthropometry. So what kind of measurements are we talking about? >> Well, the basics like weight and calculating BMI, which are easy to get, but ideally you also look at things like mid-upper arm circumference, MUAC, right? Skinfold thickness, usually the triceps, so TSF. And from those two, you can calculate the mid-arm muscle circumference or MAMC. >> And those give a better sense of muscle versus fat stores. >> They attempt to. Yeah. Trying to get a clearer picture beyond just the number on the scale. >> Now, what about the actual red flags? the specific numbers that tell us right this patient needs nutritional support. Now >> we need to look for a combination of

11:31 factors. The source gives clear criteria. Criterion one, a BMI less than 18.5 kilogram and tall and tolerance to combined with unintentional weight loss of more than 10% over the last 3 to 6 months. >> Okay. BMI under 18.5 A andd weight loss over 10%. Got it. or criterion two uh slightly higher BMI less than 20 kilogram of dollars driven but still with significant unintentional weight loss this time greater than 5% in that same 3 to sixmonth window >> BMI under 20 A andd weight loss over 5% >> right if a patient meets either of those combinations it should trigger an immediate referral to the nutrition support team or initiation of support >> but there's a big butt here isn't there especially in sick patients >> huge caveat in critically ill patients these simple anthropometric measures can

12:16 be really deceptive Why is that? >> Think about it. Aggressive fluid resuscitation, edema, massive fluid shifts that happen with sepsis or major surgery. >> Ah, so their weight might go up even if they're losing muscle. >> Exactly. A patient can gain 10 kilos of fluid overnight while simultaneously breaking down significant muscle mass. So BMI and weight alone have to be interpreted very cautiously in that acute setting. # tagbiochemistry. >> Okay. So A is anthropometry, B is for >> biochemistry. Looking at the blood tests, we're scanning for signs of inflammation, infection, and potential chronic deficiencies. >> What markers are key here? >> Well, you look at things like C reactive protein, CRP, and white cell counts. They're general flags for inflammation and infection, which we know drive

13:02 catabolism and worsen nutritional status. >> Makes sense. >> But the marker everyone always talks about is albumin, >> right? Low albumin often gets equated with malnutrition, but the source says it's unreliable in the acute setting. >> It is unreliable, yes, for a couple of reasons. First, albumin levels are heavily influenced by fluid balance. If a patient is fluid overloaded, their albumin gets diluted, making it look falsely low. But more importantly, albumin is what we call a negative acute phase reactant. Meaning during inflammation or sepsis, the liver actively suppresses albumin production and ramps up production of positive acute phase reactants like CRP. >> Ah, so a low albamin might just reflect how sick they are acutely, not necessarily their long-term nutritional state. >> Exactly. It's more a marker of illness severity in the short term. It could be

13:48 useful to track recovery over weeks, but it's not a great snapshot indicator of nutritional status today. So what are the crucial blood tests we need? Especially before starting any aggressive feeding, >> we absolutely must check hemoglobin looking for anemia. Often points to vitamin or iron deficiencies. Glycated hemoglobin HBA1C is vital if the patient has diabetes tells us about their long-term control. >> And crucially, >> we need baseline electrolytes, particularly potassium, magnesium, and phosphate. Calcium 2. These are non-negotiable. >> Why are they so critical at baseline? Because these are the electrolytes that plummet during refeeding syndrome. We need to know the starting point to anticipate and prevent those potentially fatal shifts when we start feeding. #Cintexc clinical evaluation and dietary

14:33 assessment, >> right? Makes sense. So C is clinical evaluation. This is about the history and symptoms. >> Yes. A thorough clinical evaluation. Are there symptoms actively stopping the patient from eating or absorbing nutrients? things like nausea, vomiting, difficulty swallowing, dysphasia, feeling full really quickly, early satiety, or chronic problems like diarrhea or constipation. >> And the past medical history is key, too. >> Absolutely. Conditions like cancer, inflammatory bowel disease, IBD, significant liver disease, neurological conditions that affect swallowing, or things caused by previous surgery like short bowel syndrome or a high output STO or fistula. Anything that impairs absorption needs to be flagged. Okay. And finally, D is >> dietary assessment. Trying to quantify

15:20 the gap between what they need and what they're actually getting. >> How do we estimate their needs quickly? >> A rough estimate for energy requirements in a reasonably stable adult is somewhere between 25 and 35 kilo calories per kilogram of lean body weight per day. >> Lean body weight, not total weight. >> Ideally, lean body weight. Yes. And you adjust that upwards depending on how stressed they are. trauma, fever, sepsis, all increased needs and their activity level, if any. >> And when does this assessment tell us they need artificial support? >> It's pretty straightforward. If their current estimated intake is consistently falling short of those calculated requirements, or perhaps more importantly, if you anticipate they're going to eat little or nothing for more than 5 days straight >> because of the surgery planned or

16:05 expected gut issues posttop. >> Exactly. Then they need proactive nutritional support. Don't wait for them to become visibly malnourished. # tag tagged upd. The malnutrition universal screening tool. >> This seems like a lot to pull together quickly in a busy ward setting. Is there a tool to help standardize this? >> Yes, thankfully. The malnutrition universal screening tool or must. It was developed by Bapen, the British Association for Parental and Ententral Nutrition >> and its purposes. >> It's designed as a rapid screening tool. It's objective, easy to use, and can be applied in hospitals, clinics, even in the community. It gives a score that directly guides action. >> Okay. How does the scoring work? Figure 25.2 lays it out. Three components. >> Three key components weighted equally. First is BMI. If it's less than 18.5,

16:51 that's considered severe risk. Scores two points straight away. >> Component two, >> recent documented unintentional weight loss in the last 36 months. If it's more than 10% of their usual weight, that also scores two points. Between 5 and 10% scores one point. >> Okay. And the third component addresses the immediate situation. >> Exactly. It's called the acute disease effect. If the patient has had or is likely to have very little or no nutritional intake for more than five consecutive days, >> like someone with a bowel obstruction coming in. >> Perfect example. That acute lack of intake adds another two points to the score. And then you add up the points and the total score tells you what to do >> precisely. A score of zero means low risk, just routine clinical care. >> Score a warning, >> medium risk. The protocol here is to observe. You need to meticulously

17:37 document their food intake for 3 days, then repeat the MST screening. Keep a close eye on them >> and a score of two or more. >> That's high risk. This is a hard stop. You must initiate treatment. That means referring to the specialist dietitian or the nutritional support team, implementing your local feeding policies, and getting nutritional support started promptly. >> So, it's a system designed to catch those at risk early and prevent them falling through the cracks. >> Exactly. Takes the guesswork out and mandates action. # Ivy Keen. Fluid and electrolyte replacement. >> Assessment complete. We know who needs help. >> Now, the second critical pillar you mentioned, fluids and electrolytes. These seem almost inseparable from nutrition in surgical patients. >> They are utterly interwoven, especially when you have ongoing losses from

18:22 drains, fistulas, or poor intake. You can't manage one without the other. # AI daily fluid balance and maintenance. >> Let's start with the basics again. What does normal daily fluid balance look like? Table 25.1 gives the numbers for a healthy 70 kg adult. >> Right? Roughly 2.5 L of intake should balance about 2.5 L of output. Intake comes from drinks maybe 1.2 L, water and food about 1 L and then around 300 ml the body actually produces metabolically >> and output is mostly urine about 1.5 L. But there's also this significant insensible loss. What's that? >> That's the fluid we lose without noticing it mainly through evaporation from the skin and water vapor in our breath. Usually around 900 mil well so

19:08 nearly a liter a day. >> And that amount can change. So yes, it increases significantly if you have a fever, parexia, if you're exerting yourself, or if you're in a very warm environment. >> And there's a specific surgical point about tracheosttomies. >> Yes, really important detail. A tracheosttomy bypasses the natural humidification system of the nose and upper airways. So patients lose much more water through respiration, >> meaning you have to >> you must provide humidified air or oxygen to them otherwise they can get severely dehydrated very quickly from those increased insensible losses. >> Okay, so adding it all up, what's the typical daily maintenance fluid requirement for that 70 kg adult? >> Roughly 2.2 L per day or a good rule of thumb is about 30 milliliters per kilogram per day. >> And what about the electrolytes needed just for maintenance?

19:54 >> Daily needs are around.9 to 1.2 millles per kilogram per day for sodium. Potassium is simpler about 1 millm moles per kilogram per day. >> And the others, >> don't forget calcium about 5 mill moles per day and magnesium around 1 mill per day. These baseline amounts are needed even if there are no extra losses. >> And the route of delivery, simplest is best. >> Always. If the patient can drink, oral rehydration solutions are the gold standard. If they can't swallow, but the gut works, use an entr tube. FAV fluids are really the last resort. >> Reserve for when? when the gut just can't absorb adequately or when the losses are so large they simply can't be kept up with entryally. Hashtag tag tag tag tagb introvenous fluid replacement solutions. >> So when Iv fluids are the only option, the choice of fluid becomes critical.

20:39 Table 25.2 is fantastic here comparing common solutions side by side with plasma. >> Yeah, this comparison is something everyone managing fluids needs to internalize. What's striking is just how different most standard IV fluids are from our own plasma. >> Plasma is balanced, buffered, >> right? physiologically appropriate sodium around 135 145 mill L chloride 95 105 millol physiological pH >> okay now look at 0.9% saline often called normal saline which is ironic given these numbers >> exactly it's got 154 mill of sodium and 154 mill mole of chloride both significantly higher than plasma >> and that has consequences >> certainly can especially if you give large volumes that high chloride load can overwhelm the kidney's buffering capacity and lead directly to a

21:25 hypercchloramic metabolic acidosis. Plus, look at the pH of saline itself. It can be as low as 4.5. It's acidic. >> Right? So, Hartman's solution or lactated ringers is often seen as more physiological. Why is that? >> Hartman's is much closer. Sodium is 131. Potassium is 5 mill. But the key is the lactate. It contains 29 mill. >> And the body uses that lactate. >> The liver rapidly metabolizes that lactate into bicarbonate effectively giving the fluid a buffer capacity of 29 mill. This makes it much less likely to cause acidosis compared to large volumes of saline. >> Okay. And then there's 5% dextrose, just glucose, no electrolytes, >> essentially free water. Yeah. Once the glucose is metabolized, you're left with water. It's used mainly to replace pure water deficits like insensible losses or

22:12 to correct hyperreia, but it provides no electrolytes for maintenance or replacement. So the big takeaway from this table is >> there is no single perfect 5V fluid that matches plasma exactly. The fluid you choose must be tailored to the specific patient, their underlying problem, and crucially the type of fluid they are losing. >> What about colloids? Things like jellyfine. They're meant to stay in the circulation longer. >> That's the theory. They contain large molecules designed to increase onotic pressure and hold fluid intravascularly acting as plasma extenders. But there's controversy. >> Yes, quite a bit. Large studies have questioned whether they offer significant benefit over crisids for resuscitation and some types have been linked to increased risks of acute kidney injury or problems with blood

22:57 clotting. Coagalopathy their use is much more restricted now >> and albammen >> generally not recommended for routine volume resuscitation. It has specific indications like replacing fluid to remove during paracentesis for a sites or in some specific liver failure scenarios but not as a general resuscitation fluid >> and the final rule if the loss is blood >> the best replacement for blood loss is blood period #c assessment and fluid loss composition. >> So making that tailored fluid choice requires careful monitoring. What are we watching? We look at the standard hemodynamics, pulse, blood pressure. If they have a central line, central venus pressure, CVP, gives an idea of intravascular volume. But just as important, maybe more so, is accurate fluid balance

23:43 charting, >> tracking everything in and out >> meticulously. Urine output, yes, but also output from surgical drains, nasal gastric tubes, stoomas, fistulas, even estimating significant diarrhea losses. And regular checks of serum electrolytes and hematocrit are essential to see if your replacement strategy is working. >> And table 25.3 is key here because it shows that the composition of fluid loss from different parts of the GI tract varies hugely. >> This is critical clinical knowledge. It dictates the type of replacement fluid you need. >> Give us an example. High NG tube output. >> Okay. Patient with gastric outlet obstruction putting out lots of fluid via an NG tube. They're losing gastric juice. What's in that? It's high in chloride around 110 millol and hydrogen ions it's acidic moderate sodium maybe 50 millm low potassium

24:30 >> so losing lots of chloride and acid leads to >> a hypocchloric metabolic alkyossis they become alkalotic because they're losing acid you need to replace that chloride often with saline and potassium >> and the opposite happens with lower GI losses >> exactly if the loss is from further down pancreas bile duct small bowel fistula high output iliotomy that fluid is very different. It's typically high in sodium around 140 millm similar to plasma and very rich in bicarbonate especially pancreatic fluid which can have over 100 milll of bicarb. >> So losing that fluid causes >> profound dehydration and a metabolic acidosis because you're losing base replacement here needs a balanced salt solution like Hartman's or even fluids with extra bicarbonate added plus potassium.

25:15 >> So you absolutely cannot use a one-sizefits-all approach. >> You really can't. Understanding the likely composition of the losses based on the source is fundamental to choosing the right replacement fluid and preventing dangerous electrolyte and acid base imbalances. #teagv nutritional requirements. >> Okay, assessment done. Fluids getting sorted. Now let's talk about the actual fuel figuring out the energy and nutrient requirements. # tag tagg total energy intake and calculation. Right. The starting point for planning any feed is usually estimating the basil metabolic rate or BMR. How much energy the body burns just at rest. >> And we use equations for that like Harris Benedict. >> Exactly. The Harris Benedict equations are the classic ones. They plug in the patients weight, height, age, and sex to

26:01 predict that baseline energy expenditure. >> It's amazing science developed over a century ago. Right, Harrison Benedict? >> Yeah. Foundational work adapting calorimetry for human physiology. But that equation gives us the predicted BMR. What's the actual clinical requirement for a sick patient? >> Does it go up much >> for a stable but unwell patient? Their actual requirement is typically around 20 to 30 kilo calories per kilogram of ideal body weight per day. Even with severe stress like major trauma or sepsis, the hyper metabolism rarely pushes needs beyond 120% of that predicted BMR. So maybe up to 30 kilo in those cases. >> Okay. And you emphasize ideal body weight there. Why is that distinction so important? >> Absolutely critical. If you use the patients actual weight, especially if

26:47 they're obese, you will massively overestimate their energy needs. Attapost tissue fat is metabolically much less active than muscle. >> And overestimating leads to >> overfeeding. Yeah. >> Which the source clearly states is a very common cause of complications whether you're feeding via tube or IV. >> What kind of complications does overfeeding cause? Why are we so cautious about it? Well, it puts a huge metabolic strain on the body, forcing the system to process excess calories, especially carbohydrates, generates a lot of carbon dioxide, CO2, >> which is bad if >> if the patient already has respiratory problems, maybe they're on a ventilator. That extra CO2 load can make it harder to wean them off, potentially even causing respiratory failure. Overfeeding also worsens hypoglycemia, insulin resistance, and can lead to fatty changes in the liver. >> So, the rule is start slow, especially

27:33 in high-risisk patients. Definitely if the patient is severely stressed or you know they're at high risk of refeeding syndrome, you must start cautiously. No more than 50% of their estimated target needs initially. Maybe even just 10 kiloal per kilogram per day to begin with >> and then increase gradually >> slowly increase towards the full requirement. Maybe over 24 to 48 hours for standard patient but potentially taking four to seven days for those at highest risk of refeeding. Caution equals safety here. #bm macronutrients. >> Okay, let's break down the fuel mix. The macronutrients starting with carbohydrate, >> right? Carbs usually given as glucose or the central fuel, especially for the brain and blood cells. The body needs the equivalent of at least 2 g of glucose per kilogram per day just for those basic functions.

28:19 >> And in a typical feed, what proportion should be carbs? >> Generally, carbs should make up the bulk of the energy. Somewhere between 45% and 65% of the total caloric intake. Next protein needs go up in illness. You said >> sharply. Yes. Because of that catabolic stress response we talked about. The goal of giving protein is to provide the building blocks for tissue repair and try to counteract that negative nitrogen balance. >> How much protein are we aiming for? >> Daily nitrogen needs increase quite a bit. We often aim for up to 0.25 g of nitrogen per kilogram per day which translates to roughly 1.5 g of actual protein per kilogram of ideal body weight per day. And as a percentage of total energy, >> protein should probably make up around 20% of the total energy intake. >> Okay. Lastly, fat. It's more than just

29:05 calories, >> right? Fat provides essential fatty acids, linoleic and lolinic acid, which the body can't make itself. They're vital for cell membranes, inflammation modulation, lots of things. >> And how is fat used in artificial feeding, especially IV feeding? >> When we get parental nutrition, PN, we usually use a lipid emulsion. We combine giving fat maybe 10020 grams total per week with a minimum amount of glucose say 10020 grams per day. >> Why the mix? >> This mixed fuel approach is metabolically safer. It helps the body utilize the substrates efficiently. It minimizes the risk of fluid retention compared to giving just glucose. And importantly, it significantly reduces that CO2 production we worried about with overfeeding pure carbohydrate #C

29:50 vitamins, minerals, and trace elements. Easy to focus on the big three carbs, protein, fat, but the micronutrients are just as vital, aren't they? Especially vitamins's B and C. >> Absolutely critical like the spark plugs and lubricants for the metabolic engine. Vitamin C is essential for collagen synthesis, wound healing. Post-operatively, the requirement actually increases maybe to 60 80 milligrams per day. >> And B vitamins, >> crucial co-actors in energy metabolism. Thamine vitamin B1 is probably the single most critical one to give immediately when starting any feed especially in malnourished patients to prevent the neurological damage of refeeding syndrome like vernicks and sephylopathy. >> Are there specific patient groups who need extra attention for certain vitamins? >> Definitely anyone with a history of significant alcohol abuse or patients

30:37 who've had gastric surgery like a gasterectomy needs routine supplementation with thamine, B12, and folate. Why gastric surgery specifically for B12? >> Because the parietal cells in the stomach lining produce intrinsic factor which is absolutely essential for absorbing vitamin B12 further down in the elium. Remove the stomach or bypass it and you lose that intrinsic factor leading to B12 deficiency. >> Makes sense. And what about conditions that affect fat absorption? >> If you have reduced pancreatic enzyme output or bile flow is obstructed, you'll have trouble absorbing fat. And that means you'll also malabsorb the fats soluble vitamins A, D, E, and K. They need monitoring and replacement. >> And electrolytes and trace elements. Again, continuous losses are a big issue. >> Huge chronic diarrhea. High sto output.

31:24 These can relentlessly deplete sodium, potassium, magnesium, and critically phosphate. We also need to think about trace elements like zinc, copper, selenium, iron. They're all crucial co-actors for enzymes involved in healing and metabolism. Replacement is often necessary, especially to prevent or manage refeeding syndrome. # tag6 effects of intestinal resection. >> Okay, let's shift focus now to a very specific surgical situation where nutrition becomes a central often permanent challenge. Intestinal resection, losing parts of the bowel, # tag tech, intestinal adaptation and loss. >> Right? The intestine is an amazing organ. It has this huge capacity for adaptation. After parts of it are removed, the remaining bowel can actually grow. The vi get taller. It

32:09 produces more transporter proteins to try and compensate. >> Does it matter which part of the bowel is removed? >> Oh, enormously. If you resect a portion of the proximal junum, the early part of the small intestine, the further down and the colon can often compensate remarkably well. Supplemental nutrition might be needed temporarily, but often not long term. >> But losing the different >> much more significant. Yes. The ilium has unique functions that the jigunum can't fully replicate >> like absorbing bile salts. >> Exactly. The terminal illium is where virtually all bile salt reabsorption happens. If you lose, say the last 100 cm of elium. You significantly impair that process. >> What happens then? >> The bile salts spill over into the colon. They irritate the colon lining drawing water in causing osmotic

32:55 diarrhea. They also interfere with fat absorption leading to stateria fatty greasy stools. >> Can that be managed? >> Sometimes if the loss isn't too extensive, a medication called kalistyramine which binds bile salts can help control the diarrhea. But often patients need to significantly restrict their dietary fat intake. >> And if the ial resection is even larger, >> then the fat restriction becomes essential. >> But you also get another problem. Loss of the yelium tends to increase gastric emptying and speed up overall intestinal transit. Things just rush through too quickly, >> compounding the diarrhea and malabsorption. >> It's exactly less contact time for absorption, more fluid hitting the colon faster than it can handle. Persistent diarrhea and major fluid and electrolyte losses become the norm. # tagbel

33:43 syndrome SPS. >> And when the resection is massive, we get into the realm of short bowel syndrome or SPS. The source defines this as typically less than 200 cm of remaining small intestine. >> That's the general threshold where you see the most severe consequences. Yeah. Significantly reduced absorptive surface area leads to chronic potentially life-threatening malnutrition and dehydration. >> SPS isn't static though, is it? There are phases, >> right? We think of it in two main stages. First is the acute stage right after the massive resection. This lasts for the first few weeks. >> What characterizes that stage? extremely high intestinal losses, often fluid output from stoomas or diarrhea exceeding four, five, even six liters a day. You also often see gastric hypers secretion, the stomach pumping out excess acid driven by high gastron levels.

34:28 >> Sounds incredibly unstable. >> It is. This period demands really aggressive IV fluid and electrolyte management just to prevent acute kidney injury and severe acidbased chaos. Patients are often critically ill. >> But then comes the adaptation stage. There's hope for improvement. Yes, thankfully over the next one to two years that remaining bowel undergoes those structural and functional changes we talked about villicypertrophy increased transporter expression it gradually gets better at absorbing nutrients and fluid. >> Does everyone adapt fully? >> Not everyone but many patients do improve significantly. Their symptoms lessen their nutritional status stabilizes. Some are even able to eventually wean off the parental nutrition, the IV feeding that was essential initially. >> It's a long process, >> a very long process. And even after

35:14 maximal adaptation, many patients still require specialized diets, oral supplements, specific medications like anti-diarals or agents to slow transit, often for life. The source notes that if weaning off PN hasn't happened within about 3 years, lifelong dependency is unfortunately likely. >> Let's talk about the most severe cases. Say less than 100 cm small bowel left. The fluid management here sounds really tricky, almost counterintuitive. >> It is. This is a situation where patients literally lose more water and salt in their stool or STO output than they can possibly absorb from normal drinks. Daily losses can be enormous. >> And the key management point is restricting certain types of fluids. >> Critically important. They need to strictly restrict their intake of

35:59 hypotonic fluids, meaning fluids with a low sodium concentration, typically less than 90 mil. Things like plain water, tea, coffee, juice, usually restricted to less than a liter per day. Why restrict water? That seems odd when they're dehydrated. >> It's about osmosis. In such a short compromised bowel, drinking hypotonic fluid creates a strong osmotic gradient, pulling sodium and water out of the bloodstream and into the bowel lumen. >> So, drinking water actually makes the dehydration and salt loss worse. >> Paradoxically, yes. It increases stool or sto output. So these patients must rely on isotonic or slightly hypertonic oral rehydration solutions OS like diurolyte or or similar preparations containing glucose and salt in the right proportions >> because those promote absorption rather

36:45 than secretion. >> Exactly. The glucose co-ansports with sodium helping to drive net absorption of salt and water rather than causing further losses. It's a vital management principle for severe SPS. >> Okay, we've seen the consequences of gut failure. Let's pivot back to intervention. We've assessed the patient. We know they need support. When do we actually pull the trigger and start artificial feeding? >> The general rule of thumb is if you anticipate inadequate oral intake for 5 days or more, consider artificial support. >> Sooner if they're already malnourished. >> Absolutely. If they have pre-existing chronic malnutrition or if they're about to undergo really high-risisk surgery, think major cancer operations like esophagectomies gasterectomies pancreatic resections, you should ideally start nutritional support before the operation. be proactive

37:30 >> and sometimes that means putting in a feeding tube during the surgery itself. >> Yes, very common practice now. For example, placing a feeding gunosttomy tube distal to the surgical site during a big upper GI operation anticipating that the stomach won't work properly for a while posttop but wanting to feed the patient early. #Jaga A indications and preference. Now, why is ententral nutrition feeding directly into the GI tract so strongly preferred over introvenous feeding, parental nutrition, whenever possible, even if the patient is quite sick? >> The benefits of using the gut are just profound. It's not just about delivering calories. >> What else does it do? >> First and foremost, keeping the gut fed helps maintain the integrity of the gut lining, the mucosal barrier. This is

38:15 crucial for preventing bacteria and toxins from leaking out of the gut into the bloodstream, a process called bacterial transllocation, which can drive sepsis. >> So, it supports gut immunity. >> Yes. And prevents gut atrophy, the lining becoming thin and leaky from disuse. >> Clinically, using EN is consistently associated with lower rates of infection, better wound healing, and shorter hospital stays compared to relying solely on PN. >> So, the mantra is, >> if the gut works, use it. Even if it's only working partially, try to get some feed in there. Even if you need supplemental PN alongside it, trophic feeding hashtag tagby methods. >> Okay, so how do we deliver EN? What are the options? >> Well, the simplest start is often oral nutritional supplements, ONS. Those are the liquid sip feeds, shakes, usually

39:01 providing around 200 kls and maybe 810 gram protein per 200 mill bottle. Good for boosting intake or weaning people off tubes. And if they can't manage ONS or need more reliable delivery, then it's tube feeding, >> right? And we categorize tubes mainly by where the tip sits. You have prepaloric feeding, meaning the feed goes into the stomach. >> How do we achieve that? >> Usually via naggastric NG tube like a Rialy tube, though finebore feeding tubes are better tolerated long term or via a gastrommy tube placed directly through the abdominal wall into the stomach. >> And the alternative is post pyloric feeding. >> Yes, bypassing the stomach. The feed goes directly into the small intestine, usually the jigunum. This is done via a nasogenal NJ tube or a feeding ginosttomy tube. >> Why bypass the stomach? What's the advantage there?

39:47 >> It's particularly useful if the patient has problems with delayed gastric emptying or if they're very high risk of aspirating feed from the stomach into their lungs. Post pyloric feeding allows you to feed them safely without resorting to TPN in those situations. And starting the feed itself needs careful planning. >> Always. It should be planned by a dietitian. And as we keep saying, start slow, especially if there's any risk of refeeding syndrome. >> What kind of rates are typical? >> Often start cautiously, maybe 10 or 20 milliliters per hour, and then gradually increase the rate every few hours or daily, aiming for a target rate, perhaps up to 75 or 100 mil hour, depending on the feed concentration and patient tolerance. >> Tube care is important, too. blockages. >> A meticulous flushing with water,

40:33 usually before and after feeds or medications, is essential to prevent the tube blocking up, which is a common frustration. >> And if it does block, >> try flushing gently with warm water. But the absolute safety rule, never ever try to unblock a feeding tube by reinserting the guide wire that came with it. >> What? >> Because the guide wire is stiff and sharp. If the tube has migrated slightly or kinkedked, you can easily perforate the esophagus, stomach, or bowel. It's incredibly dangerous. Got it. No guide wires. And confirming the tube is in the right place before starting the feed is mandatory. >> Absolutely mandatory. Safety check number one. For a standard NG tube going into the stomach, the first check is usually aspirating fluid and testing its pH. >> What pH are we looking for? >> A pH of 5.5 or less is generally

41:19 considered reliable confirmation of gastro placement. If the pH is higher or you can't get an aspirate or if the patient is high risk 3G unconscious sedated then you must get a chest X-ray CXR. >> And what does the CXR need to show? >> The source is specific. The tip of the tube must be clearly visible below the diaphragm and it should ideally bisect the corina or pass beyond the bronchial bifurcation ensuring it hasn't gone down an airway or coiled up in the esophagus. >> What about nasaunal tubes? They go further down. >> NJ tubes are harder to place correctly. They usually require endoscopic or radiological guidance to get the tip past the pyloris into the junum. You can't just insert them at the bedside and assume they're right. >> So confirmation for NJ tubes >> always requires an abdominal X-ray to

42:06 confirm the tip is definitely in the small bowel before you start feeding. # tagc long-term access gastrotomy and gigenostomy. >> Okay, those nasal tubes are usually for shorter term feeding. If someone needs Ian for longer, say more than four, six weeks, >> then we start thinking about more permanent access, usually gastrotomy or sometimes a gigunostomy tube placed directly through the abdominal wall. >> This sounds like a bigger decision. >> It is. It involves a procedure, potential complications, and impacts lifestyle. It really needs a proper discussion involving the patient, family, and the multi-disiplinary team. >> What's the most common type of gastrotomy? >> The perccutaneous endoscopic gastrotomy or PEG tube. This is usually done by gastroenterenterologists using an endoscope. >> How does that work? >> They pass the endoscope into the stomach, identify a suitable spot on the

42:53 abdominal wall, make a small incision, and then pull a feeding tube through, securing it so the stomach wall is held snugly against the inside of the abdominal wall, usually held by an internal bumper or cuff. >> Why is that snug fit important? It's critical to create a seal and prevent leakage of gastric contents into the peritineal cavity around the tube site which could cause peritonitis a serious infection. >> Are there alternatives if PEG isn't possible? Maybe due to anatomy. >> Yes. If endoscopy is difficult or unsafe, maybe due to previous surgery distorting things or a tumor in the head, neck or esophagus blocking the way, then a radiologically inserted gastrotomy or rig can be done. How's that different? >> Interventional radiologists use X-ray or ultrasound guidance to place the tube,

43:40 often securing it with an internal balloon or a pigtail catheter coil instead of a bumper. Surgical gastrosmy is also an option, but less common now, reserved for when PEG or rig aren't feasible. >> And these tubes aren't without risks either. >> No, definitely not. Any procedure carries risks. perforation to the bowel during insertion, bleeding, infection around the site, which is actually quite common, and the ongoing risk of leakage or peritonitis if the seal isn't maintained. >> What about removing them eventually? >> With long-term tubes, the track between the skin and the stomach can become permanent, lined with epithelium. So, when you remove the tube, sometimes the hole doesn't close on its own, leaving a persistent gastric fistula that might need surgical closure. And gigenostomies, you mentioned placing those during surgery sometimes.

44:25 >> Yes. Often placed surgically either open or laparoscopically during major upper GI operations like esophageectomies or Whipple procedures specifically to allow early post-operative feeding into the small bowel bypassing the stomach and upper GI tract which might take time to recover. >> Similar complications to gastrotomies >> generally. Yes. Bleeding, displacement of the tube, leakage causing peritonitis, which is often more dangerous with ginal contents, infection at the stoite, blockage, granulation tissue forming around the exit site. They require careful management. # tag tagd. Complications of ententral feeding. Summary box 25.3. >> Okay. Summary box 25.3 pulls together the complications of EN. We've touched on the tube related ones, malposition, blockage, leakage. What about the GI

45:12 side effects? GI issues are really common. Firstly, EN is absolutely contraindicated if there's a complete mechanical bowel obstruction or a severe paralytic ulus feeding into a non-moving gut. Massively increases the risk of vomiting and aspiration. >> What about side effects when the gut is working? >> Diarrhea is probably the most frequent problem reported in over 30% of patients getting tube feeds. It can be due to the feed composition, rate of infusion, medications, or underlying infection like CIFF. It compromises absorption and can cause dehydration and electrolyte loss. Other common issues, >> bloating, nausea, vomiting, abdominal cramps are also pretty common reasons why patients might not tolerate the feed well, requiring adjustments to the feed type or rate >> and the big systemic risk we keep coming back to >> metabolic and biochemical problems. Primarily electrolyte disturbances,

45:58 including of course refeeding syndrome if feeds are started too quickly in a malnourished patient, vitamin and mineral deficiencies can also develop over time if not monitored, and potential drug interactions via the tube. >> Right? So that's EN. But what if the gut simply cannot be used? Obstruction, massive resection, severe fistulas. Then we have to bypass it entirely. >> Then we turn to parental nutrition or PN delivering all the necessary nutrients directly into the bloodstream introvenously. If it provides everything, it's called total parental nutrition, TPN. Sometimes it's used just to supplement inadequate gut function #a. Indications and composition. >> What's the main reason someone would need TPN? The primary indication is true intestinal failure. The inability to

46:43 absorb sufficient nutrients, fluids, and electrolytes via the GI tract to maintain health. The classic example is short bowel syndrome after a massive resection. Other situations >> also used temporarily for conditions causing prolonged inability to use the gut like intractable vomiting DG hyperemmesis gravidarum >> severe prolonged paralytic alias after surgery high output intestinal fistulas where feeding makes the output worse or sometimes severe acute pancreatitis >> what's actually in the TPN bag it looks complex >> it is complex it's usually prepared aseptically by the hospital pharmacy typically is a 3in-1 mixture in a large often 2 or 3 liter bag It contains everything the patient needs. >> Meaning >> a lipid emulsion for fat calories and essential fatty acids. A solution of

47:28 essential and non-essential amino acids for protein building blocks. Concentrated glucose solution for carbohydrate energy. Plus all the necessary electrolytes, sodium, potassium chloride calcium magnesium phosphate, trace elements, zinc, copper, selenium manganese chromium and vitamins. >> Is the ratio of fuels important? >> Very important. The energy content needs to be balanced with the protein nitrogen content. Usually aim for 150 250 kilo calories per gram of nitrogen provided. This ensures the amino acids are actually used for building protein and abolism, not just burnt for energy. And typically fat provides about 30 50% of non-proin energy. >> We talked about phosphate being critical for refeeding. How much is usually in a TPN bag? >> Standard bags contain around 20 to 30 mill moles of phosphate per day. This is

48:15 essential because starting PN drives phosphate rapidly into cells for metabolism making ATP. Without adequate replacement, severe hypophosmia develops quickly, which is a hallmark of refeeding syndrome and can cause muscle weakness, respiratory failure, and cardiac arrest. >> And for patients on TN long term, do micronutrients need special monitoring? >> Yes, absolutely. The source recommends checking levels of things like zinc, copper selenium iron feritin B12 folate, and vitamin D regularly for anyone on PN for more than about 28 days and then maybe every 3 months for those on lifelong home PN. Deficiencies can sneak up and cause significant problems like skin changes, hair loss, anemia, or bone disease. #tagbad administration of parental nutrition. >> Okay, so we have this complex life

49:01 sustaining fluid. How and where do we infuse it? You mentioned it has high osmolerity, >> extremely high osmalerity, much higher than blood. That's because all those nutrients are concentrated into a relatively small volume. Because of this, TPN must be infused into a large central vein where the blood flow is very high, allowing for rapid dilution. >> Yeah, exactly. >> Ideally, the tip of the infusion catheter should sit in the lower third of the superior venneava SVC or at the junction of the SDC and the right atrium, the atrioabol junction. >> Why not a peripheral vein like in the arm? Infusing such a hyperosmolar solution into a small peripheral vein would cause immediate severe chemical thromboplabitis, inflammation and clotting of the vein. It's painful and damages the vein quickly. Peripheral PN

49:46 PPN with lower osmalerity formulations is sometimes used for very short periods less than 14 days but it's generally avoided if possible due to the high flabitis risk. >> So we need central venus access. What kind of lines are used? >> Depends on the expected duration for short to medium-term use. say weeks to a few months. A PICC line peripherally inserted central catheter is very common that's inserted into a vein in the upper arm like the basillic vein and threaded up until the tip is in the central circulation. >> Okay. >> Other options >> for shorter term acute use in hospital a standard non-tunnled central venus catheter CDC inserted into the subclavian or internal jugular vein in the neck chest is often used. And for long-term home PN >> for patients needing PN for months or years, we typically use a tunnneled

50:32 cuffed catheter like a hickman or broiac line or an implantable port device. The tunnel and cuff under the skin act as barriers to reduce the risk of infection traveling up the line tract. >> Any veins to avoid. >> Femeral lines inserted in the groin are generally strongly discouraged for PN due to a much higher risk of infection and thrombosis compared to upper body sites. And just like with feeding tubes, confirming the line position is essential before starting TPN. >> Absolutely mandatory. A chest X-ray must be done after insertion and before the TPN infusion begins. >> What are you checking for on the X-ray? >> Primarily confirming the tip position is correct in that lower SVC or atrioal junction. Also checking for any immediate complications of insertion like aumothorax collapsed lung. Starting TPN through a misplaced line, say if the

51:20 tip went up the jugular vein or too far into the heart, carries significant risks like thrombosis or arhythmias. >> Are there any special handling precautions for the TPN bag itself? >> Yes, TPN solutions containing vitamins are light sensitive. The vitamins degrade quickly when exposed to UV light. So, the bag must be covered with a special opaque light protective outer bag during infusion. >> What if the infusion gets disconnected? Because of the high risk of bacterial contamination, if the TPN line is disconnected from the patient for any reason, the bag and the remaining infusion set should be discarded. You cannot reconnect a bag once the sterile system has been broken. >> And tracking the volume infused. >> Crucial. TPN often runs at a constant rate over 12 24 hours and the total volume can be large 2 3 L or more. This

52:07 volume must be meticulously accounted for on the patients fluid balance chart to prevent inadvertent fluid overload, especially in patients who might also be getting other IV fluids or have heart or kidney problems. #tagad nutrition summary box25.4. >> Pimen is clearly life-saving in the right context, but summary box 25.4 makes it clear it also comes with significant potentially life-threatening risks. Let's break them down. First, complications related to just inserting the line. >> Yes, mechanical risks during insertion. Pumathorax a collapsed lung is the most common significant one occurring in maybe 0.51% of insertions especially with the subclavian approach usually needs a chest drain. >> What else? >> Misplacement of the catheter tip which is why that postinsertion X-ray is mandatory. Arterial puncture, bleeding,

52:54 nerve injury, air embolism. These are less common but serious potential risks of central line insertion. >> Okay. Once the line is in and being used, what are the main complications? Infections seem like a big one. Line sepsis is the Achilles heel of PN. It occurs in up to 15% of patients on long-term PN and carries high rates of morbidity and mortality. The catheter provides a direct route for bacteria or fungi into the bloodstream. >> How is it managed? >> Strict aseptic technique for all line handling is paramount for prevention. If sepsis is suspected, fever, chills, instability, you need paired blood cultures, one drawn through the line, one from peripheral vein. If they grow the same organism, especially with the line culture flags positive much faster, it strongly suggests the line is the source. The line usually has to be

53:39 removed immediately and appropriate antibiotics or antifungals started. Fungal infections are particularly nasty and can spread to eyes, uvitis or heart valves endocarditis. >> What about clots? Thrombosis >> also not uncommon. A clot can form around the catheter tip or within the vein itself. This can lead to pain, swelling, blockage of the vein like SVC occlusion or even pulmonary embolism if the clot breaks off. >> Treatment for thrombosis >> usually involves endcoagulation, blood thinners. Sometimes thrombolyis, clot busting drugs or endovvascular procedures are needed for acute severe occlusions. Regular flushing helps prevent blockage, but sometimes lines still clot off and need replacing. >> Okay, insertion risks, line risks. Now the third category metabolic complications and and top of that list

54:26 has to be refeeding syndrome. Again >> absolutely this is probably the most critical metabolic complication to understand and prevent whether starting EN or PN in a severely malnourished patient. >> Remind us again what happens >> when you suddenly provide a large nutrient load especially carbohydrate to someone who's been starved their metabolism rapidly shifts from breaking down stores catabolism back to building things up. insulin levels surge >> and this causes >> this drives key electrolytes phosphate, potassium, and magnesium rapidly out of the bloodstream and into the cells where they're needed as co-actors for all that new metabolic activity. The serum levels plummet. Fluid shifts also occur. >> How do we know who's at high risk? Summary box 25.5 gives criteria. >> Yes, NICE guidelines provide clear risk

55:12 criteria. A patient is considered high risk if they meet either one severe criterion or two moderate criteria. >> What are the severe criteria? >> Severe includes BMI less than 16 or unintentional weight loss greater than 15% in the last 36 months or little or no nutritional intake for more than 10 consecutive days or already having low levels of potassium, phosphate or magnesium before you even start feeding. Any one of those puts them in the high-risisk category. >> And the moderate criteria need two of these. Yes, moderate includes BMI less than 18.5 or unintentional weight loss greater than 10% in 3 to 6 months or little or no intake for more than 5 days or a history of alcohol abuse or being on certain drugs like insulin, chemotherapy, diuretics or antacids. Having any two of these also flags them

55:59 as high risk >> and the clinical consequences of refeeding syndrome if it's not prevented or managed >> they could be devastating and fatal. The electrolyte shifts cause cardiac arhythmias, profound muscle weakness including respiratory muscles leading to respiratory failure, heart failure due to fluid shifts, confusion, seizures, coma. >> So management is all about slow and steady, >> slow start, gradual increase, maximum 10 kilogram per day initially for high-risisk patients, sometimes even less like 5 kilo call day. Aim to reach their full nutritional requirements very slowly, maybe over four to seven days. and electrolyte monitoring. >> Intense monitoring. Check potassium, phosphate, magnesium levels daily, sometimes even twice daily in the first few days. Replace electrolytes aggressively, often needing large IV doses. And critically, give

56:45 supplementary thamine before starting the feed and continue it along with other B vitamins and trace elements. >> Beyond refeeding, what are the other major long-term metabolic issues with PN? Liver problems. Yes, liver dysfunction is common affecting perhaps 25% of long-term PN patients in some degree. It often starts as simple fatty liver steosis which might be benign but in some patients it can progress to more severe inflammation, fibrosis and even cerosis. >> What's that called? >> Severe progressive liver disease related

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