SCCM Resource Library-Everybody Has to Eat! Case-Based Approach to Nutrition in Special Populations

Everybody Has to Eat! Case-Based Approach to Nutrition in Special Populations

Video Transcription

Hello, thank you for joining us for the concurrent session titled Everybody Has to Eat, a Case-Based Approach to Nutrition in Special Populations.  This is a two-hour session with several speakers who will each have about 25 minutes. We will take your questions through the chat box throughout the session.  My name is Mary McCarthy, I'm a nurse scientist working for the Army at Joint Base Lewis-McChord in Tacoma, Washington, where I've been for the past 25 years.  My research focuses on vitamin D and nutrigenomics in military and veteran populations. I've had the distinct pleasure of working with our esteemed presenters through various  professional projects of the Society of Critical Care Medicine and the American Society for  Parenteral and Anternal Nutrition, most notably the Adult Critical Care Nutrition Guidelines in 2009 and 2016.  We are fortunate to have with us today five leading experts in the field of critical care  nutrition, not to mention their individual expertise in gastroenterology, surgery, dietetics, and research. Brief biographies are available in the session materials.  This is a session with much diversity in the topic of nutrition support in the critically ill population.  However, one common theme is the importance of meeting the ICU patient's nutrition needs as they are experiencing a life-threatening disease or condition that affects or alters  nutrient requirements or delivery. So we will be hearing from Dr. Steve McClave, who will be speaking about nutrition therapy in severe acute pancreatitis.  Stephanie Dobak will discuss the unique nutrition needs of the patient with traumatic brain injury.  Dr. Beth Taylor will help us understand the timing and determination of adequate nutrition for the trauma patient with an open abdomen.  Dr. Bob Martindale will enlighten us as to the approaches being used to deliver safe nutrition support to the patient with SARS-CoV-2 infection based on lessons learned in the  past year. And finally, Dr. Martin Rosenthal will address how chronic critical illness changes metabolism  and what impact this has on the nutrition status in the setting of persistent inflammation, immunosuppression, and catabolic syndrome.  Please enjoy the presentations and plan to put your questions in the chat box. Thank you. Hello.  In severe acute pancreatitis, possibly more than any other disease process, the status of gut barrier defenses and the microbiome have a huge impact on patient outcome.  In 20 minutes, I'm going to touch briefly on the principles of managing acute pancreatitis, and then we'll learn how the loss of gut barrier defenses and the emergence of a virulent  pathobiome impacts the course of disease. Then we can appreciate how nutritional therapy will modulate responses to pancreatitis and improve patient outcomes.  And these are my disclosures. Now, if you thought there was a difference between acute and chronic pancreatitis, they're really different ends of the same spectrum.  And this was brought into focus by the SAPE hypothesis, which was described by David Whitcomb in Pittsburgh.  In this setting, you have a trigger or an insult. Now that's not the sentinel event. The insult is the alcohol or the gallstone or the drug.  What happens next is the sentinel event, which is this vicious cycle of inflammation. And either you handle that inflammation, remove the stimulus and resolve the inflammation  and go back to a normal gland, or the process continues and you go down to lay scar tissue and become chronic pancreatitis.  The importance of this concept is that we thought early on that enteral feeding would make inflammation of the pancreas worse.  But now we know that we can utilize strategies with the gut, including enteral feeding, probiotics and other strategies to actually hasten the resolution of that inflammation.  Now when a patient comes into the ER, it's hard to determine disease severity. There are three things we look at.  We look at organ failure, circulatory shock, pulmonary or renal insufficiency. We look at local complications, which would be a pseudocyst, abscess, or necrosis.  And then we look at unfavorable prognostic science, which are really measures of the SERS response.  So an Apache 2 score of 8 or more, C-reactive protein of 150 or more, or 3 or more ransom criteria.  80% of patients are going to have mild pancreatitis, which means no organ failure and none of these local complications.  15% are going to have moderate pancreatitis, in which you might have organ failure, but it's transient and resolves within 48 hours, plus or minus local complications.  Only 5% are going to have persistent organ failure lasting more than 48 hours. And those are the patients with truly severe pancreatitis.  Now once you've figured out how sick they are, it can be equally difficult determining what they do next, whether they get better right away or get worse.  We had a 16-year-old girl with gallstone pancreatitis, and the CT and the ER showed 75% necrosis of her gland.  She did great, didn't turn a hair, and was demanding food within four days and did great. In contrast, we had a 41-year-old athletic runner with post-ERCP pancreatitis, and in  the ER, the CT scan was normal. And within 36 hours of that CT scan, he was on the ventilator with respiratory failure and stayed there for two and a half weeks.  Now for years, our hands were tied by the concept of pancreatic rest and these different levels of pancreatic stimulation.  And we knew that pancreatitis was a combination of two defects, this inappropriate activation of the pancreatic enzymes, and then a secretory defect.  The enzymes were activated, but couldn't get out of the gland, which means they would eat the gland.  For years, people were saying, like Gene DiMagno at the Mayo Clinic said that any food  anywhere in the GI tract, even in the rectum, would cause stimulation of these enzyme formations.  Steve O'Keefe said, as long as you got 40 centimeters below the ligament trites, you were safe to put food in the GI tract.  And then in our first randomized controlled trial, venerable versus venerable feeding in pancreatitis, we said it has to be past the stomach in post-biologic.  It turns out all three of these comments were overstating the fact that the majority of patients with mild to moderate pancreatitis may even tolerate solid food, that the vast  majority of patients, even with severe pancreatitis, will tolerate gastric feeding. That led to greater and greater use of enteral feeding.  And when you compare it to parenteral nutrition, we see that outcome is better. These are the forest plots that we generated for our 2016 Aspen guidelines.  And you can see that compared to parenteral nutrition, enteral tube feeding is going to reduce infection from 42% down to 16% and mortality from 16% down to 6%.  Since those guidelines were published, there have been two more meta-analyses in 2018 that showed the same thing, if not more.  In the Wu meta-analysis, enteral feeding reduced both mortality and organ failure. And in the Yao meta-analysis, the same year, done only in severe pancreatitis, enteral  feeding compared to PN reduced mortality, length of stay, and risk of complications. In fact, the American College of Gastroenterology, when they came out with their guidelines,  for the first time they said in severe pancreatitis, enteral nutrition is recommended to prevent infectious complications. That's amazing. That says this is therapy.  That means the gut affords us an opportunity to alter the course in severe pancreatitis. And that's because it's the largest immune organ and has the greatest microbial burden.  So if we're able to utilize the gut, we can promote a pattern of recovery. And in this sense, the gut becomes a modulator of the response to pancreatitis.  If we fail to do that, then the opposite pattern occurs of increasing SERS response, inflammation,  and in this case, the gut can actually serve as an accelerator of the process of acute pancreatitis.  Now in health, there's this constant crosstalk signaling between the bacteria in the gut and receptors, toll-like and nod-like receptors on the gut epithelium.  It's actually the pieces of the commensal bacteria that bind to these receptors. And when they do that, tight junction proteins are increased, mucus production is increased,  defensins, which are released into the lumen, which are proteins that bind the pathogens, their release is increased.  And when these MAMPs or microbial associated molecular pattern, these pieces of the commensal  organism bind to the dendritic cell, it influences T cell differentiation in an anti-inflammatory effect. In severe pancreatitis, all this changes.  There's a functional and physical defects which form in the barrier and the tight junctions are breached.  This means the microbes can now penetrate through the wall and bind to epithelial receptors and change immune responses.  There's thinning of the mucous layer and this toxic gut-derived lymph is formed. And then you have this induction of virulence factors because now, instead of commensal  bacteria that are binding these receptors, you have PAMPs, the pathogen-associated molecular  patterns, the virulent pathogens themselves, and DAMPs or danger-associated molecular patterns, which are pieces of necrotic S-center cells.  Now, this immune dysregulation is what causes gut sepsis. In health, the piece of the commensal organisms cause the production of anti-inflammatory, T-regulatory, and TH2 cells.  These would leave the gut, go to the circulation, and have an anti-inflammatory effect, which would modulate responses to pancreatitis.  However, if the process gets away from us, then we switch from MAMPs to the PAMPs and DAMPs, the pathogens, and these pieces of S-center cells.  And now, binding to the dendritic cells causes naive lymphocytes to form pro-inflammatory TH1 and TH17 cells.  These will emerge from the gut, go to the systemic circulation, and cause a pattern that looks like sepsis. There's no pus pocket anywhere.  This is being generated from the gut by this process. Now what's the evidence in patients that all this is occurring?  Well, in patients, they've shown that the damage to the S-center cells releases their contents and they act as these dangerous associated molecular patterns to bind to the receptors  of the epithelium. And they've listed all the parts and pieces of these S-center cells as they're destroyed that cause this.  And the level of the DAMPs correlates to disease susceptibility. There's also a shift in this number of inflammatory cells that emerge from the gut.  And in patients with pancreatitis, not lab rats, they've shown a marked increase in TH1 and TH17 lymphocytes, which are pro-inflammatory.  And simultaneously, the production of the defensins by one of those epithelial cells, the PATH cells, is reduced.  Now there's this progression from a commensal microbiome to a virulent pathobiome. And the pathogens are already there.  What happens is they get rid of the commensals and they change their appearance and their behavior.  And the impact of forming a virulent pathobiome is increasing septic morbidity, is toxic lymph, organ failure, and antibiotic resistance.  What's our evidence in patients with pancreatitis that this occurs? Well, in patients, they've documented that there's an increase in the pathogen Enterobacteraceae  and a decrease in the commensal organism Lactobacillus, and a shift or an increase in the Firmicutes to Bacteroides ratio, which promotes inflammation.  And the degree of these modifications correlates with disease severity and complications in patients with pancreatitis, because these pathogens act as the PAMPs and now will bind  to the receptors. Now in this sense, the gut becomes an accelerator. Bacterial translocation is not the issue.  It's not like the bacteria will translocate across the wall of the epithelium and somehow make it to the blood. It can make it to the blood.  Ollie Lemquist documented bacteria in the gut making it all the way to the blood in acute pancreatitis.  But by the time it gets there, the inoculum is so low and it's not important and really it just is a marker, a surrogate marker that you've had increased permeability.  Now Alberti says you're going to have more trouble with these pathogens in the lumen of the gut than you are in the blood.  And if you take a dose of Pseudomonas, Staph, or E. coli, it's going to cause threefold greater sepsis in the lumen of the terminal ileum than it is if you give the same dose  intravenously. On the other side of the coin, giving commensal organisms in patients with pancreatitis has the opposite effect.  And if you can restore the commensal to pathogen ratio through probiotics, then systemic infection is better or reduced.  Now for years we knew in lab animals that had laboratory-induced pancreatitis, if we ligated the thoracic duct, we could protect against respiratory failure.  And so we knew there was something toxic in the lymph. We used to think it was bacteria or endotoxin or cytokines, but that's not the case. It turns out it's pancreatic enzymes.  And what's happening here is that with the decreased barrier function, thinning of the mucus, the pancreatic enzymes can get into the epithelial cells.  There they destroy the epithelium called autodigestion, the same process it was doing to the pancreas.  Then that allows the enzymes to get past the epithelium into the lymphatic channel. And there are two enzymes we're talking about, pancreatic protease and pancreatic lipoprotein  lipase. Furthermore, the lipase will act on fat being transported in the lymphatics and produce free fatty acids. So the toxicity is those two enzymes and the free fatty acids.  And sure enough, they'll travel through the thoracic duct, left subclavian vein, right to the capillary system of the lungs and cause respiratory failure.  What's our evidence of this link of increased permeability and organ failure? This was shown in a landmark study by Amori, in which every day patients admitted with  pancreatitis, he would measure permeability using these lactose mannitol ratios.  These are large sugars that should go in one end of the GI tract and come out the other end unless there's increased permeability, in which case they'll show up in the urine.  He was able to link increases in permeability to both primary organ failure, which means  they had it on admission, and secondary failure, which means they developed it over the first week. And the degree of permeability was linked to disease severity.  Alverde has shown if you just take patients with a SIRS response compared to controls without SIRS, there's a reduction in their feces of the protective organisms, there's  an increase in virulent organisms, and the protective butyrate short-chain fatty acids are reduced.  And when you look at how we manage pancreatitis, everything we do compromises barrier defenses and endangers that microbiome.  So vasopressors to maintain blood pressure are going to cause spinach circulation, ischemia, and cause damage to the barrier defense. Antibiotics are going to decrease motility.  Antibiotics are going to knock down the commensal bacteria and let the virulent organisms grow.  And TPN is going to cause a nutrient deficiency in the cecum where the commensal bacteria are located, and that's going to hurt the commensals.  The timing, level of infusion, and choice of formula are all important. Two trials emphasize the importance of early enteral nutrition.  In a randomized control trial by Sun, early enteral nutrition within 24 hours was compared to delayed feeding after day eight.  And sure enough, the early enteral feeding reduced pancreatic infection and organ failure. ICU length of stay was three days shorter, and the percentage of patients with SIRS was  nearly cut in half. Olaf Bakker with the Dutch Pancreatitis Study Group did a meta-analysis in which he took  just the enteral feeding arm of eight randomized control trials comparing enteral versus parenteral.  And he looked at whether the enteral feeding was delivered within the first 24 hours or after the first 24 hours.  And sure enough, if they got the enteral feeding in early in the first 24 hours and compared to TPN, they saw a reduction in organ failure.  And a composite endpoint of organ failure plus mortality plus infective necrosis was reduced significantly as well. Does it have to be in the small bowel?  We thought that in our randomized control trial in Louisville, but that's not the case. In three randomized control trials in this meta-analysis, the degree of pain, diarrhea,  and the amount of calories or energy you get into the patient are no different gastric versus jejunal.  And the significance of this means that you can just drop a Dobhoff tube in the ER, and as you volume resuscitate the patient, you can start feeding into the stomach.  You can expect that you'll need to put the tube into the small bowel or the jejunum in only about a 15% of patients.  And the formula that we're talking about is probably just a standard polymeric fiber formula. We don't, the devenous doesn't support an immune formula, and usually we don't need  a small peptide formula. Tolerance is interesting. If you feed into the GI tract, three things can happen. You'll get enzyme stimulation probably in 100% of the patients.  20% will show an increase in clinical symptoms of pain or nausea, vomiting, and about 5% will show an increase in the SIRS response.  So if you look at this graph at the top, when we started enteral tubing in a patient with pancreatitis, the amylase levels started to go up as we were stimulating production of  the enzyme. The white count indicating the SIRS response peaked at 21,000, but actually started to come down as the amylase was going up and symptoms of pain were resolving.  The patient was becoming hungry. So we were watching all three aspects of this. But tolerance is twofold in pancreatitis.  Not only do you have to worry about the stimulation of enzymes in the pancreas, we have to worry about the usual stuff of GI dysfunction and ileus like we would in any ICU patient.  When it comes to advancing to oral diet, you have to go to clear lipids first. The answer is no.  In this meta-analysis of three randomized controlled trial, if you go straight to solid diet first, you get out of the hospital at least a day sooner than if you go to clear  liquids first and then solids. Do you have to have strict criteria or can you just ask the patient what they want to do? Go with patient wishes.  You'll get out of the hospital sooner. Should we use probiotics? Probably the scariest trial was a Dutch Proprietra study in pancreatitis in which very aggressive  use of probiotics caused worse organ failure, greater need for surgery. There was bowel ischemia in the group that got aggressive probiotics and the mortality  was two and a half times greater. But they were giving six organisms twice a day directly into the small bowel.  At least seven or eight other studies in pancreatitis showed that probiotics were beneficial.  This is a meta-analysis by Zhang in which infection was significantly less with probiotics than controls.  In a randomized control trial published after the Proprietra study, enteral feeding plus  probiotics had the lowest incidence of sepsis, organ failure, and mortality compared to enteral feeding alone or TPN.  We would use perineural nutrition if enteral feeding is not tolerated, if you're unable to get to target, or if there's a contraindication to tube feeding.  And you would expect to need perineural nutrition in about 20% of patients. Guidelines from two pancreatitis societies said that a delay of up to five days in initiating  PN may be appropriate to allow time to try oral or enteral feeding. With the Aspen guidelines, we said we would use PN when EN is not feasible after five  days from the onset of symptoms because control of hyperglycemia is worse, there may not be much of a benefit, and it may cause more problems than it may help.  Probably the most misunderstood trial in pancreatitis is the Python randomized trial by the Dutch  pancreatitis group in which patients coming into the hospital with pancreatitis were randomized to tube feeding within 24 hours versus on-demand oral diet.  On-demand oral diet meant they walked in every day and said, are you hungry? Can you eat? Can you eat? Can you eat today?  If they said no, they couldn't on day four, then day five, they finally got it tube feeding.  They showed that they were equally sick, APACHE two score were identical, about two-thirds  of the patient in each group had surge response, and the endpoint of mortality was no different  between the two groups, and a major composite endpoint, which was mortality plus infectious morbidity was no different between the two groups.  This caused most people to stand back and say, look, we don't need tube feeding, we just need to try oral diet for four or five days, and if that doesn't work, then consider  tube feeding. But look at this, the details are here, less than 20% of these patients were in the ICU,  over 80% were out on the ward, they were doing great, they did fine with feeding. Only 15% had persistent organ failure or true severe pancreatitis.  So it's really the degree of the surge response and the need to be in the ICU that's going to dictate whether or not you do tube feeding.  So in the ER, you're going to look at the surge response, the prognostic scoring, necrosis  on CT, and if they're admitted to the ICU, you're going to drop a Dobhoff and start nasogastric tubes, and you might or might not need nasodegeneral or even parenteral nutrition.  If they're out on the wards, you can go straight to an oral diet. So in conclusion, the physiologic responses in the gut can tremendously influence the  course in severe pancreatitis, and nutrition measures should maintain gut defenses and the microbiome to be effective.  In severe pancreatitis, you're going to initiate anal feeding within 24 to 36 hours of admission  to the ICU, you'll use a polymeric mixed fiber formula feeding into the stomach, you'll only need the jejunum about 15% of the time, do continuous infusion, consider probiotics,  consider tolerance, the surge response symptoms, but not residual volumes, and advance straight to a solid diet as the surge abates.  You would consider PN after five to seven days if the anal feeding is not doing the job. Thank you very much for your attention.  I'm going to be talking about nutrition in the neuro ICU. I have no disclosures. Our objectives are for you to understand the risk and impact of malnutrition in the neuro  ICU patient, to summarize the nutrient requirements during targeted temperature management to  hypothermia, also known as therapeutic hypothermia, to define the interdisciplinary roles involved  in feeding ICU patients, and to apply all this knowledge to a complicated case study. So we know there's a significant risk for malnutrition in brain injured patients.  A lot of them come in with comorbidities causing poor intake or weight loss prior to admission.  So previous neurological injury, we're also dealing with COVID right now. They also might have impaired movement, so difficulty self-feeding, making them reliant  on others at mealtimes. They might have altered hunger and thirst sensations, so have this lack of initiation to start a meal, which requires a lot of queuing at meals.  We know dysphagia is a huge negative impact on PO intake, and then on top of that, we put patients on these less palatable dysphagia diets with thickened liquids, which further  decreases their desire to eat. And then lastly, we have catabolism and proteolysis that's associated with critical illness.  Furthermore, we know that brain injured patients are more likely to not tolerate their two feeds.  So this was a retrospective study done by Dickerson et al, in which they compared gastrically fed trauma patients with and without TBI and their response to prokinetics.  So you'll see here, this plot on the left depicts the effectiveness over time of metaclopramide therapy for trauma patients with and without TBI.  In looking at the first 24 hours of metaclopramide therapy, there was no significant difference in efficacy between the groups.  However, metaclopramide's efficacy progressively declined daily to a nadir of 46% for trauma patients with TBI over the seven-day observational period,  whereas trauma patients without TBI had a more modest decline in efficacy, which appeared to plateau around the three-day mark.  This graph on the right is showing the relationship between response to metocropamide and ICP levels, and you'll note that patients who responded to initial metocropamide therapy  had a significantly lower ICP than those who had failed to respond. So in summary, the authors noted that higher ICP is associated with higher likelihood of two-feed intolerance  and decreased likelihood of responding to monotherapy prokinetics. So your TBI patients with gastric two-feed intolerance will likely require combination therapy  with both metocropamide and erythromycin, so keep that in mind when feeding patients.  But then we also have this iatrogenic risk for malnutrition. So we're not addressing nutrition early enough. The SEC and ASPEN guidelines recommend to start two-feed  within 24 to 48 hours of admission. We know that early internal nutrition is associated with better outcomes, so decreased mortality and infectious complications.  We're also not feeding what we're prescribing, so the international average is that we only give patients 50 to 60% of the two-feed that's actually ordered.  And a lot of that has to do with these frequent internal nutrition interruptions. So NPO for procedures and surgeries, which later get canceled and bumped the next day,  creating this NPO vicious cycle. And we know we can kind of mitigate that with a volume-based feeding approach, so giving them a goal two-feed volume for the day  and increasing the rate throughout the day to compensate for those NPO times. I know at Jefferson, we limited the NPO times for patients with airway protection.  So instead of making them NPO at midnight for procedures, we instead made them NPO on the way to the OR.  We may also be delaying swallowing evaluations. So there's this lack of consensus on when to conduct a swallow evaluation post-extubation.  And Leader et al., the study that I put below, they studied the swallowing function of 202 adult patients from five different ICUs. And they noted that 82% of patients  passed the Yale swallow protocol at one hour post-extubation. And by 24 hours post-extubation, nearly 92% had passed. So you know your patients, you can assess them.  And obviously, if mental status or respiratory function is tenuous, you should delay the swallow evaluation. But in most cases, there's no benefit  to delaying swallow evaluations post-extubation.  And lastly, this one-size-fits-all and set-and-forget approaches. We know that calorie needs vary between patients and even within patients over their hospital course  based off this ebb and flow phase. So we need to individualize our nutrition plans and reevaluate them routinely.  Because we know that malnutrition has a great impact on clinical outcomes. So you'll see that's associated with increased mortality risk, length of stay,  days on the vent, infection risk, impaired wound healing. And we are starting to see that the impact of nutrition, it seems to be most significant  with patients deemed at high nutrition risk and those with predicted longer length of stays. So for your previously well-nourished, healthy patient that comes from the ICU,  who might just be on the vent for a couple of days and then out the ICU door, the nutrition might not impact them as much. But those at greater risk,  you will see these outcomes associated with their nutrition.  And I will say that nutrition products, so internal nutrition, oral supplements are relatively cheap. We're talking typically $5 to $10 a day.  I'll sadly be the first to say that dieticians are cheap. So if you're able to give your patient proper nutrition, you're going to have a huge return on investment  and recoup all that money if you're able to get them off the vent a day early out of the ICU. So really keep that in mind. I included this little part about the first week.  So full feeds versus hypochloric. It's a little bit of a debate on how much we feed our patients in the first week. With patients with acute lung injury and ARDS,  it's shown that it might be more beneficial to do hypochloric feeds. And so this study by Masubian just recently came out in J-PEN and they conducted a randomized control trial  comparing hypochloric versus full energy and neural feeds in neurosurgical patients during the first week in their ICU. And they noted that hypochloric and all feeding  was associated with lower GI intolerance, as well as reduced duration on the ventilator and length of stay. Furthermore, if you feed your patients at goal rate,  just coming out of the gate, or you really ramp it up quickly, you might have those patients that might have refeeding syndrome, you might have hyperglycemia,  which we know is associated with worse outcomes.  But while starting at full or trophic rates remains a debate, we do know that there's a huge importance on starting internal nutrition early. So there are non-nutritional benefits  associated with early internal nutrition, such as supporting the immune and metabolic responses, as well as preserving gut integrity. So it's not just about calories and vitamins.  There's something just going on that could be said for starting trophic two feeds that could really positively impact your patient.  Now I'm going to switch gears a little bit here and talk about targeted temperature management to hypothermia. So we know that TTM is the control of body temperature  to improve neurological function and survival after ischemic event. And you can do TTM to normothermia or mild or moderate hypothermia, but it's used typically for neuroprotection  after cardiac arrest and hypoxic ischemic encephalopathy and neonates and the control of cerebral edema and intracranial hypertension after brain injury.  Most protocols found online specify to hold internal nutrition until the rewarming phase or until the patient is completely rewarmed.  And that might be okay if you're only cooling for 24 hours, but what if you're cooling for longer? So that made me delve into the literature  and see what it says about feeding patients that are cooled. So in all nutrition during TTM to moderate hypothermia after cardiac arrest,  the studies have shown that early internal nutrition appears safe. It's actually shows that there's sufficient GI function to absorb the nutrition  and might be associated with better neurological outcomes. After hypoxic ischemic encephalopathy, early EN is safe, not associated with increased morbidity,  but instead associated with reduced length of stay and time to full feeds. In our study after intracranial hemorrhage, we noted that early EN is safe,  not associated with increased ventilator-associated pneumonia or mortality. Now we know that peristalsis is often decreased and at least is common when the core temperature  is less than 34. So you might need some prokinetic medications to help with two-feed intolerance and further studies need to look at the role  of post-pyloric tubes or different two-feed formulas.  Calorie needs while cooling. Indirect calorimetry is always gonna be the gold standard, but it's challenging in this population. You might have shivering, spasticity,  your FiO2 or P levels might be too high to get a good study, but overall resting energy expenditure appears to be reduced by 25 to 30%.  We know predictive equations are less accurate. So Harris-Benedict equation exceeds REE by 16 to 25%.  We found the pit state to be more reliable. That's likely because this equation incorporates temperature, but if you're just gonna do a quick and dirty  calories per kg, you're probably looking at 15 to 20, although that's not studied.  Protein needs not well-studied while cooling. So there was a study after median cerebral artery infarct in which they looked at a 24 urinary nitrogen  and they noticed that it was decreased during hypothermia and then almost tripled after the patients were rewarmed. In our study, we saw no difference between 24-hour UUN  between those patients that were cooled and those at normal thermia. So for determining protein needs, if you have 24-hour UUN available, that's probably your best bet.  But if not, we recommend starting at 1.2 to 2 grams per kg per day per the Aspen SCCM guidelines.  So I'm gonna move on to our case study. So this was a 27-year-old female admitted to SAS post-motor vehicle collision. She comes with a TBI, right temporal bone fracture,  pneumothorax, L1 burst fracture, T7 compression fracture, and through a degree, electrical burns to her feet. This was a rollover vehicle.  She ran into a telephone pole, wires were on the ground.  It was raining, so it was an extremely unfortunate event for this young female.  She was intubated on the scene and transferred to us for further management. You'll see that she's sedated on fentanyl, midazolam, propofol. We started her on 3% sodium chloride  for a serum sodium goal of 150 to 155.  She's also MPO with an OG tube. You'll see her lactate's a little bit elevated on emission.  The dietician was able to assess her within a few hours of admission and noticed that she's a little bit more petite, five foot 97 pounds, a BMI of 19.  On physical exam, she appears well nourished, albeit thin. She has OG tube and her mother reported that she had good intake prior to admission.  We did estimate her needs on the higher end given her young age and her traumatic injuries. And we recommended to start with a high calorie semi-elemental 2-feed.  Ours happens to be immune modulating as well, which has shown to have some benefit in the TBI patient. We're just going to start at 10  and increase the goal of 40 over the next 24 hours and add a multivitamin because her 2-feed at goal didn't meet her complete vitamin needs.  On day one, she has some evolution of left frontal cerebral edema, no other acute changes. She's still on the vent, but awakens and follows commands.  But then she has an emesis overnight. So the 2-feeds are held. The OG tube is placed to low continuous suction. We started some Zofran and her bowel regimen  is increased to get things moving.  On days two to three, her 2-feed is resumed and advanced to goal by day three. Her lactate is now within normal limits, but then at the end of day three,  she stops following commands and becomes agitated. A repeat head CT showed no midlife shift. A right frontal ICP monitor was inserted and she was started on a rockeronium drip  and or epinephrine.  So while I was helping manage these hypothermia patients from the nutrition aspect, I noticed some discrepancies on how our different neurointensivists address nutrition.  So we did a literature review and decided on a united way to approach these cases and created this algorithm. So you'll see at the top,  this algorithm is for patients receiving hypothermia or paralytics. We want to determine calorie needs with a metabolic cart or indirect calorie tree.  The same thing, if we can. Then we're going to initiate trophic 2-feeds. If the patient is malnourished on admission, we're going to go ahead  and slap on some supplemental TPN as well, knowing that 2-feed tolerance might be an issue.  Then we're going to monitor her 2-feed tolerance. We're going to inquire daily about bowel movements. We have some recommendations if they're constipated.  We're going to do routine physical abdominal exams and we're going to check gastric residual volumes. So I know gastric residual volumes are a controversial topic,  but you'll see that we never recommend stopping for elevated gastric residual volumes alone. Instead, we have recommendations to start some gastro-motility agents  and maybe change the 2-feed.  So if everything is going smoothly, we recommend advance the 2-feed. For patients on paralytics, you'll notice that we increase it a little bit more quicker  just because the paralytics are obviously supposed to be paralyzing the skeletal muscle and not the smooth muscle of the GI tract. And then we have recommendations  that if they're not at their goal by seven days, then we're going to initiate supplemental TPN per the current CCM-ASPEN guidelines. So back to our case,  neurologically, she is not doing well. So in addition to sedating and paralyzing her, we add on TTM for a goal of 33 degrees Celsius. Her 2-feed was previously at goal by day four.  She was NPO for burn surgery for her feet, but that was postponed due to her being so instable.  TPN is recommended by the dietician just because she sees this picture and she does not think her 2-feed is stable. She does not think her patient's  going to be tolerating the 2-feed that well. And then she starts having this diarrhea. So the bowel regimen is decreased, rectal tube is placed,  but she is putting out 500 milliliters Q12 hours, so a significant amount. You'll see her FOS and MAG and potassium on the lower end  because they move intracellularly during hypothermia.  So we also created an algorithm for these patients receiving dual therapy. And first, we're going to start with that indirect calorimetry if we can,  but then we recommend to start TPN. And that was unanimous amongst our neurointensivists, but it was more of a debate as to whether or not to continue trophic 2-feed.  But then once they're weaned off one of those therapies, we recommend starting 2-feed and then advancing for the previous protocol.  On days five to six, her ICP is 17 to 23. Her 2-feed is held due to dual therapies, but then we have a change in neurointensivists and that one wanted to start the 2-feed back at 10  just to maintain any gut integrity. She has a rectal tube for diarrhea, her abdomen is soft, hypoactive bowel sounds. She's too unstable for indirect calorimetry.  And so we start TPN. She's on propofol, so we don't include any lipids in the TPN and we start at a lower dextrose and calorie goal. On day seven to 10, she's being rewarmed,  but when she hits 35 degrees, her ICP increased, so she's recooled down to 33 degrees. During a skin check, the patient vomits. And so the 2-feed's held.  She gets an abdominal X-ray that shows no obstruction. We start some metoclopramide in the 2-feed and then resume that 10. You see that we're increasing her TPN calories.  We added some soy-based supplements and we added some soy-based lipids just because propofol's weaning and we're hoping to get her to goal calories.  On days 10 to 14, she has amputations of her left toes. Her ICP is sustained at times around 40. She has a new pneumonia and transaminitis. We're holding the 2-feeds at this point.  We still think she's too unstable.  Increase the calorie goals. And then with the transaminitis, we change from the soy-based oil to the 4-oil in hopes that it will help with the transaminitis.  We also get indirect country. You'll see that this was not a great study state. Study state is not probably a great study. On the resting energy expenditure average  came out to 1,100 calories.  And so over the next days, we decrease the TPN to reflect that change. She also has an ICP monitor replaced. She remains hypothermic, still being slowly rewarmed.  She develops a pulmonary edema and hypervolumemia. So you'll note that we didn't go down to the full 1,100 calories. We thought it was a little bit low  and that the study state wasn't that great. We also recognize that it was while she was cooled, so their calorie needs would be decreased and now we're warming her.  So we went a little bit higher with 1,270 calories and we also concentrated the amino acids so we could reduce the volume in the TPN.  So we don't know if the transaminitis was from soybean oil or overfeeding combination of those two or something else, but either way, we changed the four oil  and lowered the calories.  The next couple of days, her ICP is better controlled. We start rewarming her. She remains paralyzed, sedated, and on TPN. She has a trichin peg placed.  The dietitian did recommend a J-tube given her history of two-feed intolerance, but they decided on a peg and they resumed trophic two-feeds.  On day 22, she's too unstable for waking trials. She has this high bladder pressure and so trauma didn't think the two-feed was causing that,  but nonetheless, they wanted to do a trial of holding the two-feeds, so the peg was placed to gravity.  Over the next couple of days, she has worsening ICP.  So they placed the left EVD and that allows the ICP to come under control. We had resumed the trophic two-feed and you'll see that our LFTs are improving.  And then days 26 through 27, she's weaned off rocoronium. She's still sedated. The two-feed has slowly increased the goal. She's having less diarrhea,  so only 200 milligrams per Q12 hours now. And so we discontinued the TPN.  And then her final two weeks, she's weaned off sedation. Her neuro exam is improving. We changed to a fiber-containing two-feed just because she's more stable at this time.  We're hoping the fiber will help with the diarrhea. By day 34, she is wide awake, following commands, interactive. On day 35, she goes the OR for the L1 burst fracture  and skin graft for the burns. Her rectal tube is removed. Then her trach is downsized. So we have speech pathology come in for a phase  in which she's advanced to a regular diet with thin liquids. And then prior to discharge, she's eating 50 to 75% of her meals. And we add a high calorie oral nutrition supplement  just to give her an extra boost of nutrition.  So in summary, neuro ICU patients have more difficulty tolerating two-feeds than general ICU patients. So you're probably gonna, you might benefit from adding prokinetics,  maybe a post-pyloric tube, and then not shying away from prenatal nutrition. It's not as evil as we once thought.  Hypothermia itself is not a contraindication to internal nutrition. However, in combination with other therapies, it may necessitate prenatal nutrition.  An individualized nutrition plan and close monitoring is essential in feeding these patients. In managing nutrition, the ICU requires an interdisciplinary effort.  So physicians, nurses, pharmacists that they're managing the TPN, dieticians, of course, speech pathologists to advance the diet,  respiratory therapists to conduct indirect calorimetry. So all these go into making great efforts to feed our patients.  And that's all I have. Thank you so much for joining me and feel free to write me any questions. Take care.  I'm very happy to be here today to present. As the moderator mentioned, I'm going to be talking today about feeding patients with an open abdomen.  These are my disclosures, none of which will impact my talk today.  And these are the objectives that I hope to address. And that is when, where, and what to feed our patients that have an open abdomen.  When you think of an open abdomen and you want to categorize that, you can do that in two different ways. One by the type of patient, whether it's a damage control laparotomy,  usually a trauma emergency patients, or is it open because of an abdominal compartment syndrome, but also by time to closure. And we know that those that are chronically open,  greater than seven days, nutrition becomes even more of a priority because of the needs that I'm going to discuss throughout this talk.  But I also think even those open less than seven days, perhaps nutrition should be part of that priority as well as the facial closure.  Most of us are using this negative pressure wound therapy as far as controlling the drain output from the open abdomen. Some of you may still be using a temporary closure  such as the Bogota bag. All of us use the Bogota bag at one point, right? Because that was the first thing we saw, right? When we first started using open abdomens.  Now, let me introduce you to our case. We have a 28 year old male who was in good health in a motor vehicle collision. He had a lot of injuries, fractures, chest contusion,  came in with abdominal distention. They did the FAST exam, took him to the OR, found that he had a liver laceration, had three areas of small bowel injury that required repair  and had a primary closure. And then they left him open.  He had a huge blood loss, great big fluid resuscitation, a lot of products. So they figured there's going to be some valedema for a while. He ends up on multiple pressers  and is on his way to the SICU.  I think anytime you're feeding trauma patients, you need to keep in mind they are at high risk for oxidative stress. So I need to keep in mind as the dietician,  are they going to have issues with ischemia, reperfusion injury? They're probably going to have some hemorrhagic shock. They're probably going to be on presser agents.  So I need to think about the integrity of the bowel. So I keep that in mind as I'm making my decision. But also I know these patients have increased metabolic demands.  They have a lot of tissue injury that they need to repair and drain sometimes all over the place that they have a lot of losses.  Now let's look at our case. By day two, he's intubated, but already his pressers are starting to trend down as well as his lactate level.  I say never underestimate the power of youth. They seem to turn around quickly. However, his OG tube output still putting out a lot, a liter and a half.  And his abdomen is drained over three liters that over the past 24 hours. And we talked about on rounds, what should we do about nutrition?  So when you're starting to think about nutrition, now our case is at 48 hours. You want to think about where and when should I feed? I'm going to show you some of the literature  about feeding open abdomens, but I'm not going to show you any prospective randomized control trials because they just don't exist.  So we're going to talk about retrospective reviews. This is an older one from 2007. And when you're looking at anything that's looking at early versus late internal nutrition,  you have to think about how they're defining early internal nutrition. In this study, they defined it as less than or equal to four days.  For many of us that we would think that's almost late. So it's almost like these two groups may be similar. In this study, when they did the comparison,  they saw no difference in any of the infectious complications but they did see a time to earlier fascial closure and less fistula formation and those patients that were fed earlier.  Now this analysis was actually a secondary analysis of a large multicenter trial that was looking at blunt trauma. What they did is they looked at patients that were fed  versus not fed that had an open abdomen and had no bowel injuries. So they limited it to bowel injuries. So in this a hundred patients,  they looked at those patients that got internal nutrition compared to those that did not receive any nutrition. The only significant finding they saw was those that were fed early  had less odds of developing ventilator associated pneumonia as based on a 2008 definition. And there was a trend toward earlier facial closure in those that got fed early.  The Western Trauma Association did their own retrospective review in 2012, where they looked at 590 patients, so almost 600 patients that received internal nutrition  prior to the abdomen being closed. And they actually divided it further into two groups, those with a bowel injury versus those without a bowel injury  and they compare them to those that had an open abdomen that were not fed. Now those with a bowel injury, they found no significant associations  between internal nutrition and outcomes. And those without a bowel injury, they did find some significant associations between early internal nutrition and earlier closure rates,  decreased complications, decreased mortality. Right now West recommends that internal nutrition should be started once resuscitation is complete. If we go to the East group,  they didn't do a similar study, but last year they did do a survey of their members of treating open abdomens. Primarily, they were looking at sedation and paralytics, but  they also asked some questions about nutrition. And what you see here, there was really no consensus. A third of them never fed or only gave trophic feeds. A  third of them fed, but because less than half of the patients got the full feedings, we assumed that they weren't really aggressive in feeding. And only a  third of them fed trying to progress to full feedings. Now, what also was interesting is they divided it by older and younger physicians. The older  surgeons, those practicing 15 to 20 years or greater, tended to wait until return of bowel function, whereas the younger surgeons tended to feed as soon  as they had bowel continuity, which is the newer concept in feeding. Now, the other thing we have to keep in mind for our particular patient is he did have  those three new anastomosis. So what does the data tell us about feeding across a new anastomosis? There's only two meta-analyses that help answer this  question. This was the first one in 2009. And basically, what we want to see is that there's no difference in a breakdown of an anastomosis whether a  patient is fed early, internally, or late. And that's what this one shows. There's really no difference between early and delayed internal feeding and  whether a patient will develop a leak or their mortality. The second meta-analysis that came out in 2011 actually included a wider variety of surgery patients that  had had anastomosis because they wanted to look at early feeding as in 24 hours. They also divided it into studies done before and after 2000 because feeding  practices have changed. But bottom line, again, there's no difference between early and late internal nutrition, suggesting it's safe as far as  developing an asthmatic leak. You're not at any higher risk if you feed early. So so far for our patient, using internal nutrition is looking good. We haven't  compared it to parental nutrition, which we will do, and we'll address some of these other questions here. So this is the only meta-analysis that's out there  in open abdomen patients where you're comparing EN to PN. And look, it's five retrospective studies, so these are not prospective trials. Again, there was not  too much difference, but there was a trend toward favoring internal nutrition and mortality and whether or not they developed a fistula. But on the other  hand, there was a trend toward favoring parental nutrition for pneumonia, length of stay, and time to closure. So I'm not sure how to interpret this, but I think  one thing we need to consider is adequacy of feeding. What this small study shows in just these 30 patients is can we get these patients fed with  internal nutrition alone. Guidelines tell us that we need to reach about 80% of the caloric requirements for our patients in the intensive care unit by  the end of the first week. So if you look at this figure, you will see that by day seven and those patients that were fed internal nutrition alone, they were not  even to 40% of these estimated needs. In fact, by day 21, they weren't even yet to 60%. By adding parental nutrition, they were able to get to 80% of the goal by  day 10, and not to 100% until they were a little over two weeks out. And these people, this group also did everything they could to make them tolerate  internal nutrition by, you know, trying promotility agents or placing in a small bowel feeding tube if they need it. So this shows us that we have to be  diligent in watching our patients getting what we prescribe, because remember about those increased metabolic demands I mentioned at the beginning of  this talk. So by day two, what did we do? We decided to go ahead and put a small bowel feeding tube in because of the high OG tube output, start with an  isotonic formula with the plan to advance to goal, and then we change our formula as we saw that the patient was giving, showing some tolerance to that  internal nutrition. How we choose a formula depends on not only their caloric and protein needs, but also what's happening with their drain. So  remember this patient's losing almost three liters out of that abdominal drain. You got to kind of wonder what's coming out, right? So one of the surgeons that I  worked with several years ago took the exudate from the abdominal drains of patients with an open abdomen, and we looked at it for protein and  micronutrients. This graph shows what we found as far as protein loss. You can see there was a few outliers in these patients. We think one maybe had some  blood in their output, but if we took out the outliers and we averaged it, our patients were losing around 15 grams of protein per liter of exudate. There have  been two other small studies mentioned here with 20 and 9 patients that were losing between 12 and 25 grams of protein per liter. So when you're  thinking three liters or more per day, that's a lot of protein being lost. Now micronutrients, I was a little surprised. It wasn't as bad as we thought. What I  have on these charts here is the median loss per day for each micronutrient along with the daily reference intake. So you need to keep in mind that you need  to meet the daily reference intake plus the losses for your patients when you're feeding them. The highest we saw in loss was chromium, but again you can see there  was a lot of variance between the patients. So when we decided what to feed our patient on day four, at this point he's off pressers, he's still intubated,  but he's still having a high output. We replaced the protein that he's losing from his abdominal drain when we calculated his needs. In order to do that  we had to use protein modulars to meet his needs. And also, but you'll see if we gave him goal internal nutrition, we are going to give him plenty of  micronutrients. However, if you're not giving goal, you may need to supplement with a multivitamin with minerals or something on the side until you're able  to feed these patients to goal. What do the guidelines tell us? And what you see here is the World Society of Emergency Surgeons, European Society of  Perinatal Internal Nutrition, European Society of Intensive Care Medicine, SCCM, and the American Society of Perinatal Internal Nutrition. We all say you should  feed early, you should use internal nutrition. We give some recommendation on replacing the protein from the abdominal drain, but look at the level of evidence.  Like I said, we had no prospective randomized controlled trials, so it was high consensus, but it is a low level of evidence. And I think once you start  feeding in early, you need to monitor closely. You need to watch that abdominal drain output, see if there's any change in appearance. Again, if you're  not getting to goal with internal nutrition, you need to start perinatal nutrition. In our patient, by day six, he was extubated. His abdomen was still open,  but he was tolerating two feet at his goal rate, was having bowel movements. When they extubated, he lost his OG tube and small bowel feeding tube, so we  started him on a low-residue diet. This just shows that it's okay to extubate before you close these patients. In fact, you'll see that early extubation, the  benefits that you would expect, less pneumonia, no tracheostomy, shorter length of stay. Our patient went on to tolerate that low-residue diet and had his  abdomen closed by hospital day eight without any further complications. In the next minute, I'm just going to give you one other quick example to show you an  example of when things don't go right. So this, again, was another young patient, 19 years old, had the open abdomen. We couldn't get him to go internally. We  started supplemental perinatal nutrition, extubated by day seven, though. Still, his fascia was closed, abdomen was open. We started feeding him a low-residue diet  on day eight, but then this happened. By day 10 and through 14, he had developed four what we call inter-atmospheric fistulas. And this is the toughie. This  is when they have the fistulas with inside the abdominal bed there. And this is kind of the nemesis for the surgeon because these are hard to care for. In  fact, the goal at this point is just to keep the enteric contents out of the wound. So you can see how we kind of MacGyver rigged this ostomy bag over the  fistula, be able to drain the abdominal room, and control the output from the fistula. Unfortunately for this patient, he had to go home on perinatal nutrition  and they weren't able to take those fistulas down for another six months. So he was on perinatal nutrition all that time, and we had to replace his electrolytes,  etc., from his output. So it was a challenging case. That's for another day. So I'm going to end by showing you this slide, which is an algorithm that was  developed in 2013 about the approach to nutrition and open adenovins, and I still think it holds true today. As you can see, if you have bowel continuity, you should  go ahead and think about internal nutrition. If you can't get to goal, you need to start thinking about supplemental perinatal nutrition earlier  rather than later. Again, because of these high metabolic demands and losses. And keep in mind that these patients, if we don't feed them adequately, it's just  going to worsen their muscle stores and ICU acquired weakness and make recovery that much harder. So I hope that this has helped you to tackle the  nutrition in these very challenging patients. Thanks for your time. Well, good afternoon. Today, I'm happy to be part of this symposium on ways to feed our  patients and what we feed our patients. And my topic that I was given was feed or starve a virus. Lessons learned from COVID-19. I have to say, when I got this  topic, I called Beth and I said, Beth, I don't know about this. It sounds pretty interesting. Just for the disclosures, I don't have anything to disclose. And also  the objectives today are just to talk about what are we going to do? How are we going to feed it? Is the virus really feeding different than is bacterial  feeding? So the bottom line is today, you know, I was very privileged to be asked to help write some SCCM guidelines and Aspen guidelines for this COVID-19  crisis. This is back in early March, actually. Beth Taylor, myself and Steve McClave helped were the sort of the directors of the SCCM guidelines in 2016  for nutrition in the ICU. So we were asked if we could help and make some, is there anything different about this virus that we should be looking at? So we  got in some people that pulled them in Jay Patel, and Dr. Rabi and Melissa Warren, we got pulled them in because they work daily with COVID patients, we  got some expertise. And so in reality, we got some people that really knew a lot about it. And as I started preparing for this talk, I started asking the  question, well, shouldn't it be different? Should we just give the routine ICU recommendations? Or should we, have we learned anything about this  COVID-19 virus that may make us change the way we do nutrition support? Well, you've all heard the saying, starve a fever and feed a cold. And really, that  kind of fits in this case. And that was actually stated first in 1574. Fasting is a great remedy for fever with this concept. The concept at that time really  was that eating food generates body warmth, and then food may help cool when overheated. So I think we've, you know, that's the concept there that we don't  want to make the body more warm, if it's already hot. So now, the current dogma, what happens? Is there a difference between virus and bacterial infections?  The current dogma when an animal, any animal, whether it be an insect, a small mammal, large mammal, what happens when it gets sick? It undergoes anorexia. Most  animals undergo, have anorexia, especially things like insects and low mammals. You can watch their diet change overnight. It's fascinating to see even  insects. If you give them choices to what to eat, and you infect them with bacteria, they will fast, they will quit eating. If you give them a viral  infection, guess they eat carbohydrate. So that really made people wonder, what happens? Should we have a different species? Well, I think that we have to  remember that virus is very different to cell metabolism. The viruses have no ability to store energy. They have to get that energy from the host in which  they're attacking. Remember, they require the host to supply all of their needs. The viral infection triggers metabolic reprogramming of the host, and  the viral infected cells exhibit a Warburg metabolism, which is glycolysis. As you might remember from cancer cells, upregulation of  glycolysis, several thousand fold in many cases, to actually increase the end products of carbohydrate metabolism of glycolysis, which would be  pyruvate and lactate if it's unused. That way, making a somewhat acidic media from the area. Well, guess what? Viruses do the same thing, and that allows them  to upregulate this glycolytic metabolism and increasing the pentose phosphate pathway, which are required for RNA synthesis. It makes sense. The virus  would want to say, I need to make more RNA, especially RNA virus, so it's going to hijack the pentose phosphate pathway, which is carbohydrate  metabolism. So, it's very interesting that essentially these viruses need the host machinery and the host biomolecules for survival, for replication, and for  spread before they can make new viral capsules for the next set of viruses. Now, is this just speculation, or am I just pontificating about no data? Well,  actually, it's a very interesting work done in this area. Probably one of the best papers, this article in Cell in 2016 by Dr. Andrew Wang. What he did  here, using a mouse model, he compared viral and bacterial infections with feeding and fasting, and he showed that with bacterial infections, which he  stimulated with Listeria monocytogenes versus LPS, which is the, obviously, the end product of gram-negative sepsis there, and he showed that when he  infected animals with either one of those, not both, but either one, that the anorexia protected the animal, whereas they gave extra nutrition, they yielded  poor outcome, and that glucose was needed to show the detrimental effect of the extra feeding. So, glucose supplementation increases reactive  oxygen species, and actually, they showed on the show it caused some brain damage, where ketogenesis was necessary to limit the reactive oxygen species. Now, if you  think back, is this how we're doing in critical care now? In reality, it is. There's been about six or seven major papers in the last two or three years,  actually four years, that show that small amounts of feeding are probably equal during that first five to seven days of ICU care. So, we don't push  calories like we did in the past. Some of you may remember five years ago, we pushed calories. Got to get in there. Got to get up to goal. We don't do that  anymore. Based on the good data, started with Todd Rice's work at Vanderbilt, and now we've got seven papers showing that. Okay, now, how is that  different than viral infections? In the same paper, they stimulate with either influenza virus or poly-LC, which is a DNA, synthetic DNA  product, basically to simulate a virus. So, like LPS equivalent to a viral infection. Now, what they showed there was nutritional supplementation actually  protected against mortality, the exact opposite of a bacterial infection. And if we, in fact, block glucose metabolism, high rates of glycolysis, it was lethal  to the animal. So, glucose mediated tissue tolerance of the virus, while glucose exaggerated the mortality in the bacterial infection. So, it showed that  they did this by maintaining the endoplasmic reticulum stress responses. Very interesting data. So, the body handles viruses very different than it  does bacteria. So, if we look at that, and we look at the viral story here, what happens? We get a SARS-CoV-2 virus infection. We see the rapid, rapid  response here of viral replication. Okay, and then we see, you know, disease tolerance, antiviral effluents, the body's inflammatory response, and then we  have resolution, hopefully. So, should we then be modulating what we normally would do? Normally, if we'd looked at critical care, we'd start here, feeding  the patient slowly, and by day 7 to 10, or day 5 to 7, we're up to speed with goal. Maybe we should be going rapidly like we did before, get to goal  with these patients, especially with a carbohydrate source, and then taper off and maybe give more even later during rehab. So, again, interesting thought. And  so, we have to look at some of the inferences we can make about a COVID-19 infection. They're older patients. Clearly, many of them are sarcopenic. Many have  pre-existing malnutrition. They have more comorbidities, diabetes, hypertension, you know, the whole thing we've heard about for months now. Severe acute  respiratory distress syndrome. How do we safely feed these? Can it be prone? ECMO? What do we do? There's some issues here. Circulatory failure, multiple organ  failure, cytokine release syndrome. We got to monitor triglycerides. So, there's a lot of issues here that we have to think about when we're feeding. So, let's  look about first, let's look at the lipids. Should we change the way we give lipids in this? Well, as you know, we give, usually, if we're giving intra, we're  giving a mix. If we're giving parenteral, now we're giving, in most cases, giving a mixed oil, which only became available a few years ago. Some people are still  using soy, but I would guess most people will transition to a mixed oil as we get the data as it continues to come out. There's news data, there's several papers  showing that. But now, if we look at the back end here, short-chain fatty acid butyrate, we have to remember, not just all lipids, that's a short-chain fatty  acid, not a medium or long-chain. Medium-chain triglycerides are sort of neutral, okay? And now, also, we now know that the fish oils go on to produce what  we call SPM, specialized pro-resolving mediators. So, let's look at the choice of lipid for a minute, and keeping in mind, what do we have? We have people that  are tremendously inflamed in COVID-19, right? So, we want to have enhanced resolution. We got to think about inflammation as two phases. We don't just  think about stopping it. We got to think about how we're going to resolve it, because we can't stop it right now. So, we know that by giving fish oils, our body  will produce SPM, specialized pro-resolving mediators, and they come from DHA and EPA. These then enhance the resolution phase of inflammation. Now,  what else do these SPMs do? Well, in some very nice work published in the England Journal of Medicine in 2013, showed very nicely that the SPMs lower  mortality in viral illnesses. By producing protectin, one of the SPMs, they inhibit viral replication. So, not only do we decrease the, or we enhance the  resolution of inflammation, we now can show that these SPMs decrease viral replication. Well, there's all kinds of conflicting results. You've seen, almost  weekly now, another one will say, oh, we should give this amount of vitamin C, and give us pharmacologic doses of vitamin D, and how about some  niacin? Well, we better throw in some quercetin. I'm not even sure what that is.  You know, so we got, these are well-respected researchers in nutrition, but they have these things with, I think, very little data. They have some good  theory, but we need some prospective data to show it. So, let's kind of review those. So, let's look at vitamin D. Well, we know in the ICU setting, we've got  two ICU randomized clinical trials showing no benefit, even if the patient presented within a deficient. The immunological effects of vitamin D  appear transient. The antiviral activity reported remains very vague. So, we really have no big benefit. There's no data currently to show that vitamin D  makes a difference in a randomized clinical trial, okay? So, for viral abacteria, for any kind of sepsis in the ICU. Well, vitamin A, we know that they  benefit animal models we see, but not necessarily COVID's not been tested, but in multiple viral models, if the animal's deficient in vitamin A, giving  back vitamin A helps survival. And also, that was mostly shown with the polio virus years ago. But again, we don't have any data on COVID-19. We have no  data that extra vitamin A makes a difference. What about vitamin C? We have no data in basically a good randomized clinical trial data in COVID, but we  know we have two large randomized clinical trials in sepsis for all comers in the ICU with ARDS, and there was shown to be no benefit for large  doses of vitamin C. Well, what about trace minerals, or these antioxidant based trace minerals? Well, again, what do we show? We know that when animals  are deficient in selenium, they can increase viral replication. We know when animals are replete with selenium, we reduce viral replication. It's a  cofactor for the antioxidant enzymes, superoxide dismutase and glutathione peroxidase. We know they're required for optimal immune function. But again, we  have no data that supraphysiologic doses of selenium makes a difference. Zinc is basically the same. It impairs viral replication when an animal's deficient.  We don't have COVID data, but we do know in other RNA coronaviruses, we can actually show we can decrease viral replication if the host is deficient in  zinc. Again, that's the key. Only when they're deficient do we see a difference. Cofactor for antioxidants, basically, the key thing with zinc is  it's required for taste and smell. So there is data to say that if the person is deficient, we should replace it early and hopefully we'll get taste and  smell to come back. So when we summarize these, what do we see? We know that zinc is antioxidant, has antiviral actions again in animal models, immune  function. What do we have the literature for COVID-19? Editorials and case series. Selenium, same thing. Vitamin D, same thing. Look at this. These are not  randomized clinical trials. These are editorials or maybe some observational trials, but very little data there. Vitamin C, same story. So again, we've  got to be very careful. So if we look at that, what can we say? We can also talk about pre and probiotics. Well, we know that probiotics are beneficial in viral  upper respiratory tract infections, 30% of which in America are caused by coronavirus, not our COVID virus, obviously. But we know that we can  decrease incidence and duration of symptoms. They enhance our immunity, they prevent colonizing pathogens, and they produce bioactive compounds that  we talked about before, which actually block the ACE receptor, which is how the virus enters our cell. So we could argue, theoretically, we could benefit from  those. Good thing is there's no real downside to the probiotics. Prebiotics, same sort of thing. We know that butyrate gives a systemic as well as a  local anti-inflammatory effect. So again, indirect evidence, but no hardcore data.  So when we look at vitamin and mineral supplementation, we can look at all these things. They decrease the oxidative burden, you know, in COVID-19 infections.  We know they're pleomorphic in their function, but really we can make a couple of bigger statements. We can say there's significant research gaps in  micronutrient therapy and SARS-CoV-2 infection. We have to look at that first. We can say that there's improvements in surrogate outcomes. It doesn't  necessarily translate in improvement in clinical outcomes. So we can look at that. So again, watching a few labs change, getting a level up to what we  think is, quotes, normal, does that not correlate to days on ventilator, days in the ICU, length of stay or mortality? So really we've got to be very careful  with what we're saying. We've got, there's no direct evidence at large doses or there's certainly no randomized clinical trials currently on  antioxidant cocktails in megadoses or pre and probiotics. So remember, we're talking about theory here, not data. So we should look at those. We should  go with our standard ICU requirements for now until we get more data. Now, conclusion, what can we say? Optimizing function of immune system would make sense, right?  So we know that supplementation of micronutrients, omega-3 fats and pre and probiotics are low cost, they're safe and they're effective in most to eliminate nutritional gaps.  Remember, nutritional gaps are not mega doses. We're talking about eliminating nutritional gaps and supporting optimal immune function.  So that really should be our guiding light there. Low cost, safe and effective. They eliminate nutritional gaps and that's what we should be going after to optimize immune function.  Currently considering supplementation above the RDA for vitamin C and D only in patients who are deficient or high risk for deficiency. So don't go with mega doses  until we see some randomized clinical trials. Now, what have we learned from all this? What have we learned about feed or starve a virus?  Well, almost all critically COVID-19 patients can be fed interally. We've seen that nationwide now when we've just finished a big survey and most are fed interally and successfully.  We know that blood sugar is difficult to control in these viral infected patients and severe insulin resistance is common. So be careful there.  We need to consider the concept that feeding a virus may be more beneficial than feeding a bacteria. That would be new, but that we have to wait and see again.  We've got some interesting basic animal work but we need to see it in humans. We haven't done that yet. I mean, that needs to be done but it's a very exciting concept  that maybe we should change the way we treat viral infections from bacterial infections. Our current recommendations regarding nutritional therapy  and critical illness of viral etiology clearly needs reevaluation and more study. That's the big issue. So if we look back at our graph here, the timing of the viral infection.  So our key is get into the system, stay healthy, eating a good, well-balanced diet, maintain your healthy microbiome. So if you do get infected, you're at a good state, okay?  Maintain your trace minerals. They'll take a well-balanced diet, not supplements, but a well-balanced diet. If you do get infected, then here's where it becomes interesting.  Make sure we've got to inhibit viral replication. Things like zinc, selenium, fish oils. Again, adequate numbers, not super pharmacologic.  Early feeding, considering carbohydrates and MCT. MCTs now we know inhibit viral replication. Okay, that's in the early phase. Stopping the virus inflammatory response,  enhancing resolution, minimizing viral replication. And then we go into second phase. Adhere the antioxidants to decrease damage from reactant oxygen species.  Increased proteins support acute phase response. Now we're talking about inflammatory disease and how do we treat that. High protein, decrease reactive oxygen species.  And then during our rehab phase where the patient's lost amount, they become sarcopenic from this viral infection, we should go with high protein resistance exercise,  maintaining vitamins, minerals, and trace minerals, because this is where we're going to have to get them back after this illness.  So maybe we should be looking at a SARS-CoV-2 infection as phases of diseases and we change our nutritional support depending on the phase of disease they're in.  So I think we're in good shape now. What does the future hold for us? Well, certainly manipulating specific metabolism to reduce viral replication is on the horizon.  We already know that osteo-CoA carboxylase inhibition is shown to reduce RNA viral replication and treatment. It's a new treatment. So we're looking now using these osteo-CoA.  Now what's the importance of osteo-CoA carboxylase? That's what's required to produce melanocoA, which is a rate limiting step for both RNA and DNA virus.  So very interesting data there. They cannot make a capsule to go out and infect another cell if they can't make melanocoA. So I think that's exciting areas  about metabolic manipulation to go after these viral infections, using things like ketogenic diets or intermittent fasting where MCT utilization increases.  That way MCT inhibits a viral envelope formation. I think the data is nothing but exciting to use nutrition as a tool to go after these infections.  I think there's lots of viral COVID-19 nutritional resources available to you. If you go to the website, you'll see several papers on cronying  and the ECMO during ECMO, ICU, et cetera. The CDC's website's got some, USDA and Aspen all have websites with COVID specific nutritional recommendations.  So thank you for your attention today. And I eager to talk and discuss in the question session. We'll see, have a live question session later. Thank you very much.  Hello and good morning, good afternoon and good evening. My name is Martin Rosenthal. I'm one of the assistant professors over at University of Florida.  I'm here to present 20 days and counting should I change what's on the menu. And I appreciate this opportunity to share my thoughts  and some of my research as well as share the presentation with some of my esteemed colleagues. Without further ado, our learning objectives are to discuss evolution of inflammation  to the chronic critical illness, as well as the persistent inflammatory immunosuppressed catabolic syndrome. And to help elucidate some of these ideas, I have a case report for you.  We're gonna discuss some of the recent evidence and as gold standard enough and what anti-inflammatory nutrition is going forward, at least some of the compelling evidence.  Here are my disclosures. So without further ado, our case report is a 22 year old female who was admitted to the surgical ICU, status post motor vehicle crash.  She was alcohol and marijuana positive. She sustained a traumatic brain injury, grade four splenic injury. She had hemo pneumothorax on the left side.  She had seven rib fractures on the left side as well as sigmoid perforation and traumatic flank hernia. And she was also found to be COVID-19 positive.  The ironic thing with this patient was that she was sharing her marijuana with her boyfriend who was COVID positive and she ended up having COVID  through the vehicle of her inhalation drugs.  She was actually intubated on scene for respiratory distress. She was unstable in the trauma bay and went for an emergent laparotomy.  During this emergent laparotomy, she had a splenectomy. She had a left tube thoracostomy to relieve the hemo pneumothorax, but not too much blood came out.  She had a sigmoid resection and was left in discontinuity. Her sigmoid resection was for a shear injury that she sustained, which is evidenced by her left flank hernia.  During that mechanism, you can have a tear in the splenic mesentery, which she had, and she had a de-gloving injury in her subcutaneous as well as she had a mesenteric rent  and what we call a bucket handle injury. Radiographs demonstrated bilateral diffused patchy infiltrates and the list of the injuries above.  Neurosurgery was consulted for the traumatic brain injury. It was small, but because her GCS or her common Glasgow scale was less than eight, an ICP monitor was placed.  She returned to the operating room hospital day two for an N-colostomy and repair of her flank hernia and a sequential abdominal closure.  Hospital day three, aggressive ventilatory management starting to fail. She was placed onto our bi-level. She was paralyzed. She was having to go on Flolan.  Nitric was an idea at that point because we couldn't rule out that she wasn't having any right heart strain, but it looked more like an ARDS pulmonary contusion picture,  but now because she was COVID positive, the idea that her COVID infection wasn't contributing to this clinical scenario could not be ruled out.  And ultimately she was evaluated for ECMO, but she improved.  By hospital day four and five, the patient is now in septic shock and is on pressers with early signs of organ dysfunction on her SOFA score.  She got a CT scan and a pelvic abscess was identified and our IR colleagues were able to train it. Hospital day six, she's stable on pressers and steroids  for adrenal insufficiency was initiated only because her cortisol came back less than 10 on labs, but we still were able to trickle two feeds at this point  because her pressure requirements were below our threshold for feeding.  Hospital day seven, she was started on supplemental pro nutrition because of our SCCM aspen guidelines. In hospital day 10, she was off pressers  and started to increase to goal two feeds. She's weaned from her TPN and weaned to virtually supplemental pro nutrition.  On hospital day 11, she had emesis abdominal distension. The KUV was confirmed in ileus. So we had to back off of our goal two feeds and we had to equilibrate for her caloric goals  with our supplemental pro nutrition. By day 16, she had returned to bowel function through her OSMI with well-formed stool and gas in the bag, advanced her two feeds to goal  and weaned off supplemental pro nutrition. By two days later,  she was still trached and on the vent at this time. She was actually trached hospital day, I wanna say five or six,  just because of everything that was going on.  And then ultimately our patient had a prolonged clinical course. She stayed in the ICU for virtually 32 days. She was able to tolerate two feeds at goal post-pyloric.  It was felt her aspiration risk, despite even having a cuff tracheostomy would be too high and could kill her because of everything that happened with her lungs.  Whether it was the COVID infection, whether it was ARDS or pulmonary contusions, we don't really understand the full mechanism, but I do believe everything contributed  to that clinical picture. And had she been COVID negative, could this have potentially actually happened? Sure, but we still couldn't rule out that there was a COVID-19 infection  that was actually contributing to this clinical picture. She was MPO and went to a long-term acute care facility for vent wean. Ultimately, she suffered considerable weight loss  and loss of functionality.  So here's the early concept of what multi-organ failure was. We used to believe that there was a SERS response or systemic inflammatory response syndrome,  and you had a lot of disarrayed immunologic function.  You had cytokines, you had cytokine storm, and ultimately this all got bracket back down to homeostasis through a CARS response. But we also thought that maybe a CARS response  could be maladaptive and you can remain immunosuppressed and fall prey to latent infection or nosocomial infections. Either way, what we now know is that  both the SERS and the CARS response happen simultaneously. You have an innate immunity as well as an adaptive immunity response, and both of those happen simultaneously.  And whether or not the patient remains persistently inflamed and catabolic or progressively immunosuppressed is dependent upon multifactorial response,  genetics being a large component of the predisposition. But because of our definition of chronic critical illness happening at ICU day 14,  which you can see at the bottom of the slide,  anything that progresses after that, we call that chronic critical illness. But if you have the phenotypic and the biomarker array  of persistent inflammation off of biomarkers, persistent immunosuppression, catabolism, you fall into this kind of PICS phenomenon that we're describing at University of Florida,  and you ultimately have dismal outcomes. And one of the things that we always look at is why does this actually matter? So five to 7% of all admissions to any ICU,  whether it's MICU, PICU,  chronic critical illness is becoming more and more prevalent. And that's also because we have advances in technology. We have bundles, we have whatever have you in the ICUs  that are starting to become more prevalent.  They are gold standard. They're all evidence-based, and we're doing a really good job of keeping these patients alive. And a lot of these patients that would have expired  50 years ago are still staying alive,  but they developed this chronic critical illness picture. And we know that in the surgical population,  the CCI folks develop about 20% of the time. And after sepsis, it can be as high as 50% of the time. More than 380,000 cases with 170,000 hospital deaths.  Patients that develop CCI devour 30% of ICU utilization  and resources. And we spend over $26 billion in healthcare expenses toward this patient population.  Recently we published this paper, chronic critical illness patients fail to respond to current evidence-based intensive care nutrition secondarily to persistent inflammation,  immunosuppression, and catabolic syndrome. And what it was, was a kind of retrospective review on a prospective database that we picked up  for the P50 grant, looking at this chronic critical illness  and looking at the PICS patients. We were trying to figure out an epidemiologic structure. Was there anything driving this mechanism? And figuring out from a multidisciplinary  team science grant award through the P50, is there anything that we could potentially offer for this patient population? And what I found was that out of the 56  chronic critical illness patients that we matched, double fold for the rapid recovery, RAP stands for rapid recovery. We matched the 56 to the 112 just to increase the power  for the analysis. And we matched them for the Charleston Comorbidity Index age, sex, and Apache 2 score. That within the first month of their ICU stay,  all the patients received 75% of their goal calories, which is actually pretty good looking at evidence on how we are performing at getting our patients  to goal calories across the board.  75% is actually a reasonable number, but you also have to remember that this is a strong patient population that is very surgically heavy in the sense that these are trauma patients  and these are acute care surgery patients. So whether or not we're going back and forth to the operating room, whether or not we're having to get source control  or damage control for surgical sepsis or penetrating trauma for blunt trauma, these patients within the first week of their hospital stay  actually are going back and forth. And usually by the end of a week in our intensive care unit for the trauma care and the surgical care side of our two ICUs,  we can usually get a good source control by the end of the week. So if we exclude the first week from our actual data set,  the next two, three, and four weeks, we actually fed our patients at 88% of their goal calories, which is really, really good.  The thing to understand is that when you look at the data,  the chronic critical illness group compared to the rapid recovery group, when I say a non-home discharge, 81% of the CCI group are not going home.  And non-home discharge for us is death. They're going to the morgue or they're going to a long-term acute care facility. They're going to a nursing home. They're going to rehab.  They're going to subacute rehab. 81% of those patients are not going home, which is truly something to be aware of. And it's also something that's super frightening.  You know, when you're a patient and you survive the ICU, all you want to really do is just get home, but sometimes that's not appropriate,  versus only about roughly a third of the rapid recovery  go to a non-home discharge, excuse me. That means two thirds of them get to go home. And then 12 months survival in this patient population, a third of the CCI folks die,  whereas only 8% of the rapid recovery die. So what about the biomarkers that I was talking about? Here's inflammation. So what you see in the pink line,  and that's the CCI or chronic critical illness, and the blue line is rapid recovery. So IL-6, IL-8 are significantly more in the CCI folks.  Immunosuppression, we use absolute lymphocyte count and the soluble programmed death ligand or SPDL-1.  The absolute lymphocyte count was not statistically significant until the third and fourth week,  but there was a trend toward it. And then the SPDL-1 was statistically significant throughout. And then catabolism and stress metabolism.  So glucagon-like peptide is a good biomarker for stress metabolism. Urinary 3-methylhistidine is interesting because it's a marker that when you break down  your lean muscle mass or your muscles, you release 3-methylhistidine in your bloodstream and it's cleared through your kidneys and so you can track it in your urine.  But oftentimes, these patients that we have, the trauma patients, the sepsis patients, they have AKIs. So sometimes creatinine is not indicative  of how stressed they are or how catabolic they are.  I do have that graph also as a ratio of urinary 3-methylhistidine to creatinine and it follows the exact same trend. Though it's not statistically significant,  the trend is very much in favor that the CCI folks remain highly catabolic. Here you have a Zubrod score. So I wanna touch base with this. And the next graph I'm gonna show you  is gonna be what we actually look at. So Zubrod is zero to five, zero is fully functional and five is death. Four is completely disabled, cannot carry on self-care  and totally confined to bed chair. Here's the graph. So CCI folks on the top line, the one that's in white, have an average Zubrod score of about 3.75 to four  throughout their one year. Whereas the rapid recovery, they're back to almost baseline, if not a little bit diminished at one to 1.5.  So what do we do?  Can we look at additional literature? Can we glean anything from it? Here is the publication we just recently came out with,  2020. It was a meta-analysis that's looking at fish oil. Here's the actual publication. So do omega-3 fatty acids enrich parenteral nutrition in hospitalized patients?  It says systemic review, meta-analysis. So looking at omega-3 fatty acids, I get it, it's a parenteral supplement, but at the same time,  omega-3 fatty acids decreased infection by about 40%.  Sepsis was 56% lower in this meta-analysis. Length to stay was upwards of 2%, I mean, sorry, two days shorter. And though it wasn't statistically significant,  the mortality had a reduction of about 16%. And so what about SPMs? This is a novel substrate of omega-3 fatty acids.  It's a bio-engineered,  using your own endogenous pathways, breakdown of omega-3 fatty acids. You get three different classifications of SPMs, resolvins, mericins, and protectins.  Protectins used to be called neuroprotectins because we thought it was more nerve related, and mericins come from macrophages,  but helps resolve inflammation using endogenous pathways. Maybe the actual bioactive component, why fish oil helps decrease inflammation.  The other thing that I really wanted to kind of talk about is something that I recently found. So here is a GLU grant project that they looked at.  So gene expression and pro-resolving lipid mediators, the SPMs, pathways associated with clinical outcomes in trauma patients. So looking at just trauma patients,  it's a post hoc analysis of the GLU grant database. It's where genomic storm came from. And what it looked at is resolvin score versus leukotriene score. And these scores looked at,  numerators went on the top, and were everything that builds either resolvins or leukotrienes. And the denominator was everything that breaks it down,  you know, catalytic process of breakdown or excretion.  And so they enrolled 96 patients, complicated versus uncomplicated. I hope that sounds familiar. Complicated is RCCI versus uncomplicated, which is our rapid recovery.  And when all genes were combined into scores, patients with uncomplicated recoveries had differential and higher resolvins, resolvins scores, excuse me,  which was statistically significant and lower leukotriene scores, which if you look at this, this is from their paper.  You see on the top left resolvins score, blue is the actual recovery or uncomplicated. And excuse me, yes, sorry. So blue is the uncomplicated and they resolved.  And the lower red line is for the complicated patients and same with the leukotriene score. So the patients that had really complex recoveries  or had complications period, red is higher. Here's our data from University of Florida. So chronic rival illness versus RAP, blue is CCI, RAP is red.  The leukotriene score is lower in the rapid recovery and higher in the chronic rival illness. This fits their picture perfectly,  which is nice. But what I have to show you on the next slide is our cohort of chronic critical illness patients had a much higher resolvins score.  And so the one thing that this has as a question  or hypothesis driving stance is that  what is missing from the equation? Do the chronic critical illness patients ramp up their genes to build up a resolvin  producing mechanism, but they lack the substrate to actually produce their resolvins? Or is there a breakdown somewhere thereabouts and that this is a broken feedback loop,  much like a thyroid? Like are we not able to utilize the genes  and the proteins that we're making to build resolvins? And so this is very interesting in my world. I'm trying to figure this out, but ultimately I think that this has potential  for answering a lot of questions and it could be a therapeutic benefit to a lot of these chronic critical illness PICS patients.  So is gold standard evidence-based nutrition good enough for our CCI PICS patients?  It may not be good enough. Can we utilize other nutrients? Sure we can.  I ultimately think that there's a evolving body of anti-inflammatory literature, pro-resolving literature,  anti-catabolic literature, anti-sarcopenic literature that we can use to understand what we need to be feeding our patients  in the chronic critical illness and PICS patient population.  I do appreciate you guys listening to me and I appreciate any questions at this time. Thank you so much for including me in this presentation. ♪♪

Video Summary

This presentation titled "Everybody Has to Eat: A Case-Based Approach to Nutrition in Special Populations" focuses on the importance of nutrition in managing patients in special populations. The speakers discuss specific populations such as those with severe acute pancreatitis, traumatic brain injury, open abdomen, SARS-CoV-2 infection, and chronic critical illness. They emphasize the role of enteral feeding in improving outcomes and provide evidence-based guidelines for nutrition therapy. <br /><br />The speakers cover various topics related to nutrition in special populations. They discuss the management of acute pancreatitis and the benefits of enteral feeding. They also highlight the unique nutrition needs of patients with traumatic brain injury, including the challenges of feeding patients on targeted temperature management. The importance of monitoring and individualized nutrition plans for patients with an open abdomen is also emphasized. The speakers address the delivery of safe nutrition support to patients with SARS-CoV-2 infection and discuss the potential role of probiotics. Finally, they discuss the concept of chronic critical illness and its impact on metabolism and nutrition status. They highlight the need for tailored nutrition interventions and mention the potential benefits of omega-3 fatty acids and specialized pro-resolving mediators. <br /><br />Overall, the speakers stress the importance of meeting the nutritional needs of patients in special populations and providing individualized nutrition therapy. They also emphasize the need for further research to develop specific nutrition interventions for patients with chronic critical illness.

Asset Subtitle

GI and Nutrition, 2021

Asset Caption

The Society of Critical Care Medicine's Critical Care Congress features internationally renowned faculty and content sessions highlighting the most up-to-date, evidence-based developments in critical care medicine. This is a presentation from the 2021 Critical Care Congress held virtually from January 31-February 12, 2021.

Learning Objectives

Describe the nutrition approach in the ICU patient with severe acute pancreatitis
Assess how nutrition needs differ in patients with traumatic brain injury
Examine timing and adequate nutrition in the trauma patient with an open abdomen
Review which critical care nutrition principles work for COVID-19 and lessons learned
Discover the metabolism changes and impact on nutrition status in chronic critical illness

"Don't Mess With the Pancreas" Doesn't Mean Starve It! Stephen McClave My Head Hurts and I'm Hungry! Stephanie Dobak Look in My Belly, and Then Feed It! Beth Taylor

Feed or Starve a Virus: Lessons Learned From COVID-19 Robert G. Martindale Twenty Days and Counting: Should I Change What's on the Menu? Martin Rosenthal

Meta Tag

Content Type Presentation

Knowledge Area GI and Nutrition

Knowledge Level Foundational

Knowledge Level Intermediate

Knowledge Level Advanced

Membership Level Select

Tag Pancreatitis

Tag Enteral Nutrition

Tag Calorimetry

Year 2021

Keywords

nutrition

special populations

acute pancreatitis

traumatic brain injury

open abdomen

SARS-CoV-2 infection

chronic critical illness

enteral feeding

nutrition therapy

evidence-based guidelines

monitoring

individualized nutrition plans

probiotics

omega-3 fatty acids

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