So, at the end of the session, we'll have a review of relevant gastrointestinal anatomy and physiology and then common GI normalities in terms of their management and diagnostic features. We're going to start with GI physiology in terms of structure, motility, circulation, common ICU conditions, and then common GI abnormalities that lead to critical illness. So small intestinal epithelial structure, so you have the small intestine with villi in crypts to increase the surface area, about the size of a tennis court, and that stem cells at the base of the crypt renew the epithelial cells, so your entire GI tract every seven days is new in terms of the epithelial surface. Various cells serve different functions but derive from these stem cells to secrete mucus, control electrolyte absorption, water absorption, and provide another set of digestive enzymes. Importantly, the jejunum is the site of the majority of nutrient absorption. The ileum is where you're absorbing bile acid, some fluid, and B12, if that ever becomes a question, where is B12 absorbed? And then, importantly, the microvilli and brush border and mucus layer are the site of terminal carbohydrate digestion and act to protect the cells themselves, the mucus layer, from digestive enzymes. So motility, which is often abnormal in the Pediatric Intensive Care Unit, occurs in phases and stages of health. So control is through extrinsic and intrinsic nervous system and endocrine system. In the interdigestive phase, right, in a normal person who's eating bowl-less meals throughout the day, the migrating motor complex basically preps the GI tract for the next meal. So cyclophasic contractions to empty the stomach, and it's controlled by parasympathetic input GI hormones and the enteric nervous system. During the feeding state, you have various phases. It's in the longer, larger talk in terms of cephalic phase, digestive phase, et cetera. But there are stretch receptors in the proximal stomach, which trigger receptive relaxation. And then in the distal stomach, you have cycles of contraction and relaxation. And the control of gastric emptying is regulated by this neuronal and hormonal feedback loop, where the duodenum is exposed to macronutrients and osmolar load to trigger these feedback loops and control gastric emptying and ensure complete digestion. This list is sort of the, on the exam, I imagine the, which one of these things is not like the other. So I've listed stimulatory and inhibitory hormones. It's not important that you know exactly what these hormones do, but very likely if you were to be asked a question, it's sort of like they'd only give you one stimulatory hormone on the list, right, versus other inhibitory hormones. And so it's more a matter of knowing that ghrelin and modelin are stimulatory and the other hormones are inhibitory in terms of what's going to promote or decrease gastric emptying. I have a question. With the GLP-1 inhibitors being so prevalent now, like we've had a couple kids come into my ICU just with like horrible vomiting, diarrhea, dehydration. Do you think there'll be any questions like that on the... No, I would not. I think that's too new. And I don't think children are being placed on those medications. I mean, certainly they can impact gastrointestinal motility, but I think more likely is the low-hanging fruit of the other medications we're giving to patients in terms of opioids, et cetera, that slow... Yeah. Yeah. And then in terms of gastric motility and poor gastric emptying, I think this is under-diagnosed in the Pediatric Intensive Care Unit. And when it's looked at, about 50% of critically ill children have slow gastric emptying related to sympathetic activation, parasympathetic inhibition, and a dysregulated enteroendocrine system. Small intestinal absorption is also impaired. And all of the commonly used promotility agents that we have in our arsenal lack evidence for their use and are legitimately probably poorly effective. Drugs that decrease GI motility in the Pediatric Intensive Care Unit are those that we commonly use, opioids, catecholamines, clonidine, anesthetics, plus or minus 6-metatomidine. And so we introduce a lot of medications, and then critical illness itself results in slow GI transit, slow gastric emptying. And so there are a lot of factors slowing that whole process. And then in terms of actual circulation during enteral nutrition, this is the cause of a lot of consternation. I showed you some of the data saying that actually enteral nutrition provision based on VIS score was not associated with an increase in complications. The concern is really that there's this steal from cardiac output in patients with hemodynamic instability where baseline, the splenic blood flow is about 20% of your circulation, but with meals can increase to 40% to 60%. So is your watershed area, your splenic flexure, which is the area between the SMA and IMA, and is at a higher risk for ischemia if you feed your patient who's hemodynamically unstable? Might you get ischemia and a bowel catastrophe? That's the worry. This is more a reference table to just go over the effect of various inotropes and pressors on GI mucosal flow. Wanted to kind of provide this because this is a difficult piece of information to find in the literature. You could spend hours looking for a table that describes this. Wanted to provide it here as a reference. But essentially from a practical and pragmatic standpoint on the exam, if you have resuscitated your patient and based on current national guidelines that after the patient is resuscitated and has achieved hemodynamic stability irrespective of whether or not they're on pressors, sepsis guidelines currently recommend initiating enteral nutrition and monitoring your patient and trying to achieve goal calories at the end of the first week of ICU hospitalization. So common ICU conditions, so I'll address stress ulcer, prophylaxis, and dysbiosis briefly because it's an emerging topic in the literature, although I think probably at this stage unlikely to show up on the board exam. So in terms of stress ulcer, prophylaxis, we don't have national or international guidelines that are clear and established for stress ulcer, prophylaxis in critically ill children. What might appear on the exam is that the two greatest risk factors for significant gastroduodenal bleeding are mechanical ventilation greater than 48 hours and the presence of a coagulopathy. Enteral nutrition is in the literature protective against clinically important GI bleeding. One of the reasons why sepsis guideline, for example, is recommending early initiation of enteral nutrition and may help in terms of an experimental standpoint to prevent dysbiosis. So how do our drugs work? Again, I'm including this more because it's testable, easy to ask in terms of the site. So the hydrogen potassium ATP secreting pump is located at the parietal cell. Proton pump inhibitors irreversibly bind this receptor to suppress acid secretion by parietal cells and are superior to H2 blockers for acid suppression. That's essentially, I think, what you might need to know for the exam. And this is sort of maybe if it shows up, but I doubt it, but I thought it was important to just introduce the topic. So functional consequences of an altered microbial community composition. Dysbiosis is common in adult and pediatric critical illness. What you see here in terms of relative abundance of firmicutes and actinobacteria decreased and an increased relative abundance of proteobacteria and bacteroidetes. And so kind of so what, right? So the transient perturbations in the emerging literature are that transient perturbations in the microbiota early in infancy are associated with adult long-term illnesses and that dysbiosis in pediatric critical illness is associated with longer length of stay and worse severity of illness. And there is ongoing investigation to identify if there is any link between dysbiosis and necrotizing enterocolitis. The functions of the gut microbiome are a multitude in terms of modulating bone density, development and training of the immune system, metabolism of therapeutics, biosynthesis of vitamins and amino acids, importantly, vitamin K, breaking down food compounds and providing resistance to pathogens. Now I'll go through a whirlwind of common GI abnormalities starting with necrotizing enterocolitis. But first, normal KUB is where we're going to start from because there will be several images throughout the talk. There are no distended loops. There are no air fluid levels. There are no masses, no paucity of gas, normal stool in the colon and no extra luminal or free air. I'll add the caveat, my husband's a radiologist and he will say a flat plate abdomen is only good for identifying feeding tubes. It's worthless for anything else. Also importantly, hopefully on the exam you will see an upright or a lateral or decubitus KUB that will be described that way. So necrotizing enterocolitis, this slide is filled with information and meant as a reference. So you could look at it as this is what I need to know about necrotizing enterocolitis. So 1 in 1,000 lives birth, incidence is higher in very low birth weight infants or infants with congenital heart disease with specific lesions, truncus arteriosus and hypoplastic left heart syndrome are the most common, or if patients or infants have significant periods of poor perfusion, right? And pathogenesis is really unknown, thought to be multifactorial. And then in 95% of cases is after the introduction of enteral nutrition, there's actually a lawsuit currently by parents to formula companies because they think that there's this clear, they're proposing this clear association between formula nutrition and necrotizing enterocolitis. The risks for the preterm gut are listed there. And then presentation is feeding intolerance, increased gastric residuals, abdominal distension, bilious vomiting, gross or occult blood in the stool. Treatment is, right, initially for stage 1 and 2 bowels, bowel rest, broad spectrum antibiotics, and stage 3 is typically surgical and usually associated with perforation. Findings on KUB, pneumatosis is the most common, but you can have perforation, portal venous air and, but usually the story is going to be fairly clear on the exam. Esophageal atresia, again, easy picture to show you and ask the question. This picture is the two blind pouches, right, because you have the feeding tube that ends at the top of, in the esophagus and no distal air in the GI tract, right? So it's one of the easier questions to ask on exam because there's no air in the GI tract and this is a blind pouch that stops at the top. The incidents are listed there. And then hypertrophic pyloric stenosis, 3 in 1,000 births, male to female ratio of 5 to 1, diagnosis median about 6 weeks of age, but 2 to 8 weeks of age. Associated abnormalities, esophageal atresia, TE fistula, renal abnormalities, Turner's or trisomy 18. Typically non-bilious projectile vomiting. And in the textbook it's going to say a palpable mass, but I think we all know you don't actually feel them in a wriggly infant unless they're anesthetized. Potentially a paraseltic wave and hypochlorimic, the classic feature, right, it's going to be a hypochlorimic metabolic alkalosis with a bicarb that's high and a chloride that's very low in a baby, in a 6-week-old male infant that comes in vomiting, right? And the treatment is pyeloplasty, diagnosis is by ultrasound and a single bubble assigned on the dilated stomach. Duodenal atresia, 1 in 10,000 life's births, site of re-cannulation failure is the ampulla of Votter, has this list of associated disorders, typically bilious vomiting in the first day of life. Treatment is surgical. Importantly, however, the double bubble sign is not solely associated with duodenal atresia. It's most classically described in a textbook that way, but there are other things that are associated with double bubble simply because they have that same site of obstruction. Intussusception is telescoping of one segment of bowel into another. Typical instance is three months to two years of age. You have your lead point, right, which may be tumor, in spasticity feces, lymphoma in older children, crampy abdominal pain that's intermittent, may or may not have bloody stools depending on how long this has been going on. Patient could be shocky depending on how long it's been going on. Maybe require some fluid, some resuscitation. Ultrasound is the imaging of choice and an air enema reduction with surgery plan if that's not possible. Here you can see image on the top left is an upper GI with water-soluble contrast. Did identify it's kind of a mass in the bowel. And then there's a hint of a target sound, which I've kind of like drawn in to see that. And then midgut volvulus, again, fair game. This is a surgical emergency, so this is a surgical emergency and carries risk of bowel necrosis if not recognized. So this is failure of normal embryonic rotation of the bowel. So the duodenal-jejunal junction doesn't reach its intended location to the left of the spine. And the small bowel is suspended on a narrow vascular pedestal and can rotate and cut off your blood supply, essentially. And so the duodenal-jejunal junction is to the right of the spine. Most of the small bowel is to the right of the abdomen, and the cecum in this picture is in an abnormal location mid-pelvis. So bleeding, again, a reference table to more so be able to understand infants, younger children, and older kids and causes of upper GI bleeding. Not meant for me to walk through all of this with you. And then lower GI bleeding by age, same thing, infants two to five years and older. So significant GI bleeding, important to assess exam, comorbid history, contributory mechanisms, and likely on the exam is really the assessment of blood loss and management and what's your next step in management for this patient is a likely question. Localization temps are often not successful. I think you guys probably know that. And may, depending on the rate of volume of loss, may need initiation of a massive transfusion protocol. And then black, tarry stool, classic, right, upper GI bleed, characterized proximal to the ligament at trites. And then hemodynamic instability, orthostatic or supine hypotension, plus or minus abdominal pain may be part of the story or the stem. And then NG lavage can be a little bit of a red herring in terms of fresh blood or coffee ground, yes, probably an upper GI bleed, but a false negative for a now it's over bleed and you're dealing with the consequences or post-pyloric bleed. And then CBC, right, could be normal, microcytic anemia or could just look normal. And then the appropriate laboratory evaluation. Management in terms of resuscitation, classic, right, two large borer peripheral IVs, perhaps an early small volume balanced fluid resuscitation, but the goal is they're bleeding, replace the blood. And then a PPI or H2 agonist simultaneously. And then with somatosatin or a treatide, gram-negative antibiotic coverage empirically. And then OG tube or NG tube, and for infants, potentially a Foley for tamponade that carries risk of esophageal perforation or aspiration. And then following serial crit and correcting coagulopathy. And then GI consult in terms of evaluating for upper GI endoscopy, for band ligation of varices if that's what's suspected, Klipsch-Cotterie or local, epi for bleeding vessels, excision of bleeding polyps, et cetera. And then contraindicated if perforation is suspected. And then surgical consult potentially. And then I will, acute pancreatitis, there's the INSPIRE criteria, anytime there's a guideline that's published or Clear Credit Society guidelines, right, questions are likely to come from those areas. So acute pancreatitis is defined as requiring two of the following three criteria by INSPIRE criteria, abdominal pain compatible with acute pancreatitis, serum amylase or lipase more than three times the upper limits of normal, or imaging findings of acute pancreatitis. Predictors of poor outcome for children with pancreatitis are age less than seven years at admission, weight less than 28 kilos, white count greater than 18.5, and an LDH greater than 2000. And then during the initial 48 hours post-admission, calcium less than 8.3, or total calcium, serum albumin less than 2.6, requiring more than 75 per kilo fluid resuscitation, and a BUN greater than five. Management is initial conservative treatment with crystalloid fluid resuscitation, maintenance IV fluids, oxygen, and algesia to treat electrolyte and metabolic abnormalities as they occur. And then if you have necrotizing pancreatitis, carbapenem, time 14 days, and then percutaneous ultrasound or CT-guided fine needle aspiration. And then biliary pancreatitis, so cholangitis, persistent jaundice, endoscopic sphincterotomy. And then in terms of necrotizing pancreatitis, typically surgical treatment is delayed, or potentially an interventional radiology for management. Prior to 15 years ago, you wouldn't have fed these patients or you would have fed them just post-ampullavator. And now enteral nutrition is thought to decrease complications of acute pancreatitis, typically still provided via the NJ route. And parenteral nutrition is more so preserved for prolonged fasting due to ileus, complex fistula, or abdominal compartment syndrome. Subdominal compartment syndrome is complex physiology, so dilated, boggy bowel with edema causes upward movement of the diaphragm, which causes atelectasis, impaired gas exchange. And then you have negative effects on preload, afterload, and contractility. There is activation of the renin-angiotensin-aldosterone pathway, leading to secretion of catecholamines, impacting afterload. There's also direct compression, potentially, on the RV and LV, such that end-diastolic volumes and compliance are reduced. And then you have renal dysfunction due to two mechanisms, which are decreased cardiac output with stimulation of the renin-angiotensin-aldosterone system and due to direct renal compression. This is a self-feeding cycle that continues, but really the characteristic of abdominal compartment syndrome is the elevated pressure in the abdominal compartment plus additional organ dysfunction. So, ACS in children is defined. This is from 2013 international guidelines regarding abdominal compartment syndrome in children. So, a sustained elevation in intra-abdominal pressure greater than 10 associated with new or worsening organ dysfunction that can be attributed to the elevated intra-abdominal pressure. Usually, on an exam, it's going to be a little bit more of a no-brainer in terms of they'll give you a pressure of high 20s or something quite elevated. And measuring intra-abdominal pressure is really, like, first recognize that this is happening and it's under-recognized in children, so a protocolized pathway for monitoring and treatment, so monitoring fluid balance, resuscitation, preventing gross fluid overload in at-risk patients, and then potentially evacuation of intestinal intraluminal contents, extraluminal contents, elevating the head of bed considering your muscular blockade, and then percutaneous peritoneal catheter drainage. And then for overt cases of ACS with refractory oxygenation or ventilation, decompressive laparotomy and mortality for this condition is high. Thank you.

GI anatomy

small intestine

GI motility

PICU

enteral nutrition

GI conditions