This is the multi-professional critical care review course for pediatrics. I'll be speaking about gastrointestinal abnormalities. My name is Katri Tippo. I'm the division chief of pediatric critical care and an associate professor of pediatrics at University of Arizona, and I am the immediate past chair of the PICU NutriNet subgroup at Felici. My research interests are on the gut microbiome and nutrition and pediatric critical illness. These slides were originally developed by Nilesh Mehta, and I edited and updated them for this talk today. My one disclosure is I've been a consultant to leading biosciences to aid in study design. Learning objectives for today are to review relevant gastrointestinal anatomy and physiology, common GI abnormalities and diagnostic features such as obstruction, bleeding, intra-abdominal hypertension or abdominal compartment syndrome, and necrotizing enterocolitis, and discuss management of common GI emergencies. The outline is here. We will start with GI motility and gastric emptying. Here's a question. Please select the correct options that describe GI motility during critical illness. A, delayed gastric emptying is seen in less than 10 percent of patients in the PICU. B, use of gastric residual volume measurement prevents aspiration and pneumonia in enterally fed patients in the PICU. C, gastric emptying is stimulated by ghrelin and motelin, or D, gastric residual volume is an accurate marker of intramutrician intolerance. The correct answer is C, gastric emptying is stimulated by ghrelin and motelin and we'll review all these concepts in the coming slides. Gastric motility increases after a meal, so you have receptive and adaptive relaxation. Gastric contractility activity or peristalsis is induced by the cells of cassol which act as a pacemaker within the stomach and induce a wave every three minutes towards the pylorus. They deliver chyme to the duodenum or back for more mixing. Looking at the feedback loop for gastric emptying and regulation in the cartoon on the right. If you have the presence of fatty hypertonic or acidic chyme in the duodenum, then that stimulates duodenal enteroendocrine cells to secrete enterogastrin such as secretin, CCK, and G1P. Then chemoreceptors and stretch receptors, which then are target by a short and long reflexes, enteric neurons, and then CNS centers to increase sympathetic nervous system activity and decrease parasympathetic activity. This results in the contractile force and rate of stomach emptying to decline. Then that feeds back to duodenal stimuli decline. Gastric emptying is regulated by hormones that are stimulatory or inhibitory. Ghrelin or the hunger hormone is released by gastric mucosal cells and requires post-translational isolation for activity. It stimulates gastric emptying by inducing phase 3 activity in the stomach to induce contractions. During critical illness, conversion to the active form, acyl ghrelin is reduced and may be partially responsible for decreased gastric emptying in critical illness. Modulin is released by endocrine cells in the small intestine. It stimulates the migratory motor complex to induce phase 3-like activity, which are high amplitude phasic contractions. Modulin agonists are medications such as erythromycin and erythromycin. Inhibitory hormone signals, which cause delays in gastric emptying, are cholecystokinin, a mediator of enterogastric response inhibits gastric emptying and promotes intestinal motility. Glucagon-like peptide 1 is secreted by endocrine cells in the small intestine and also slows gastric emptying. Secretins regulate secretions in the stomach, pancreas, and also slows gastric emptying. In the pediatric intensive care unit, the key points to realize are that gastric emptying is slow in up to 50 percent of critically ill patients. Those at risk include patients with trauma and sepsis. There is abnormal anteroduodenal motility and a short MMC cycle during fasting. MMC is really intended to empty the stomach in preparation for the subsequent meal. Small intestinal absorption is also impaired even when gastric emptying is normal, and small intestinal transit appears to be grossly normal in critical illness. Many drugs decrease GI motility. Many of these you're familiar with opioids, catecholamines, clonidine, and there's the suggestion perhaps that dexmedetomidine may also affect GI motility. There are promising new agents for the treatment of gastrointestinal dysmotility in critical illness, and they include non-antibiotic motilin agonists and methylnitrexone. We'll move to acid secretion next. Now we will review regulation of gastric acid secretion. Gastric acid secretion by the parietal cell is regulated mainly by three stimuli, acetylcholine, gastrin, and histamine. Acetylcholine is the principal neurotransmitter modulating acid secretion and is released from the vagus and parasympathetic ganglion cells during the cephalic phase of digestive secretion. There are three phases to digestive secretion, the cephalic, gastric, and intestinal phases. The cephalic phase begins with the sight, smell, thought, or taste of food. Acetylcholine directly increases acid secretion by parietal cells, but also stimulates other cell types to release peptides, such as gastrin-releasing peptide. The gastric phase of secretion begins when food enters the stomach. Protein products of food interact with microvilli of enteral G-cells to stimulate gastrin release. Food also stimulates acid secretion by causing mechanical distention of the stomach and activation of stretch receptors. Enteral distention also causes gastrin release. Gastrin secreted from G-cells stimulates the release of histamine from gastric enterochromaffin-like cells or ECL cells, which is the major stimulant of acid secretion from gastric parietal cells. The gastric phase accounts for 60-70 percent of meal-stimulated acid output. Finally, the intestinal phase actually decreases gastric acid secretion. It is stimulated by kind reaching the duodenum and intestinal distention. There's a decrease in pH in the duodenum. This is mediated by the release into the circulation of somatostatin, secretin, CCK, and other peptides, but primarily regulated by somatostatin, to then provide a negative feedback to inhibit parietal cell secretion of gastric acid, and to decrease peristalsis. Let's review parietal cell acid secretion. Within the stomach, we have several drugs that are often used to suppress acid production. Sometidine and ranitidine are histamine or H2 receptor antagonists. They work on the H2 receptor via a cyclic AMP-dependent pathway to inhibit the hydrogen potassium ATPase pump. Omeprazole and pantoprazole are two examples of proton pump inhibitors, which they work by irreversibly binding the hydrogen potassium ATPase to suppress acid secretion by parietal cells. They are superior to H2 blockers for acid suppression. These medications are typically used for stress ulcer prophylaxis in the PICU. There are no national or international guidelines for stress ulcer prophylaxis in critically ill children. A systemic review identified pharmacologic treatment effective to prevent clinically significant upper GI bleed as compared to no treatment. Two greatest risk factors for significant gastro duodenal bleeding are mechanical ventilation for greater than 48 hours or coagulopathy. Clinically, there is both under and over-utilization of H2 blockade and PPIs. Stress ulcer prophylaxis is associated with hospital-acquired pneumonia and gut dysbiosis in adults, but there is no such clear association with VAP in children. In fact, there are some small studies demonstrating that there is no increase in VAP. Enteral nutrition, on the other hand, does seem to be protective against clinically important GI bleeds and may help to prevent dysbiosis. Next, we'll turn to absorption in the GI tract. I'll go over some of the small intestinal structure. Within the small intestine are folds in the intestinal wall, and then within those folds are villi, which have a vascular supply with venule and arteriole and lymphatic lacteal, and then the epithelial cells on these villi then have microvilli and are bound together by tight junctions, which are the primary determinants of intestinal epithelial barrier function. The intestinal epithelium is the site of nutrient absorption. The purpose of villi and crypts and microvilli are to increase the surface area for absorption, and it does this very well. The surface area of the intestinal tract is the size of a tennis court or 250 meters squared. There are stem cells at the base of the crypts, and this is the source of renewal for the epithelial cells. The entire GI tract surface renews every seven days. The microvilli form a dense glycocalyx, also known as the brush border. It protects cells from enzymes, but also houses hydrolyzes and is the site of terminal carbohydrate digestion. Covering the villi is a mucus layer. Enterocytes have their apical surface covered by these transmembrane mucins and globlet cells that produce the secreted gel-forming mucins that form mucus. The small intestine has a single unattached mucus layer, and in the colon and stomach, there are two layers of mucus. In the colon, importantly, the outer mucus layer is the habitat for commensal bacteria. Even after short periods of enteral fasting, critically ill patients develop gut mucosal atrophy. This is a study of 15 critically ill patients as compared to 28 healthy controls. The median fasting period was four days. They measured the laculose mannitol tests, which is an assessment of gut epithelial permeability, and then do a adenal endoscopy with biopsy for histopathology. In the two pictures, on the left is the critically ill patient population where you see decrease in villus height and crypt death signifying gut mucosal atrophy, and on the right is preserved histopathology. They also identified altered gut permeability with abnormal laculose mannitol tests. Monosaccharide 3-O-methylglucose is used to assess the absorptive function of the small intestine. In this study of 28 critically ill patients, they were randomized to early antinutrition within 24 hours versus delayed where they were fasted for four days. The results were that gastric emptying was not significantly different between the groups. The 3-OMG absorption, again, a marker of the absorptive function of the small intestine, the peak and area under the curve were lower in the delayed group, and notably the length of stay and duration of mechanical ventilation were higher in the delayed group. The next topic is intestinal perfusion with a discussion of necrotizing enterocolitis and a brief review of the gut microbiome. The splanchnic circulation utilizes 20% of cardiac output. The liver does have a dual source of blood supply, venous from the portal and arterial from the hepatic circulation. The stomach, duodenum and rectum also have multiple collaterals. There is relative protection against ischemia in the splanchnic circulation. However, the splenic flexure is the watershed between the superior mesenteric artery and the inferior mesenteric artery and is high risk for ischemia. In terms of regulation, splanchnic vasoconstrictors are catecholamines, the endothelin-1, and splanchnic vasodilators are nitric oxide and prostaglandins. When we look at a portion of individual loop of bowel, so the top of this cartoon is the outside of the bowel and the bottom of the cartoon is the bowel lumen. So you have a small mesenteric artery piercing and then several generations of arterioles down to the mucosa and villus. This picture is a blown up view of the villus and crypt and you can identify the arteriole and venule and in green the lacteal circulating into the villus. There is within the villus countercurrent exchange of oxygen and a descending gradient of partial pressure of oxygen from the base to the tip. The degree of oxygen diffusion is flow rated and the pressure of oxygen at the tip of the villus is less than 10 millimeters of mercury with an increasing gradient down to the base with a partial pressure of oxygen of 85 millimeters of mercury. So then we think about the effect of glucose or a meal on splanchnic blood flow. In this study, they examined the change in splanchnic blood flow with oral versus IV glucose administration and at 15 and 30 minutes and subsequently, but the peak was at 15 and 30 minutes, there was a significant difference in splanchnic blood flow. Corresponding to this difference in splanchnic blood flow, when they examined changes in cardiac output in comparison with oral versus IV glucose administration at 15 and 30 minutes, there is an increase in cardiac output in response to oral glucose challenge. So splanchnic circulation during enteral nutrition can be compromised. In baseline settings, splanchnic blood flow increases by 40 to 60% with meals and with large meals, it can be up to double. There is redistribution of cardiac output to the splanchnic circulation after ingestion of a meal. Enteral nutrition also increases mucosal oxygen requirements and there is a corresponding increased mucosal permeability. The consequence we all fear when feeding patients who are hemodynamically unstable is that there may be steel from cardiac output and then subsequent intolerance or mucosal ischemia and in the worst case scenario, small bowel infarction. So now we will review the effect of inotropes and pressors on GI mucosal flow. Dobutamine is known to increase GI mucosal blood flow and gastric pH. Dopamine in septic shock patients decreases gastric pH and increases oxygen delivery, does cause precapillary basal constriction with diversion of blood flow away from the gut mucosa. Norepinephrine in septic shock increases gastric pH and splanchnic perfusion. In the setting of hypovolemia, it's associated with decreased mucosal blood flow. Epinephrine is known to decrease splanchnic blood flow and vasopressin in sepsis with intractable hypotension does increase arterial pressure but causes direct intestinal vasoconstriction which can be associated with severe gastric mucosal acidosis. It does appear to enhance pressor response to catecholamines. Necrotizing enterocolitis is a significant problem both in the neonatal ICU and PICU and cardiovascular ICU. It occurs in one in 1,000 life births. Incidence is highest in very low birth weight infants at 7% but elevated in patients with congenital heart disease such as truncus arteriosus and hypoplastic left heart syndrome, so ductal dependent lesions or in patients with periods of significant corporefusion. In prematurity is a clear risk factor. In term infants, necrotizing enterocolitis is seen in sepsis, hypotension, congenital heart disease. The pathogenesis is multifactorial and not elucidated at this point but seems to represent an overreaction of the immune system to an insult and that insult may be ischemia, infectious enteral feeds gut dysbiosis or response to bacterial translocation. In greater than 95% of the cases, it occurs after introduction of enteral nutrition which raises the question of infant formula potentially having harmful components versus human milk having bioactive protection. So presentation is typically feeding intolerance, increased gastric residuals, abdominal distension, bilious vomiting and then gross or occult blood in the stool. There can, patients may have abdominal tenderness, wall erythema or ecchymosis or palpable distended loops of bowel. In severe cases, patients may develop lethargy, apnea, bradycardia and temperature instability. Risk factors in the preterm gut include dysmotility of normal microbiota, decreased mucin barrier, increased gut permeability, reduced immune globulin and gut immunity, increased risk for ischemia and slow gastric emptying. Here's a closer look at the radiographic findings in necrotizing enterocolitis. These are two separate films taken at different times but both show evidence of necrotizing enterocolitis. The overall evaluation of these films reveals nonspecific elongated bowel loops which are indicative of a dysfunctional gut filled with air. On both films, you can find pneumatosis intestinalis. The arrows are pointing them out. It's more subtle on the left, seeing the air in the bowel wall. On the right film, it is more obvious with multiple areas of air in the bowel wall. And in that top arrow, what I'm trying to point out is that there is portal venous gas within the liver seen as darker central branching which is superimposed on the liver. Other signs of necrotizing enterocolitis include crescent shaped gas collections, an unchanged bowel gas pattern, free intraperitoneal gas or air for representing an occult perforation. This can be seen as regular sign which is a sharpening of the density around the bowel because of air existing in between bowel loops. The football sign you think, I think you're probably all familiar with which is sort of a impression of air in a large amount of free air in a supine film. I'll shift to discussion of the gut microbiome which has a variety of functions both locally within the GI tract and systemically and these functions are still being elucidated. But important to children is the development and training of the immune system, biosynthesis of vitamins, amino acids, metabolism of therapeutics, breaking down of food components and resistance to pathogens. What are the functional consequences of altered microbial community composition within the GI tract? Dysbiosis is common in adult and pediatric critical illness. It's demonstrated by decreased relative abundance of firmicutes and active bacteria and increased relative abundance of proteobacteria and bacteroidetes and characterized by a increase of pathogens and a decreased relative abundance of protected commensal organisms. So does this matter in our patient populations? That is being worked on and ultimately yet to be seen. So transient perturbations in microbiota development in infancy are linked to adult diseases and dysbiosis is associated with longer length of stay and worse severity of illness in children. And there are ongoing investigations to identify a link between dysbiosis and necrotizing enterocolitis. What happens to the gut microbiome during pediatric critical illness? There is disruption of the microbiota across multiple body sites in critically ill children. So there is dysbiosis of the GI tract, skin and oral compartment. In this study, they compared pediatric ICU patients to healthy pediatric controls and to the human microbiome project. What they identified was that in pediatric critical illness, there is the identification of a dominant pathogen. So a dominant organism within the gut microbiome that is a pathogen and then loss of site specificity such that the oral samples were starting to look more like the GI tract. Which was concerning in terms of the overall development risk for VAP. So question, factors that might increase the risk of developing necrotizing enterocolitis in preterm infants includes a low energy density formula, use of specialized elemental semi-digested preterm enteral formula, duct dependent lesions or exclusive use of human milk and human milk based fortifiers. The answer is duct dependent lesions. Next, we'll move to common GI abnormalities. First, we will go over intestinal obstruction. So here's another question. This chest radiograph was obtained in this newborn infant due to failure to advance the NG tube. Which of the options below is the most likely diagnosis? So you see the NG tube coiled in what looks like probably the upper esophagus. This x-ray represents esophageal atresia with distal fistula. And in the subsequent slides, we'll describe why. Here is an NG tube. It abruptly ends within the esophagus. Notice there is no gastric bubble. This is isolated esophageal atresia. There is an absent gastric or fundic air indicating that there's no tissue. Here is a cartoon of the different types of esophageal atresia. The most common type is esophageal atresia with distal fistula. And the subsequent types are all far more or less common with pictures and diagrams listed, as you can see. Hypertrophic pyloric stenosis occurs in 3 in 1,000 live births with a male-to-female ratio of 5 to 1. Typically, it's diagnosed between 2 to 8 weeks of age, but can be diagnosed up to 6 months of age, and it is associated with other abnormalities such as esophageal atresia, T.E. fistula, renal abnormalities, Turner syndrome, and trisomy 18. Typically, presentation is with non-bilious projectile vomiting in a palpable mass, although this mass in an active infant is likely very difficult to feel. You can observe a parasaltic wave, and there's the classic presentation of severe hypochlorimic alkalosis. Surgical treatment with pyloroplasty is treatment of choice, and on a radiograph, you see here on the left the typical single bubble sign of dilated stomach. In this fluoroscopy study, the patient is positioned left side down and oblique. If that kind of helps orient you to the picture, on the top of the picture is the esophagus entering the stomach. I've outlined the hypertrophy pylorus, and you can see faintly the narrowed canal and then contrast within the duodenal bulb, which creates this mushroom appearance or Kirkland sign. In duodenal atresia, we see on the x-ray this flat abdominal film shows the classic double bubble sign of duodenal atresia. Duodenal atresia reflects obstruction in the second portion of the duodenum, which is why you see this bilious vomiting occur. It is diagnosed in 1 in 10,000 life's births, often prenatally diagnosed in the United States. The ampulla vauter is the typical site of recanulation failure, and there may be associated disorders such as Down syndrome, malrotation, heart disease, renal anomalies, T.E. fistula, bacterial, and treatment is surgical. So this is sort of a, what do you think is going on in this one? It's a little bit of a trick, because this is a normal bowel gas pattern. There are no descended loops, there are no arid fluid levels, there are no masses, no areas of paucity of gas, there is normal stool content in the colon, and no extraluminal free air. Hopefully you can adjust the contrast on your computer to kind of see all of that. This film is an obviously abnormal flat plate abdomen. The first questions we'll ask ourselves is, is there free air as evidenced by pneumatosis, portal venous error, air under the diaphragm, air between bowel loops, etc. The dilated bowel is so descended that it is anonymized with loss of characteristics, smaller large bowel markings. You have an NG tube in place so you can determine position of the stomach and can visualize a stomach bubble. This is actually a case of intussusception. Intussusception is the telescoping of one segment of bowel into another, typically three months to two years when it's diagnosed. It can occur after viral illness with Peyer's patches acting as the lead point. The lead point can also be tumor, inspasated feces, lymphoma in older children. It typically presents with crampy abdominal pain or emesis, can have bloody stools or at least may be absent. Ultrasound is really the imaging of choice for diagnosis. The image on the top left is an upper GI with water soluble contrast and identifies a mass in the bowel. This is evidenced by the look of sort of a shoulder hump, shoulder outline by contrast. There is a hint of a target sign or bowel within the bowel creating a functional obstruction. Patients may also present with altered mental status that waxes and wanes with irritability, Patients may also present with altered mental status that waxes and wanes with irritability, if severe or prior to your reduction. Typically, you're going to treat with an air enema reduction and then surgically if it's not reducible. So, radiographic signs of intussusception. This is another film, a plane x-ray of intussusception in a two-month-old female. Additional radiographic signs of intussusception include the target sign, which I've drawn here on the picture, the crescent sign, which I've also drawn on the right. There can also be the absent liver edge sign, also called absence of the sympathetic angle. There could be bowel obstruction and in turn, the x-ray can also be completely normal. Air contrast enema will typically have this, I put the arrows here, this coiled spring appearance at the site of intussusception. And here is a series of fluoroscopy pictures showing you the air enema reduction of intussusception. There's the progression from picture A, B to C with the air un-telescoping the bowel. In C, you can see air passing through the previously obstructive segment all the way into the small bowel. In Hirschsprung's disease, this is aganglionosis of the colon or failure of normal cranial-clonal migration. of ganglion cells. There is typically a transition site. In this abdominal film, you see proximal colonic distension as a result of a partial functional obstruction, which is the agangliotic segment of the colon. The rectosigmoid ratio is abnormal, although the rectum may be normal appearing in 33% of cases. The incidence is 1 in 5 to 8,000 births. And then the classic presentation is failure to pass meconium at 24 hours or later and treatment is a surgical pull-through. So here is a case. This is a three-week-old infant who presents with acute onset bilious vomiting, abdominal distension, and a GI contrast study is obtained with two key images above with red arrows that maybe your radiologist has added in there for you. The infant continues with symptoms now with tachycardia, cool extremities, and hypotension. Here's the next question. Initial management of this infant must include one, fluid resuscitation, NPO, IV antibiotics, serial examinations, two, air enema, three, CT scan with contrast, or four, emergent surgical consult for XLAP due to risk of bowel necrosis. The answer is number four, emergent surgical consult for XLAP and risk of bowel necrosis. This was a case of midgut lobulus and is a surgical emergency due to risk of bowel necrosis. So midgut malrotation represents failure of normal embryonic rotation of the bowel. The duodenal-jejunal junction does not reach its intended location to the left of the spine. And the small bowel is then suspended on a narrow vascular pedicle, which then normal peristalsis can cause it to twist and turn around that pedicle and at some point, cause twisting such that there is vascular compromise. If we go back to the original images, then you can look back to see that the duodenal-jejunal junction is to the right of the spine. You're missing the typical sweep down and to the left side of the body of the second and third portions of the duodenum. Most of the small bowel is on the right side of the abdomen. And on the right-sided picture, the arrows are pointing at the fact that the cecum is in an abnormal location in the mid-pelvis. Next, we will talk about bleeding. This is a pretty typical differential diagnosis list for the causes of upper GI bleeding by age and anatomical location. In infants, the causes are not that varied. In the stomach, you can see gastritis from stress and then variable locations due to vitamin K deficiency or sepsis trauma from NG2 placements, for example, and cow milk protein allergy. At two to five years of age, the etiologies are slightly more varied. Within the esophagus can be esophagitis, varices, or Malory-Weiss tears. In the stomach can be gastritis or gastric ulcers or varices. And in the duodenum, duodenitis or a duodenal ulcer. And then in variable locations due to caustic ingestions, foreign bodies, or NSAID use. In older children, esophagitis in the esophagus or Malory-Weiss tears or varices. In the stomach can have a Julephoid lesion or portal hypertensive gastropathy or hemophilia. And then in variable locations, there can be polyps that could cause bleeding, Crohn's disease, telangiectasias, aortoenteric fistulas, coagulation disorders, caustic injections, and foreign bodies and NSAID use. Here is a similar table for causes of lower GI bleeding by age. So in infants, nonspecific colitis, anal fissures can cause lower GI bleeding as well as milk allergies, duplication of bowel or volvulus. Hirschsprung's disease can also be a cause for lower GI bleeding, necrotizing enterocolitis, or an underlying bleeding diathesis. At two to five years of age, polyps, or anal fissures, or infectious enterocolitis, intussusception, and Meckel's diverticulum. There can be systemic diseases like Henoch-Schollen-Purpura or Hemolytic Uremic Syndrome. We can see lymphonodular hyperplasia or angio-dysplasia. In older kids, anal fissures continue to be a potential cause of lower GI bleeding as well as infectious enterocolitis and polyps. Inflammatory bowel disease becomes more common, and we can see lymphonodular hyperplasia here as well, in addition to Henoch-Schollen-Purpura and angio-dysplasia. We also see lower GI bleeding due to Hemolytic Uremic Syndrome and underlying bleeding diathesis. I want to specifically cover Meckel's diverticulum. It is an incomplete obliteration of the vitiline duct, so the omphalo-mesenteric duct. It is in two to three percent of the population, and it is the most common GI abnormality. And it follows the rule of twos, which you probably remember from training previously. So it's in two percent of the population. Two percent are symptomatic. Symptomatic usually before age two, located within two feet of the ileocecal valve, length of two inches. Patients typically present with bleeding because of ectopic gastric mucosa within the Meckel's that causes focal inflammation or perforation or intussusception. We diagnose Meckel's using nuclear scintigraphy, doing a technetium-99 protectonate scan. It demonstrates accumulation of radioactivity in the right lower para-umbilical region, and this is consistent with the most frequent location of Meckel's diverticulum. The time course pattern of radioactive accumulation in possible Meckel's mirrors the pattern of tracer concentration in the gastric region, which you can see in these pictures here, and the arrows indicating the Meckel's. Now I'll shift to discussion of GI bleeding. So management of significant GI bleeding involves initial stabilization. Localization attempts are not always successful. The presentation and initial management in the setting of black tarry stool stool may be an upper GI bleed, which is defined as proximal to the ligament of trites. Patients may have hemodynamic instability, may be orthostatic, or have supine hypotension. The presence of abdominal tenderness should raise a concern and evaluation for perforation. NG lavage can help determine the localization of the bleed. If it's fresh blood or coffee ground that may represent an upper GI bleed. So you can localize upper GI versus lower GI bleeding. It can be falsely negative if there is transient or post-pyloric bleeding. And then also looking at the CBC to assess for normal or microcytic anemia. Look at chemistries, coagulopathy, liver function tests, and type and cross the patient as they may need blood. Management of brisk upper GI bleeding requires resuscitation, placement of two large for peripheral IVs, fluids, and likely packed for blood cells. Typically we follow serial hematocrit, correct any coagulopathy of present by providing plasma and platelets and obtain a pediatric GI consult typically. With regard to the role of urgent upper GI endoscopy, NASPGN has issued a statement. So after initial stabilization, efforts have been initiated. Endoscopy should be considered for active recurrent hemodynamically significant GI bleeding. It may allow differentiation between variceal and non-variceal bleeding and help definitive therapy. So treatment in the setting of varices involves ligation, band ligation of varices, clips or cautery, or local vasopressin or epinephrine for identified bleeding vessels. There can be excision of bleeding polyps, although endoscopy is generally contraindicated if perforation is suspected. Further treatment involves acid suppression with proton pump inhibitors such as omeprazole or a histamine antagonist. At times treatment with somatostatin or arctreotide coverage for gram-negative organisms out of concern for gut translocation. And then a small bowel tube or foley in infants can be used to try to tamp a non-suspected esophageal variceal bleeding, but there is risk of esophageal perforation or aspiration with its use. A surgical consult may be needed for suspected intestinal necrosis of alveolus or Meckel's and for patients with end-stage liver failure they may be candidates for TIPS procedure. Our next two topics are pancreatitis and intra-abdominal hypertension and abdominal hypertension. Acute pancreatitis occurs when enzymes such as amylase and lipase which are normally secreted by acinar cells of the exocrine pancreas into the duodenum are released into the circulation due to pancreatic damage. Consensus criteria are developed for the diagnosis of acute pancreatitis requiring two of the following. One, abdominal pain compatible with acute pancreatitis. Two, serum amylase or lipase greater than or equal to three times the upper limits of normal and imaging findings of acute pancreatitis. With regard to etiology in children, the majority, the greatest etiology is idiopathic with 24 percent, then trauma and systemic illness and structural abnormalities in decreasing frequency. Drugs are implicated with the greatest players being valproic acid, L-asparaginase, prednisone, and 6-MP, and then infectious etiologies at eight percent with viruses listed there. Of note in the idiopathic category many of these are presumed to be due to a viral illness. There is a consensus statement regarding determination of severity of acute pancreatitis and here is the decision algorithm. So first is diagnosis of acute pancreatitis by inspired criteria and then it's really based on the determination of organ dysfunction. If there is organ dysfunction and it has been present for less than 48 hours then it is moderately severe acute pancreatitis and if you have organ dysfunction greater than 48 hours it's classified as severe acute pancreatitis. In the absence of organ dysfunction then the decision tree is determined by any local pancreatic or systemic complications or exacerbation of prior comorbid disease. If these are present then it is categorized as moderately severe acute pancreatitis and if these are absent then it's mild acute pancreatitis. Predictors of poor outcome include age less than seven years, weight less than 28 kilos, a white blood cell count of greater than 18.5, LDH greater than 2000, and then during the initial 48 hours a serum calcium less than 8.3, an albumin less than 2.6, fluid sequestration greater than 75 mils per kilo or a BUN greater than five. In the setting of severe pancreatitis consensus recommendations for diagnosis include the previously described inspired criteria and that initial imaging be via transabdominal ultrasound. The first time diagnosis should include liver enzymes triglyceride level and calcium level. In terms of the underlying pathogenesis the thought is that is the progression to severe forms is secondary to altered microcirculation of the pancreas which is a result of hypovolemia and microthrombi and that fluid resuscitation may improve both hypovolemia and limit microthrombi formation. Consensus guidelines for the management of acute pancreatitis recommends initial conservative therapy with initial crystalloid fluid resuscitation with 10 to 20 mls per kilo and then maintenance fluids delivered at 1.5 to twice the usual maintenance rate, oxygen as needed, and analgesia for pain. There is some controversy regarding analgesic choice because morphine had in the past been reported to cause sphincter of od dysfunction but in fact no clear evidence exists to support this theory and in the consensus guidelines and in prior literature morphine can be used safely in patients with acute pancreatitis. Meparidine has been used successfully in the past but has the drawbacks of a short half-life and the potential for neurotoxicity. So in the guideline the consensus statement is that opioids can be used for acute pancreatitis pain when not responding to acetaminophen or NSAIDs. In terms of the workup and management if the patient has infected necrotizing pancreatitis recommendation is to initiate antibiotics typically carbapenem times 14 days and the patient may need percutaneous ultrasound or CT guided fine needle aspiration with interventional radiology. Surgical treatment is actually best done in a delayed fashion for at least four weeks after initial diagnosis as this delayed treatment is associated with improved outcome. For biliary pancreatitis with cholangitis or persistent jaundice the recommendation is for endoscopic sphincterotomy. With regard to nutritional support during acute pancreatitis enteral nutrition is thought to decrease complications of acute pancreatitis. It is typically in practice provided via the NJ route with a polymer formula with parenteral nutrition reserved only in the setting of prolonged fasting due to ileus complex fistulae or the development of abdominal compartment syndrome. That's a great introduction into our next topic of abdominal compartment syndrome. First we will review the pathophysiology. So typically ACS occurs after fluid resuscitation for critical illness and in a patient with total body fluid third spacing edema this leads to then elevated intra-abdominal pressure due to bowel edema with then being a cable compression from the increased abdominal contents then reduced blood return to the heart in the form of preload, reduced cardiac outputs, reduced blood flow to distal organs, and then potentially multi-system organ failure for within the organs of the body. The upward movement of the diaphragm results in bibasal or atelectasis and ventilation perfusion mismatch for the cardiovascular system. There are negative effects on preload, afterload, and contractility. There is activation of the renin, angiotensin, and aldosterone pathway leading to secretion of catecholamines which impacts afterload. There is also direct compression of the RV and LV such that end diastolic volumes and compliance are reduced. There is false elevation of CVP and wedge pressures as well. Renal dysfunction is due to the two mechanisms of decreased cardiac output with stimulation of the renin, angiotensin, and aldosterone system and also due to direct renal compression. There is now a specific definition for ACS in children so intra-abdominal hypertension is a sustained or repeated elevation of intra-abdominal pressure greater than 10. Grades 1, 2, 3, and 4 are described and then abdominal compartment syndrome is described as a sustained elevation intra-abdominal pressure greater than 10 associated with new or worsening organ dysfunction that can be attributed to elevated intra-abdominal pressure. Abdominal compartment syndrome is further classified as primary, secondary, or recurrent. Primary is a condition associated with injury or disease in the abdominal pelvic region. Secondary refers to conditions that do not originate from the abdominal pelvic region and recurrent refers to the condition in which IAH or ACS redevelops following prior surgical or medical treatment of primary or secondary IAH or ACS. The way we typically evaluate for intra-abdominal hypertension is with bladder pressure monitoring using a similar system to what is described in this cartoon. Measurements are expressed in millimeters of mercury and measured at end expiration with the patient in supine position. They are zeroed at the iliac crest in the mid-axillary line and the installation volume is no greater than 25 mils of saline or 1 ml per kilo for kids under up to 20 kilos and then measured 30 to 60 seconds after installation to allow for bladder detrusor muscle relaxation and measure the absence of active abdominal muscle contractions. With regard to ACS prevention and treatment is to first recognize this is a problem so measure intra-abdominal pressure in at-risk patients. Normal bladder pressure in mechanically ventilated children is 7 plus or minus 3 millimeters of mercury. ACS is an under-recognized phenomenon in children and then protocolized monitoring and management with particular attention to fluid balance and prevention of fluid overload in patients at risk. Evacuation of intestinal intraluminal contents and extraluminal contents to elevate the head of the bed and consider neuromuscular blockade. Consideration of percutaneous peritoneal catheter drainage may prevent ACS from developing and for overt cases of ACS the treatment is decompressive laparotomy. Mortality is variably reported at 16 to 100 percent. I'd like to thank you for listening to this talk and I have listed my email below if there are any questions. Thank you.

Dr. Katri Tippo

pediatric critical care

gastrointestinal abnormalities

anatomy and physiology

common GI abnormalities

diagnostic features

gastric motility

pediatric critical illness