tube with normal saline lavage can be diagnostic If physical examination findings reveal significant abdominal tenderness with guarding or rebound tenderness, plain radiographs of the abdomen including an upright view should be obtained to evaluate for perforation or secondary bowel obstruction IV access should be obtained in all patients who have significant emesis, dehydration, weight loss, or concerning abdominal examination findings An initial bolus of isotonic fluid (20 mL/kg) should be given and vital signs monitored frequently, with additional boluses given as needed to achieve hemodynamic stability An upper GI series is not recommended for the routine evaluation of PUD given its relatively poor sensitivity However, it may be useful in diagnosing children with gastric outlet obstruction secondary to PUD Practice guidelines by the North American Society for Pediatric Gastroenterology, Hepatology, and Nutrition (NASPGHAN) recommend initial diagnostic H pylori testing with positive histopathology on EGD plus a positive rapid urease test or a positive culture Culture of the organism may assist in the determination of appropriate antibiotic therapy, particularly in communities where antibiotic resistance is high Serologic tests based on the detection of antibodies (IgG, IgA) against H pylori in serum, whole blood, urine, and saliva are not reliable for use in the clinical setting These noninvasive H pylori tests are not recommended for initial H pylori diagnosis; however stool antigen testing or 13C-urea breath testing can be used to assess the outcome of H pylori treatment weeks after completion therapy A number of approaches are available for the treatment of PUD Therapies can be categorized as those that neutralize acid (i.e., antacids); those that block acid secretion; those that are cytoprotective; and the anti-infective treatments (e.g., H pylori regimen) Antacids are a low-cost, safe, primarily short-term means of treating PUD in children They can be prescribed for patients of any age Adverse effects of antacids are related to the metal ion present in the preparation: Magnesium-containing products may cause diarrhea, whereas aluminum-containing products may cause constipation Some products are available as a combination of the two to minimize these effects The usual dosage for children is 0.5 mL/kg, given hour after eating and before going to the bed Patients with food-related or nocturnal abdominal pain without associated signs of serious illness can be started on empirical therapy with antacids, and followed by a primary care physician H2 -receptor antagonists (e.g., ranitidine or famotidine) are used to block acid secretion and treat ulcer disease Alternatively PPIs (e.g., omeprazole or lansoprazole) can be used and are more effective at decreasing gastric acid secretion than H2 -receptor antagonists PPIs should be used in patients with anemia or who have moderate to severe PUD Potential short-term adverse effects with PPI usage include headache, abdominal pain, diarrhea, nausea, and vomiting When initiating therapy, follow-up is important, as is providing a sufficient quantity so that the child can take the medication until the outpatient visit has occurred Sucralfate (40 to 80 mg/kg/day by mouth every hours) is a sucrose sulfate and aluminum hydroxide salt that creates a gel over the mucosal surface and insulates the gastric mucosa from further damage by acid, pepsin, or bile It is recommended to be given on an empty stomach hour before meals and at bedtime, and not given at the same time as other medications given its ability to bind them Current protocols for first-line therapy for H pylori include a PPI plus two antibiotics (choosing two of the following: amoxicillin, clarithromycin, or metronidazole for 10 to 14 days) Compliance is an important consideration because it is a major determinant of the success of treatment Antibiotic susceptibility testing for clarithromycin is recommended before initial clarithromycin-based triple therapy in areas/populations with a known high resistance rate (>20%) as this will adversely affect eradication rates MALLORY–WEISS TEARS/PROLAPSE GASTROPATHY Mallory–Weiss tears are mucosal lacerations of the distal esophagus and proximal stomach induced by forceful retching Patients typically present with a recent history of repeated vomiting prior to onset of the hematemesis and less frequently, with pain from the tear While the amount of blood can vary, Mallory–Weiss tears usually are self-limited and not require any medical or surgical intervention Upper GI bleeding after retching or vomiting may also be due to prolapse gastropathy, when the stomach prolapses through the lower esophageal sphincter causing mucosal injury Management is generally conservative with antiemetic therapy, PPI, and observation LOWER GI BLEEDING Inflammatory Bowel Disease Goals of Treatment The goals of emergency therapy include initial supportive care and the identification of any IBD complication These complications may include perforation, intra-abdominal or perirectal abscess, toxic megacolon, severe anemia, electrolyte imbalances, superinfection, and dehydration In severe cases initial supportive care may include rehydration, addressing electrolyte abnormalities, and packed red blood cell transfusions Diagnostic tests to assess the presence and/or severity of the disease include laboratory markers, stool testing, and radiologic imaging Communication with gastroenterologists and, when needed, surgeons helps to ensure efficient and directed care CLINICAL PEARLS AND PITFALLS Lower GI bleeding in a child with IBD should not immediately be attributed to a flare of the chronic underlying disease as these children often receive immunosuppressive therapies and are at high risk for infections (e.g., Clostridium difficile ) In an ill-appearing child with Crohn disease and fever, the clinician should consider intra-abdominal abscess and perforation in the differential diagnosis Children with IBD may have extraintestinal manifestations including arthralgia, arthritis, muscle diseases, erythema nodosum, and ocular manifestations such as uveitis Narcotic and anticholinergic usage should be avoided when possible in children with IBD colitis to avoid toxic megacolon Pancreatitis should be considered with acute worsening of abdominal pain in children with IBD, particularly those on thiopurine (e.g., azathioprine or 6-mercaptopurine) therapy Current Evidence IBD is primarily used to describe two chronic lifelong intestinal disorders: (i) ulcerative colitis (UC), characterized by inflammation and ulceration confined to the colonic mucosa; and (ii) Crohn disease, manifested by transmural inflammation that may affect any segment of the GI tract The incidence of IBD, particularly of Crohn disease, has been increasing in children and adults with an estimated 1.17 million Americans having IBD The etiology of IBD is unclear but is thought to result from a confluence of host genetic makeup and environmental factors One of the most important risk factors is a family history of the disease IBD likely results from the inappropriate and ongoing activation of the GI mucosal immune system driven by the presence of normal bacterial flora Growth failure is common in children with IBD The cause of growth failure in patients with IBD is multifactorial, but inadequate nutrient intake is most likely the final common pathway Malabsorption, especially with small bowel involvement of the disease, may also occur and micronutrient deficiencies may result in part from the area of intestine affected (e.g., duodenal inflammation is associated with iron deficiency) Hematochezia, proteinlosing enteropathy, and increased fecal losses of cellular constituents result from chronic inflammation and damage to the intestinal mucosa The cause of diarrhea is also multifactorial, resulting from extensive mucosal dysfunction, bile acid malabsorption in terminal ileal disease, bacterial overgrowth secondary to strictures and disordered motility, and protein exudation from inflamed surfaces Extraintestinal manifestations of the disease may be related to the activity of the IBD (e.g., oral manifestations) or may typically a run an independent course (e.g., hepatobiliary disease) Clinical Considerations Clinical Recognition Clinical manifestations of IBD can be varied and related to either GI inflammation or the development of either GI tract or extraintestinal manifestations Many clinical features are common to both UC and Crohn disease, including diarrhea, GI blood and protein loss, abdominal pain, fever, anemia, weight loss, and growth failure Children with UC are more likely to present with rectal bleeding, diarrhea, and tenesmus In contrast, children with Crohn disease are more likely to present with chronic abdominal pain, weight loss, and failure to thrive Perianal disease, including fissures, skin tags, fistulae, and abscesses, occurs in 15% of children with Crohn disease but not in UC Perianal disease may precede the appearance of the intestinal manifestations of Crohn disease by several years Extraintestinal manifestations involving the joints (arthritis), skin (erythema nodosum), eyes (uveitis), and liver (chronic hepatitis or sclerosing cholangitis) are seen with both disorders, although they are generally more common with Crohn disease ... PPI, and observation LOWER GI BLEEDING Inflammatory Bowel Disease Goals of Treatment The goals of emergency therapy include initial supportive care and the identification of any IBD complication