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864 SECTION 12: Pediatrics Acute causes include dehydration, electrolyte abnormalities (hypercalcemia or hypokalemia), or drug ingestions. Constipation may still be present with a recent, watery bowel movement if the child is passing soft stool around a mass of hard stool. Pencil-like stools suggest a stricture. Spasticity or delayed motor milestones may be signs of occult spinal dysraphism. Toilet training is a common inciting event for functional constipation. While constipation may be very painful, it should not cause an ill or toxic appearance. The abdomen may be distended, and firm columns of stool may be felt in the descending and ascending colons. A rectal exam with an empty vault and increased sphincter tone that emits a burst of gas on insertion of a finger suggests Hirschsprung’s disease. Examine the anal and sacral area for tufts of hair, dimples, and lipomas, which may suggest neurologic malformations including spina bifida and tethered cord. 66 An anteriorly displaced anus (more than two thirds the distance from the coccyx to the scrotal-perineal junction in males and the posterior four chette in females) should prompt outpatient surgical referral. Check lower extremity tone, reflexes, and gait for signs of spasticity. Botulism may present as a hypotonic child with constipation. Fissures may cause painful defecation, leading to a cycle of retention and functional constipation.  TREATMENT If the constipation is presumed to be causing acute pain, the physician may wish to treat in the ED with response guiding further evaluation (Table 133-5). 67,68 Oral polyethylene glycol is as effective as enemas for outpatient treatment. Children with constipation refractory to ED management may require hospitalization for polyethylene glycol by nasogastric tube. REFERENCES The complete reference list is available online at www.TintinalliEM.com. TABLE 133-5 Treatment of Constipation in Children •   Dietary management: Fruits, vegetables, avoidance of processed foods, water or nonsugar fluids to avoid dehydration. •   Glycerin suppositories: ED treatment of constipation in infants <2 years; 1 suppository × 2. •   Normal saline enemas: ED treatment of acute constipation; 0–6 months, 120–150 mL; 6–18 months, 150–250 mL; 18 months–5 years, 300 mL. Enemas are most effective when held as long as possible. •   Sodium phosphate enemas: ED treatment of acute constipation in children 2–11 years, 2.25-oz pediatric enema. Children >11 years, 4.5-oz adult enema. May repeat. •   Polyethylene glycol (PEG): Initial treatment 1–1.5 grams/kg/d divided to two to four times per day for 3 days. Then decrease to 0.78 gram/kg/d divided daily or twice daily for maintenance therapy. Inpatient treatment for cleanout by nasogastric tube with PEG plus electrolyte solution is 14–40 mL/h. Gastrointestinal Bleeding in Infants and Children Sarah M. Reid INTRODUCTION AND EPIDEMIOLOGY GI bleeding varies in its epidemiology and presentation depending on whether it originates from the upper or lower GI tract. Upper GI (UGI) bleeding is bleeding proximal to the ligament of Treitz, whereas lower GI (LGI) bleeding originates distal to this ligament. A recent study demonstrated a 14% increase in pediatric GI bleeding associated ED visits between 2006 (82/100,000 children) and 2011 (94/100,000 children). 1 In CHAPTER this sample, 20% of visits were for UGI bleeding, 30% were for LGI bleeding, and the remainder were unspecified.

ng originates distal to this ligament. A recent study demonstrated a 14% increase in pediatric GI bleeding associated ED visits between 2006 (82/100,000 children) and 2011 (94/100,000 children). 1 In CHAPTER this sample, 20% of visits were for UGI bleeding, 30% were for LGI bleeding, and the remainder were unspecified. More than three-quarters (81%) of the patients were discharged home from the ED. The signs and symptoms of GI bleeding in children vary and include the following: bright red blood in small strands or clots in emesis or bowel movements, vomiting of gross blood (hematemesis), black tarry stools (melena), or the passage of bright red or marooncolored blood from the rectum (hematochezia). Occult bleeding may result in unexplained pallor, fatigue, and anemia. Severity is assessed by vital signs, physical appearance, and the hemodynamic status of the patient, all of which lead to an estimation of the vol ume of blood loss. Worrisome symptoms and signs include pallor, diaphoresis, lethargy, abdominal pain, tachycardia, hypotension, and altered mental status. GI bleeding can be life threatening. Advances in endoscopy and radiology and newer therapeutic modalities have helped identify the causes of bleeding more accurately and have pro vided more treatment options. CLINICAL APPROACH Assess bleeding and institute resuscitation if the child has signs of hemorrhagic shock. Next, obtain a history and perform a physical examination, and try to establish the level of bleeding as UGI or LGI, because the subsequent diagnostic and treatment steps differ. Then, narrow the differential diagnosis based on history, physical examination, laboratory studies, and the categorization of age-related causes of UGI and LGI bleeding. The presence of any one of melena, hematochezia, unwell appearance, or moderate to large volume of fresh blood in the vomitus was associated with a clinically significant UGI bleed (defined as a hemoglobin drop of >20 g/L, need for blood transfusion, need for emergent endoscopy, or need for surgical procedure).  ASSESS BLEEDING AND BEGIN RESUSCITATION There are several important questions to consider. Is the patient stable or unstable? Is this really blood, and is it coming from the GI tract? Is it a small amount of blood or a large volume? Has the child had prior episodes of bleeding, and if so, do the parents know the cause and prior treatment?  IS THE PATIENT STABLE OR UNSTABLE? The presence of tachycardia, pallor, tachypnea, prolonged capillary refill time, altered mental status, metabolic acidosis, and/or hypoten sion indicates significant GI bleeding. Tachycardia and tachypnea are the first clinical signs, followed by delayed capillary refill, decreased urine output, altered mental status, metabolic acidosis, and pallor. Orthostatic changes in heart rate and blood pressure indicate that sig nificant bleeding has occurred. Hypotension is a late sign and indicates uncompensated hemorrhagic shock. Any signs of hemorrhagic shock require simultaneous resuscitation, diagnosis, and treatment. Maintain the airway, monitor oxygen saturation and provide oxygen, place two large-bore IVs (20 gauge or larger), and administer boluses of crystalloid and, if necessary, blood products.  IS THIS REALLY BLOOD? Determine whether or not the vomit or stool really contains blood. Beets, food coloring, and fruit juices can look like blood. Black and tarry stools can result from vitamins with iron, bismuth (Pepto- Bismol ® ), spinach, cranberries, blueberries, or licorice. Urinary (urate) crystals in the neonatal diaper are often orange in color and may be interpreted by a caregiver as blood. The Gastroccult ® and Hemoccult ® tests (Beckman Coulter, Brea, CA) can be used to document the pres ence of blood in gastric contents or stool, respectively.

cranberries, blueberries, or licorice. Urinary (urate) crystals in the neonatal diaper are often orange in color and may be interpreted by a caregiver as blood. The Gastroccult ® and Hemoccult ® tests (Beckman Coulter, Brea, CA) can be used to document the pres ence of blood in gastric contents or stool, respectively. These guaiacbased tests rely on the peroxidase activity of the heme portion of hemoglobin. False-positive results are associated with foods that have peroxidase activity such as red meat, melons, grapes, radishes, turnips, cauliflower, and broccoli. False-negative results can result from the ingestion of vitamin C due to its antioxidant properties. Newer guaiac kits have improved specificity. Tintinalli_Sec12_p0669-0996.indd 864 8/2/19 7:53 PM

d with foods that have peroxidase activity such as red meat, melons, grapes, radishes, turnips, cauliflower, and broccoli. False-negative results can result from the ingestion of vitamin C due to its antioxidant properties. Newer guaiac kits have improved specificity. Tintinalli_Sec12_p0669-0996.indd 864 8/2/19 7:53 PM CHAPTER 134: Gastrointestinal Bleeding in Infants and Children 865  IS BLOOD COMING FROM THE GI TRACT? Evaluate the child for epistaxis, recent dental work, or gingival bleeding, because swallowed blood may lead to hematemesis. The neonate can swallow maternal blood during delivery or from breastfeeding if the mother has fissures on her nipples. In the toddler, blood could come from an injury to the oropharynx or nose. Make sure that blood does not originate from the throat or lungs. Distinguish whether the blood in the diaper is from a GU or GI source. Examine the perineum and ure thra. Neonatal girls may develop some vaginal bleeding from maternal hormone withdrawal.  IS IT A SMALL OR LARGE AMOUNT OF BLOOD? It is difficult to gauge the amount of bleeding from caretaker descrip tions, because even small amounts of blood can appear alarmingly large. Assess the clinical status of the patient, vital signs, results of laboratory studies, and results of serial clinical examinations to determine the amount of bleeding. The hemoglobin and hematocrit are unreliable indicators of blood loss in the early stages. See Tables 134-1, 134-2, and 134-3 for potential recurrent causes of GI bleeding organized by age and symptoms. 4,5  HISTORY Ask whether the child had prior episodes of bleeding. If so, ask whether the caregivers know the cause and prior treatments. There are many causes of UGI and LGI bleeding in children, and the causes vary sig nificantly by age (Tables 134-1 and 134-2). In addition to the age-based approach to the differential diagnosis of GI bleeding, the clinical pre sentation and constellation of associated symptoms are often useful in narrowing the differential diagnosis for a particular child. Table 134-3 describes symptom complexes along with the differential diagnosis of GI bleeding. The type and implications of questioning differ depending on the age of the child (Tables 134-1 and 134-2). If the child is verbal, obtain the history from both the child and the parent or caregiver. Elicit an accurate chronology of events, and ask questions to help frame the differential diagnosis (Table 134-4). Vomiting of bright red blood or coffee-ground emesis is the classic presentation of UGI bleeding. Bloody diarrhea and bright red blood mixed with or coating normal stool are the classic presentations of LGI bleeding. Hematochezia, melena, or occult GI blood loss could represent UGI or LGI bleeding.  PHYSICAL EXAMINATION Obtain vital signs and pulse oximetry. Assess the airway, breathing, and circulation of the patient. Perform a complete physical examination. Gain the confidence of the child before any painful examination or procedures are performed. Examine the nose for any signs of epistaxis and the oral pharynx for any signs of injury, infection, bleeding, or ulcers. Examine the skin for bruises or petechiae (a sign of coagulopathy), jaundice and abnormal venous pattern on the abdomen that would point toward liver disease, cutaneous vascular malformations that may signal lesions of the GI tract, or the palpable purpura associated with Henoch- Schönlein purpura. Allow the young child to rest on the caregiver’s lap while examining the abdomen. Start with visual inspection, then auscultate for bowel sounds, and finally, palpate the abdomen for tenderness, guarding, rebound, rigidity, organomegaly, ascites, or masses.

he palpable purpura associated with Henoch- Schönlein purpura. Allow the young child to rest on the caregiver’s lap while examining the abdomen. Start with visual inspection, then auscultate for bowel sounds, and finally, palpate the abdomen for tenderness, guarding, rebound, rigidity, organomegaly, ascites, or masses. External examination of the anus and digital rectal examination are necessary to identify fissures, skin tags, fistulae, hemorrhoids, polyps, and impacted stool and to test for fecal blood.  DIAGNOSIS Try to determine if the source of bleeding is UGI or LGI. In cases where it is unclear if UGI bleeding is occurring, consider nasogastric lavage. Nasogastric lavage is performed with a 12-French nasogastric tube in small children and a 14- to 16-French tube in older children. Instill 50 mL of warmed saline for infants and 100 to 200 mL for older children TABLE 134-1 Age-Based Causes of Upper and Lower GI Bleeding Upper GI Bleeding Neonate Infant/Toddler Child/Adolescent Common Common Common Swallowed maternal blood Non-GI source (e.g., epistaxis) Mallory-Weiss tear Milk/soy protein allergy Mallory-Weiss tear Gastritis (especially Helicobacter pylori gastritis) Trauma (nasogastric tube in NICU) Esophagitis Esophagitis Uncommon Gastritis Peptic ulcer disease Stress ulcer/gastritis Uncommon Uncommon Esophagitis Stress gastritis or ulcer Esophageal varices Vascular malformation Peptic ulcer disease Toxic/caustic ingestion Hemorrhagic disease of newborn (vitamin K deficiency) Vascular malformation Foreign body Coagulopathy/bleeding diathesis GI duplication Vasculitis Coagulopathy associated with infection

n Uncommon Esophagitis Stress gastritis or ulcer Esophageal varices Vascular malformation Peptic ulcer disease Toxic/caustic ingestion Hemorrhagic disease of newborn (vitamin K deficiency) Vascular malformation Foreign body Coagulopathy/bleeding diathesis GI duplication Vasculitis Coagulopathy associated with infection Gastric/esophageal varices Bowel obstruction Toxic/caustic ingestion Coagulopathy/bleeding diathesis Foreign body Vascular malformation Bowel obstruction Crohn’s disease Coagulopathy/bleeding diathesis GI stromal tumors Dieulafoy’s lesion Lower GI Bleeding Neonate Infant/Toddler Child/Adolescent Common Common Common Swallowed maternal blood Anal fissure Anal fissure Anal fissure Milk/soy protein allergy Infectious gastroenteritis Milk/soy protein allergy Infectious gastroenteritis Polyps; benign, familial Infectious gastroenteritis Uncommon Uncommon Uncommon Intussusception Henoch-Schönlein purpura Meckel’s diverticulum* Meckel’s diverticulum* Hemorrhoids Necrotizing enterocolitis GI duplication Inflammatory bowel disease Vascular malformation Hemolytic-uremic syndrome Meckel’s diverticulum* Hemorrhagic disease of newborn (vitamin K deficiency) Henoch-Schönlein purpura Hemolytic-uremic syndrome Intussusception Malrotation with volvulus Vascular malformation Malrotation with volvulus Polyps; benign, familial Celiac disease Hirschsprung’s-associated enterocolitis (toxic megacolon) Coagulopathy/bleeding diathesis GI duplication Vascular malformation Abbreviation: NICU = neonatal intensive care unit. *Most common cause of severe LGI bleeding in all ages. while keeping the child’s head elevated to 30 degrees to reduce the risk of aspiration. After 2 to 3 minutes, gently aspirate gastric contents. Bloodflecked or coffee-ground aspirate suggests a slow rate of UGI bleeding, whereas bright red blood suggests serious hemorrhage. The usefulness of nasogastric lavage is limited, because clear aspirate does not exclude major bleeding from the UGI tract. For example, a duodenal ulcer distal to the pylorus may not reflux blood into the stomach and could yield a negative gastric aspirate. Tintinalli_Sec12_p0669-0996.indd 865 8/2/19 7:53 PM

morrhage. The usefulness of nasogastric lavage is limited, because clear aspirate does not exclude major bleeding from the UGI tract. For example, a duodenal ulcer distal to the pylorus may not reflux blood into the stomach and could yield a negative gastric aspirate. Tintinalli_Sec12_p0669-0996.indd 865 8/2/19 7:53 PM 866 SECTION 12: Pediatrics Laboratory studies are guided by the results obtained from the history and physical examination, the child’s appearance (ill or not), and the differential diagnosis (see Chapter 133, “ Acute Abdominal Pain in Infants and Children, ” and Chapter 131, “Vomiting, Diarrhea, and Dehydration in Infants and Children”). The stable child with minimal or self-limited bleeding may require no further diagnostic evaluation. A CBC, type and screen or cross-match of blood, serum electrolytes, renal function tests, liver function tests, coagulation panel, urinalysis, and stool testing for enteric pathogens or Clostridium difficile toxin should be obtained, as needed. For minimal or moderate GI bleeding, it may be difficult to deter mine the exact cause in the ED. Diagnosis may require ultrasonography, radiographic imaging, endoscopic evaluation, or a technetium-99m (Meckel) scan.  DIFFERENTIAL DIAGNOSIS FOR UPPER GI BLEEDING BY AGE GROUP Although the differential diagnosis is guided by the results of history and physical examination and age-related causes, there is considerable overlap among age groups (Table 134-1). Mucosal lesions such as gas tritis, esophagitis, ulcer disease, and Mallory-Weiss tears can be seen in children of any age. Massive bleeding can occur from esophageal varices, ulcer disease, vascular malformations, Meckel’s diverticulum, and GI duplication. Neonates Hematemesis in the newborn is most likely the result of swallowed maternal blood at delivery or during breastfeeding from cracked nipples. The Apt test is a qualitative test that distinguishes fetal from maternal hemoglobin. The blood in question is mixed with alkali to detect conversion of oxyhemoglobin to hematin. Fetal hemo globin is more resistant to denaturation than adult hemoglobin. If the supernatant stays pink after the addition of alkali, the blood is fetal in TABLE 134-2 Causes of GI Bleeding by Type Hematemesis Infant Swallowed maternal blood Vitamin K deficiency Vascular malformation Child/adolescent

866 SECTION 12: Pediatrics Laboratory studies are guided by the results obtained from the history and physical examination, the child’s appearance (ill or not), and the differential diagnosis (see Chapter 133, “ Acute Abdominal Pain in Infants and Children, ” and Chapter 131, “Vomiting, Diarrhea, and Dehydration in Infants and Children”). The stable child with minimal or self-limited bleeding may require no further diagnostic evaluation. A CBC, type and screen or cross-match of blood, serum electrolytes, renal function tests, liver function tests, coagulation panel, urinalysis, and stool testing for enteric pathogens or Clostridium difficile toxin should be obtained, as needed. For minimal or moderate GI bleeding, it may be difficult to deter mine the exact cause in the ED. Diagnosis may require ultrasonography, radiographic imaging, endoscopic evaluation, or a technetium-99m (Meckel) scan.  DIFFERENTIAL DIAGNOSIS FOR UPPER GI BLEEDING BY AGE GROUP Although the differential diagnosis is guided by the results of history and physical examination and age-related causes, there is considerable overlap among age groups (Table 134-1). Mucosal lesions such as gas tritis, esophagitis, ulcer disease, and Mallory-Weiss tears can be seen in children of any age. Massive bleeding can occur from esophageal varices, ulcer disease, vascular malformations, Meckel’s diverticulum, and GI duplication. Neonates Hematemesis in the newborn is most likely the result of swallowed maternal blood at delivery or during breastfeeding from cracked nipples. The Apt test is a qualitative test that distinguishes fetal from maternal hemoglobin. The blood in question is mixed with alkali to detect conversion of oxyhemoglobin to hematin. Fetal hemo globin is more resistant to denaturation than adult hemoglobin. If the supernatant stays pink after the addition of alkali, the blood is fetal in TABLE 134-2 Causes of GI Bleeding by Type Hematemesis Infant Swallowed maternal blood Vitamin K deficiency Vascular malformation Child/adolescent Swallowed blood from epistaxis, dental work, oral trauma Mallory-Weiss tear Esophagitis/gastritis Peptic ulcer disease Esophageal varices Vascular malformation Toxic ingestion Foreign body Coagulopathy/bleeding diathesis Hematochezia and melena Infant

Swallowed maternal blood Vitamin K deficiency Vascular malformation Child/adolescent Swallowed blood from epistaxis, dental work, oral trauma Mallory-Weiss tear Esophagitis/gastritis Peptic ulcer disease Esophageal varices Vascular malformation Toxic ingestion Foreign body Coagulopathy/bleeding diathesis Hematochezia and melena Infant Upper GI sources Anal fissure Milk/soy protein allergy Infectious gastroenteritis Meckel’s diverticulum Intussusception Malrotation with volvulus Ischemic bowel Child/adolescent Upper GI sources Anal fissure Infectious gastroenteritis Polyps Henoch-Schönlein purpura Hemorrhoids Inflammatory bowel disease Intussusception Meckel’s diverticulum Malrotation with volvulus Ischemic bowel Hemolytic-uremic syndrome Celiac disease Vascular malformation TABLE 134-3 Symptom Complexes and Differential Diagnosis for GI Bleeding Symptom Complex Differential Diagnosis Painless hematemesis Swallowed blood (non-GI source) Coagulopathy/bleeding diathesis Hematemesis and abdominal, epigastric, or chest pain Peptic ulcer disease Helicobacter pylori–associated gastritis Esophagitis/gastritis Hematemesis, hematochezia, or melena with underlying systemic disease Esophageal varices Inflammatory bowel disease Vomiting, hematochezia, or melena with abdominal pain Intussusception Malrotation with volvulus Ischemic bowel Henoch-Schönlein purpura Necrotizing enterocolitis Vomiting, hematochezia, or melena with fever Infectious gastroenteritis Inflammatory bowel disease Painless rectal bleeding Polyp Meckel’s diverticulum GI duplication Vascular malformation TABLE 134-4 Focused Historical Questions Chief complaint

Intussusception Malrotation with volvulus Ischemic bowel Henoch-Schönlein purpura Necrotizing enterocolitis Vomiting, hematochezia, or melena with fever Infectious gastroenteritis Inflammatory bowel disease Painless rectal bleeding Polyp Meckel’s diverticulum GI duplication Vascular malformation TABLE 134-4 Focused Historical Questions Chief complaint Frequency and volume of vomiting Blood-streaked, coffee-ground, or bloody vomitus Frequency and volume of diarrhea Bloody diarrhea Constipation with blood-streaked stool Blood on toilet paper or blood in toilet bowl Abdominal pain along with bloody vomitus or stool Dyspepsia; heartburn; dysphagia Fever Review of systems Rashes; joint pain; oral ulcers; perianal lesions; ocular symptoms; weight loss; fatigue; delayed puberty; failure to thrive; abnormal bleeding; dehydration Medications Iron; aspirin; NSAIDs; steroids; alcohol; recent antibiotics Environment Foreign body ingestion; foreign travel; sick contacts; raw meat/poultry; unpasteurized milk/cheese; animal contacts; water source Trauma Injury to abdomen (especially epigastrium or right upper quadrant) or significant body surface area burns Past medical history Term or premature; umbilical artery catheter; postpartum care; abdominal surgery; sepsis; liver disease; GI disease (enterocolitis, intussusception, congenital anomalies); coagulopathy/bleeding diathesis Family history GI bleeding; polyps; vascular anomalies; coagulopathy/ bleeding diathesis; inflammatory bowel disease Tintinalli_Sec12_p0669-0996.indd 866 8/2/19 7:53 PM

rtum care; abdominal surgery; sepsis; liver disease; GI disease (enterocolitis, intussusception, congenital anomalies); coagulopathy/bleeding diathesis Family history GI bleeding; polyps; vascular anomalies; coagulopathy/ bleeding diathesis; inflammatory bowel disease Tintinalli_Sec12_p0669-0996.indd 866 8/2/19 7:53 PM CHAPTER 134: Gastrointestinal Bleeding in Infants and Children 867 origin (reported as a positive test). If it turns brown, it is maternal blood. Hemorrhagic disease of the newborn is rare, but if there was failure to administer vitamin K in the immediate postpartum period (e.g., home birth), a prolonged prothrombin time can result in neonatal bleeding. Infants and Children Infants and children with severe gastroesophageal reflux may develop esophagitis and hematemesis. Mallory-Weiss tears after acute forceful vomiting or retching can also cause hematemesis. Any child with significant illness or injury (shock, polytrauma, respiratory failure, burns, head injury, renal failure, or vasculitis) can develop stress-related peptic ulcer disease. Ingestion of a sharp foreign body or button battery can occasionally cause GI bleeding. Removal by endoscopy is indicated. See Chapter 77, “Esophageal Emergencies, ” for further discussion of button battery ingestions. Preschool and older children can develop idiopathic ulcer disease. Peptic ulcer disease in the child is similar to that in adults, and there may be a positive family history. Y oung children may have poorly localized abdominal pain, bleeding, or even signs of obstruction or perfora tion. The adolescent will describe epigastric burning pain in a pattern more typical of the adult. If the bleeding is low grade, chronic symptoms of weakness and fatigue may develop. Helicobacter pylori is a leading cause of secondary gastritis and peptic ulcer disease in older children. Diagnosis should be made using endoscopy and is based on either positive culture or H. pylori gastritis on histopathology with at least one other positive biopsy-based test. 7 H. pylori eradication is confirmed using either the two-step monoclonal stool H. pylori antigen test or the 13C-Urea Breath Test (Kimberly-Clark Corp., Roswell, GA).7 Variceal bleeding is the most common cause of severe UGI bleeding in children.5 Consider esophageal variceal bleeding in older children and those with underlying chronic hepatic or vascular disease resulting in portal hypertension. Primary diseases of the liver that may lead to portal hypertension include biliary atresia, cystic fibrosis, hepatitis, α 1-antitrypsin deficiency, or congenital hepatic fibrosis. Portal hypertension may occur following liver transplant or operative repair of liver diseases such as biliary atresia. Other predisposing factors to portal hypertension include neonatal omphalitis, umbilical venous cannulation, abdominal sepsis, and abdominal/ surgical trauma, although many cases remain idiopathic. Reactive gastritis can occur due to anti-inflammatory drugs, alcohol, cocaine ingestion, iron ingestion, H. pylori, Crohn’s disease, Henoch- Schönlein purpura, or foreign bodies. Rarely, GI stromal tumors can arise from the wall of the GI tract mesentery or omentum. Most of these are found in the stomach and are associated with genetic disorders such as neurofibromatosis. An unusual cause of UGI bleeding in children is Dieulafoy’s lesion. Symptomatic lesions result when an abnormal submucosal artery erodes through a tiny mucosal defect, typically in the fundus of the stomach, causing massive bleeding. The characteristic history is recurrent massive hematemesis without any prodromal symptoms. Definitive diagnosis is usually made during endoscopy.

lesion. Symptomatic lesions result when an abnormal submucosal artery erodes through a tiny mucosal defect, typically in the fundus of the stomach, causing massive bleeding. The characteristic history is recurrent massive hematemesis without any prodromal symptoms. Definitive diagnosis is usually made during endoscopy.  DIFFERENTIAL DIAGNOSIS FOR LOWER GI BLEEDING BY AGE GROUP The presence of melena, hematochezia, or bright red blood per rectum can help to differentiate causes of LGI in children ( Figure 134-1). The differential diagnosis for LGI bleeding is also age dependent (Table 134-1). The approach to LGI bleeding in the neonate can be organized based on whether the baby appears well or unwell (Figure 134-2). Neonates and Infants The neonate with dark, tarry stools likely has swallowed maternal blood from delivery or breastfeeding. Birth history is important because failure to replace vitamin K can lead to coagulopathy and massive bleeding. As the infant ages, other disorders become important. Anal fissures are a common cause of bright red rectal blood on the surface of wellformed stools or toilet paper in children of all ages and highlight the importance of a careful rectal examination and spreading of anal skin folds. Milk protein allergy has a prevalence of 2% to 3% in infants, and cross-reactivity with soy protein exists in at least 10% of cases. Protein-induced allergic enterocolitis, proctitis, or proctocolitis may lead to blood-streaked, mucousy, loose stools. Food protein–induced enterocolitis is a rare, delayed non–immunoglobulin E–mediated reaction typically presenting with profuse vomiting and diarrhea 1 to 4 hours after ingestion of the offending allergen, most commonly cow’s milk, soy, rice, or oats. 11 The diarrhea may be frankly bloody, and in 15% of reactions, the infant may develop profound dehydration and lethargy. The basis of therapy in milk or soy protein allergy is removal of the offending protein using hydrolyzed or elemental formula. Breastfed infants whose mothers ingest dairy or soy may also suffer from this condition, and the offending protein must be eliminated from the maternal diet. 10,11 LGI bleed Melena Swallowed blood UGI bleed Henoch-Schönlein purpura Henoch-Schönlein purpura Hemolytic-uremic syndrome Infectious gastroenteritis Inflammatory bowel disease Milk/soy protein allergy Intussusception Malrotation with volvulus Necrotizing enterocolitis Significant UGI bleed Meckel’s diverticulum GI duplication Vascular malformation Coagulopathy Significant UGI bleed Anal fissure Polyp Hemorrhoid Hematochezia NoYes Abdominal pain? Bright red blood per rectum FIGURE 134-1. Diagnostic algorithm for lower GI (LGI) bleeding in children. UGI = upper GI. Tintinalli_Sec12_p0669-0996.indd 867 8/2/19 7:53 PM

iverticulum GI duplication Vascular malformation Coagulopathy Significant UGI bleed Anal fissure Polyp Hemorrhoid Hematochezia NoYes Abdominal pain? Bright red blood per rectum FIGURE 134-1. Diagnostic algorithm for lower GI (LGI) bleeding in children. UGI = upper GI. Tintinalli_Sec12_p0669-0996.indd 867 8/2/19 7:53 PM 868 SECTION 12: Pediatrics Necrotizing enterocolitis is most commonly seen in preterm infants in the neonatal intensive care unit, but may rarely be seen in term infants. Infants will be systemically unwell and present with abdominal disten tion and hematochezia. Plain radiographs reveal ileus and the pathog nomonic pneumatosis intestinalis diagnostic of this condition. Infants with Hirschsprung’s disease (congenital aganglionic megacolon) may develop Hirschsprung’s-associated enterocolitis, also characterized by abdominal distention and hematochezia. Hirschsprung’s-associated enterocolitis should be considered in any infant who appears toxic and has bloody diarrhea. In older infants who develop sudden painless hematochezia, congenital malformations such as Meckel’s diverticulum and GI duplication must be considered. Meckel’s diverticula are remnants of the omphalomesenteric duct in the distal ileum and are present in approximately 2% of the population. They may be lined with ectopic gastric mucosa and typically present with painless rectal bleeding in the 2-month to 2-yearold age group. 13 Diagnosis is made using a Meckel scan. Intussusception is another important consideration in infants and young children with a peak incidence between 5 and 10 months of age. 14 Intussusception is associated with episodes of colicky abdominal pain and vomiting. As the intussusception progresses, painful episodes may alternate with periods of lethargy, and gross blood (“currant jelly”) may be noted in the stool. Diagnosis is made using US or contrast/air enema. Painful LGI bleed ing in the infant can also be a symptom of malrotation with volvulus. Volvulus most commonly presents with abdominal pain, distention, and bilious vomiting, but may lead to bowel ischemia and subsequent LGI bleeding as the condition progresses. Both intussusception and volvulus represent true surgical emergencies and are further discussed in Chapters 131 and 133. Children Age 2 to 5 Y ears Old Children in the 2- to 5-year-old age range have a different spectrum of disorders causing LGI bleeding: juvenile polyps, infectious gastroenteritis, hemolytic-uremic syndrome, and Henoch-Schönlein purpura. A review of recent literature suggests an estimated detected prevalence of colorectal polyps in 12% of all children with LGI bleeding undergoing colonoscopy. 15 Manifestations of polyps range from chronic heme-positive stools to acute hematochezia from autoamputation of the polyp at its stalk. Juvenile polyps are usually benign hamartomas, and most have no malignant potential. Multiple adenomatous polyps should suggest diagnoses such as familial adenomatous polyposis. Infectious gastroenteriti s should be evident by history and physi cal examination (Table 134-5). 16 Also see Chapter 131. When bloody diarrhea is present, stool cultures should be obtained. 12 Patients with typical diarrhea-associated hemolytic-uremic syndrome caused by Shiga toxin–producing strains of Escherichia coli have an antecedent episode of hemorrhagic enterocolitis within 2 to 12 days before the onset of thrombotic microangiopathy. 17 Children who have recently been exposed to antibiotics may develop bloody diarrhea from pseudo membranous colitis associated with C. difficile infection . In Henoch- Schönlein purpura, 50% to 75% of patients have episodic abdominal pain and/or blood in their stool from intestinal vasculitis.

ombotic microangiopathy. 17 Children who have recently been exposed to antibiotics may develop bloody diarrhea from pseudo membranous colitis associated with C. difficile infection . In Henoch- Schönlein purpura, 50% to 75% of patients have episodic abdominal pain and/or blood in their stool from intestinal vasculitis. One-third of Henoch-Schönlein purpura patients develop acute intestinal bleed ing manifested as gross or occult blood per rectum. 18 Intussusception develops in 1% to 5% of children with Henoch-Schönlein purpura. 18 Henoch-Schönlein purpura is further discussed in Chapter 133. Children >5 Y ears Old In children >5 years of age, juvenile polyps and infectious gastroenteritis remain common causes of LGI bleeding. Both Crohn’s disease and ulcerative colitis also become evident in this age group, and the incidence of these diseases is increasing. 19 Symptoms are varied and involve multiple systems: skin lesions such as erythema nodosum and pyoderma gangrenosum; extraintestinal GI problems such as nonspecific hepatitis, cholelithiasis, sclerosing cholangitis, and pancreatitis; skeletal involvement including aseptic necrosis of bone, arthralgias, and arthritis; ocular problems with uveitis and scleritis; renal disorders such as stones and nephritis; hematologic abnormalities such as anemia, thrombocytopenia, and hypercoagulability; and general failure to thrive. Crohn’s disease is twice as common as ulcerative colitis and is characterized by abdominal pain, weight loss, growth failure, and anemia. 19 Ulcerative colitis often presents with rectal bleeding, bloody diarrhea, urgency/ tenesmus, and abdominal pain. 19 In the acutely ill patient, diagnosis can be made with a combination of laboratory studies (blood count, erythrocyte sedimentation rate, C-reactive protein, albumin, liver function tests) and CT or MRI enterography. 19 Imaging can show areas of inflammation and can identify complications such as abscess or perforation. 20 Definitive diagnosis requires upper endoscopy, colonoscopy, and biopsy. TREATMENT Severe bleeding requires acute resuscitation and teamwork with the pediatric surgeon and/or gastroenterologist, depending on the suspected cause of bleeding. Treatment goals for UGI and LGI bleeding are: (1) resuscitation from hemorrhagic shock and restoring the intravascular volume; (2) restoring normal oxygen-carrying capacity by transfusion with packed red blood cells; (3) identifying the source of bleeding; and (4) stopping ongoing blood loss. Swallowed maternal blood Anal fissure Milk/soy protein allergy Infectious gastroenteritis (early) Hemorrhagic disease of the newborn (early) GI duplication (early) Meckel’s diverticulum (early) Vascular malformation (early) Appears unwell: Toxic appearance Abnormal vital signs Poor perfusion Distended/acute abdomen Volvulus/ischemic bowel Hirschsprung’s-associated enterocolitis Necrotizing enterocolitis Intussusception Coagulopathy due to systemic disease Infectious gastroenteritis (late) Hemorrhagic disease of the newborn (late) GI duplication (late) Meckel’s diverticulum (late) Vascular malformation (late) Neonate with LGI bleed Appears well: Alert Active Stable vital signs Well-perfused Benign abdomen FIGURE 134-2. Approach to lower GI (LGI) bleeding in a neonate. Tintinalli_Sec12_p0669-0996.indd 868 8/2/19 7:53 PM

ease of the newborn (late) GI duplication (late) Meckel’s diverticulum (late) Vascular malformation (late) Neonate with LGI bleed Appears well: Alert Active Stable vital signs Well-perfused Benign abdomen FIGURE 134-2. Approach to lower GI (LGI) bleeding in a neonate. Tintinalli_Sec12_p0669-0996.indd 868 8/2/19 7:53 PM CHAPTER 134: Gastrointestinal Bleeding in Infants and Children 869 TABLE 134-5 Infectious Causes of Bloody Diarrhea in Children Infectious Agent Historical Facts Symptoms Diagnosis Treatment Salmonella <4 y Foodborne Reptiles/Amphibians Fever Abdominal pain Stool culture Supportive; antibiotics if enteric fever, sepsis, <3 months old, or immunosuppressed Shigella <5 y Child care center Travelers Fever Abdominal pain Stool WBC count (nonspecific) Shiga toxin Stool culture Supportive; antibiotics unless very mild disease Yersinia Uncommon Livestock transmission Foodborne Contaminated water Abdominal pain (pseudoappendicitis) Fever Scarlatiniform rash Stool culture Supportive; antibiotics for neonates, immunosuppressed, sepsis, or extraintestinal manifestations; otherwise, clinical benefit not established Campylobacter jejuni Unpasteurized milk, improperly cooked poultry Contaminated water Often self-limited +/– Fever Abdominal pain 10%–20% have severe, prolonged, or relapsing illness Stool culture Supportive; antibiotics Escherichia coli (Shiga toxin) Ground beef Petting zoos Contaminated raw fruits Abdominal pain Fever Hemolytic-uremic syndrome Stool culture for O157:H7 Shiga toxin Supportive; antibiotics not proven beneficial and may increase risk of hemolytic-uremic syndrome E. coli (enteroinvasive) Foodborne Contaminated water Travelers Fever Vomiting Stool cultures not helpful (normal flora) Supportive; antibiotics Entamoeba histolytica Resource limited countries Low socioeconomic status Travelers from endemic areas Increasing severity of diarrhea Lower abdominal pain Tenesmus Stool for ova and parasites may be negative (serial testing may be necessary) Stool antigen test kits Serology with enzyme immunoassay kit Supportive; antibiotics followed by luminal amebicide Aeromonas hydrophila Warm weather Waterborne Chronic diarrhea Stool culture (requires special media) Antibiotics only in special populations Clostridium difficile Recent antibiotic usage or hospitalization

Stool for ova and parasites may be negative (serial testing may be necessary) Stool antigen test kits Serology with enzyme immunoassay kit Supportive; antibiotics followed by luminal amebicide Aeromonas hydrophila Warm weather Waterborne Chronic diarrhea Stool culture (requires special media) Antibiotics only in special populations Clostridium difficile Recent antibiotic usage or hospitalization Pseudomembranous colitis Toxic megacolon (rare) Stool culture not helpful C. difficile toxin studies on diarrheal stool Antibiotics if symptomatic Note: C. difficile can be normal flora in infants. Management begins with an assessment of the airway, breathing, and circulation, followed by the rapid administration of serial 20 mL/kg crystalloid fluid boluses. If three boluses of crystalloid do not restore volume, administer 10 mL/kg of packed red blood cells. Avoid overexpansion of intravascular volume, particularly if the bleeding is from varices. Correct for shock and restore urine flow, but then titrate additional fluid volume or blood administration based on estimated blood loss and response of the vital signs ( Figure 134-3).  UPPER GI BLEEDING Emergency endoscopy is needed for children with moderate to severe, persistent or recurrent bleeding, and may be both diagnostic and therapeutic (e.g., coagulation, sclerotherapy, banding). Variceal Bleeding For unstable patients in whom endoscopy cannot be performed, octreotide is the drug of choice for esophageal variceal bleeding. Octreotide is administered as a bolus followed by a continuous infusion (1 to 2 micrograms/kg bolus up to 50 micrograms, followed with a continuous infusion of 1 to 2 micrograms/kg/h, which may be increased hourly by 1 microgram/kg up to 4 micrograms/kg/h). 6,20 The major adverse effect of octreotide is hyperglycemia, which requires monitoring of serum glucose. If octreotide is unavailable, consult with a pediatric gastroenterologist regarding the use of a vasopressin infusion (0.002 to 0.005 unit/kg/min titrated as needed, maximum 0.01 unit/kg/min). If bleeding stops for 12 hours, then vasopressin is tapered off over 24 to 48 hours. 21 Intensive care unit admission is needed. Vasopressin use is limited by the side effects of peripheral and central vasoconstriction. There are limited pediatric data on the use of both octreotide and vasopressin. Nonvariceal Bleeding Medical treatment of bleeding from mucosal lesions, such as peptic ulcers, can include proton pump inhibitors, histamine-2 receptor antagonists, antacids, and sucralfate. Proton pump inhibitors are more efficacious than histamine-2 receptor antagonists. Intravenous pantoprazole, given as a bolus dose followed by an infusion, is used for control of active bleeding (Table 134-6). If bleeding is persistent and endoscopy fails to identify a bleeding site, angiography may be indicated, although it is technically difficult in young children and a minimum rate of bleeding of 1 to 2 mL/min is required for diagnosis using this modality.  LOWER GI BLEEDING Hemorrhagic shock is not common as a result of LGI bleeding. There are some important exceptions, however. Meckel’s diverticulum may result in significant blood loss in children of any age and requires surgical excision. Painless hematochezia should point to this diagnosis, and a Meckel scan is diagnostic. Definitive treatment is surgical resection. Bleeding associated with Henoch-Schönlein purpura can be severe, but resuscitation and stabilization are the mainstays of treatment. GI duplications and vascular malformations may also cause significant bleeding. Tintinalli_Sec12_p0669-0996.indd 869 8/2/19 7:53 PM