1 What is the most common cause of vomiting in older children?

Acute gastroenteritis. Although usually associated with diarrhea, vomiting can occur alone in the early stages of gastroenteritis. The most common infectious viral etiology is rotavirus. Salmonella, Shigella, Yersinia, Campylobacter spp. and Escherichia coli can also cause bacterial gastroenteritis with vomiting.

Stevens MW, Henretig FM: Vomiting. In Fleisher GR, Ludwig S, Henretig FM (eds): Textbook of Pediatric Emergency Medicine, 5th ed. Philadelphia, Lippincott Williams & Wilkins, 2006, pp 681–689.

2 What are other medical causes of vomiting in children?

Metabolic disorders, such as galactosemia, fructose intolerance, or amino acid or organic acid defects (phenylketonuria, urea cycle defects) usually present in infancy. Along with vomiting, symptoms such as lethargy, seizures, or coma may occur. Diabetes mellitus can cause vomiting because of ketoacidosis or slowed gastric motility (gastroparesis may occur after 10 years of diabetes mellitus). Other causes include milk/soy protein allergies, pancreatitis, urinary tract infection, neurologic disorders associated with increased intracranial pressure (tumor, hydrocephalus), migraines, pregnancy, and psychological causes (rumination, bulimia).

Stevens MW, Henretig FM: Vomiting. In Fleisher GR, Ludwig S, Henretig FM (eds): Textbook of Pediatric Emergency Medicine, 5th ed. Philadelphia, Lippincott Williams & Wilkins, 2006, pp 681–689.

3 What are the most common anatomic regions to find a coin that has not passed?

In the esophagus, the cricopharyngeus/thoracic inlet (proximal third) is the most common place, followed by the level of the aortic arch (middle third), then the gastroesophageal junction/sphincter (lower third). Other areas of the gastrointestinal (GI) tract include the stomach, pylorus, ligament of Treitz, and ileocecal valve. Objects larger than 2 cm in diameter or longer than 5 cm are more likely to get “caught” at the pylorus.

Karaman A, Cavusoglu YH, Karaman I, et al: Magill forceps technique for removal of safety pins in upper esophagus: A preliminary report. Int J Pediatr Otorhinolaryngol 68:1189–1191, 2004.

4 What is the best way to remove an esophageal coin?

This is a highly controversial topic. One study demonstrated that when the foreign body is lodged for less than 24 hours, no respiratory symptoms are present, and the child has no prior esophageal disease or surgery, 28% pass spontaneously, including 22–33% of those in the upper esophagus and midesophagus. In such cases, observation for 12–24 hours with repeat radiography may be appropriate.

There are several methods of coin removal in infants and children with no respiratory symptoms and no history of esophageal disease. Some advocate the use of Foley catheter extraction under fluoroscopic guidance for coins that have been lodged less than 24 hours, while others extend this time to 3 days. Others use esophageal bougienage for coins lodged in the distal esophagus less than 24 hours. Laryngoscopy with Magill forceps removal, esophagoscopy, or endoscopy under general anesthesia are also options. In the presence of respiratory symptoms, a history of esophageal disease, esophageal edema, or focal narrowing of the adjacent trachea (seen on the lateral neck radiograph), the best way to remove the foreign body is under direct vision via esophagoscopy or endoscopy. The choice of method is often based upon the expertise and availability of the specialists (radiology, otolaryngology, surgery, or gastroenterology) at a particular hospital.

Harned RK, Strain JD, Hay TC, et al: Esophageal foreign bodies: Safety and efficacy of Foley catheter extraction of coins. AJR 168:443–446, 1997.

Karaman A, Cavusoglu YH, Karaman I, et al: Magill forceps technique for removal of safety pins in upper esophagus: A preliminary report. Int J Pediatr Otorhinolaryngol 68:1189–1191, 2004.

Macpherson RI, Hill JG, Othersen HB, et al: Esophageal foreign bodies in children: Diagnosis, treatment and complications. AJR 166:919–924, 1996.

Schunk JE, Harrison M, Corneli HM, et al: Fluoroscopic Foley catheter removal of esophageal foreign bodies in children: Experience with 415 episodes. Pediatrics 94:709–714, 1994.

Soprano JV, Fleisher GR, Mandl KD: The spontaneous passage of esophageal coins in children. Arch Pediatr Adolesc Med 153:1073–1076, 1999.

5 What is the “big deal” about button batteries?

Although they are small (watch or hearing aid batteries), the risk is corrosion of the ingested battery. If the battery remains in the esophagus, there is fear of tissue damage, with resultant erosions, tracheoesophageal fistulas, and strictures. When a child swallows a button battery, obtain a radiograph to determine the battery’s location. If it remains in the esophagus, it should be removed under direct visualization (not a Foley catheter) to assess for any damage to the esophageal mucosa. The proposed mechanisms of injury include electrolyte leakage, alkali production, mercury toxicity, and pressure necrosis.

Fun fact: Many batteries are made of mercuric oxide. There is little risk of mercury poisoning, however, because mercuric oxide is poorly absorbed from the GI tract.

Lin VYW, Daniel SJ, Papsin BC: Button batteries in the ear, nose and upper aerodigestive tract. Int J Pediatr Otorhinolaryngol 68:473–479, 2004.

6 How should a caustic ingestion be managed?

First, ensure that there is a patent airway. Next, determine what was ingested. This may require calling the poison control center (1-800-222-1222) or going to a computer-based system that determines treatment, signs/symptoms, and toxicity in the emergency department. The child may have symptoms such as drooling, mouth pain, pain on swallowing, chest pain, or cough. Examine the mouth for mucosal and oral burns. Alkali ingestions (lye, drain cleaners) are more damaging to the oropharynx and esophagus than are acid burns because they cause deeper injury. In addition, after an alkali burn, esophageal burns can occur without an oral burn. The amount of caustic ingested does not correlate with the degree of burns, or the symptoms. Induced vomiting is contraindicated in these children because of the risk of injury and aspiration. After a thorough examination, if any burns are seen, or if the child ingested alkali, the child should undergo endoscopy under general anesthesia. If there are no burns and no symptoms, and if a weak or very dilute formulation of an acid was ingested, observation is indicated.

Erickson TB: Toxicology: Ingestions and smoke inhalation. In Gausche-Hill M, Fuchs S, Yamamoto L (eds): APLS: The Pediatric Emergency Medicine Resource, 4th ed. Sudbury, MA, Jones & Bartlett Publishers, 2004, pp 244–245.

7 Distinguish among hematemesis, hematochezia, and melena

Squires RH: Gastrointestinal bleeding. In Altschuler SM, Liacouras CA (eds): Clinical Pediatric Gastroenterology. Philadelphia, Churchill Livingstone, 1998, pp 31–42.

8 Distinguish between upper GI and lower GI bleeding in terms of site of bleeding

Squires RH: Gastrointestinal bleeding. In Altschuler SM, Liacouras CA (eds): Clinical Pediatric Gastroenterology. Philadelphia, Churchill Livingstone, 1998, pp 31–42.

9 What are some of the common tests used to determine the presence of blood? What causes them to be falsely positive or falsely negative?

The Hematest is a qualitative stool test that uses orthotolidine (a leukodye). False-positive results occur when the patient has ingested red meats, iron preparations, or plant peroxidases (found in horseradish, turnips, tomatoes, and fresh red cherries). False-negative results occur in the presence of ascorbic acid (vitamin C). The Hemoccult test is a qualitative stool test that uses guaiac (also a leukodye). False-positive results occur with red meats, broccoli, grapes, cauliflower, iron preparations, plant peroxidases, and cimetidine. False-negative results occur with hard stool, penicillamine, antacids, and ascorbic acid. The HemoQuant test is the only quantitative test (2 mg hemoglobin/gm stool) and uses a fluorescent antibody to porphyrin. It is falsely positive with red meat. Gastroccult tests check gastric fluids for blood.

Cadranel S, Scaillon M. Approach to gastrointestinal bleeding. In Guandalini S (ed): Textbook of Pediatric Gastroenterology and Nutrition. London, Taylor & Francis, 2004, pp 639–654.

Squires RH: Gastrointestinal bleeding. In Altschuler SM, Liacouras CA (eds): Clinical Pediatric Gastroenterology. Philadelphia, Churchill Livingstone, 1998, pp 31–42.

10 What ingested foods can cause red stools?

Fruit punch, Kool-Aid beverage (especially cherry or strawberry), red beets, tomatoes, and gelatin. Note that commercial dyes can also be found in breakfast cereals.

Cadranel S, Scaillon M: Approach to gastrointestinal bleeding. In Guandalini S (ed): Textbook of Pediatric Gastroenterology and Nutrition. London, Taylor & Francis, 2004, pp 639–654.

Markel H, Oski JA, Oski FA, McMillan JA: The Portable Pediatrician. Philadelphia, Hanley & Belfus, 1992.

11 What foods or items can cause black stools?

Bismuth (Pepto-Bismol), iron preparations, charcoal, licorice, beets, spinach, blueberries, grape juice, dark chocolate, and swallowed blood.

Cadranel S, Scaillon M: Approach to gastrointestinal bleeding. In Guandalini S (ed): Textbook of Pediatric Gastroenterology and Nutrition. London, Taylor & Francis, 2004, pp 639–654.

12 What is the APT-Downey test? How is it used?

This test is for fetal red cells and is used when an infant spits up blood. If the infant is breast-feeding, it is often unclear if the blood is from the baby’s GI tract or maternal milk. Adult hemoglobin, eluted from erythrocytes, is denatured to alkaline globin hematin in an alkaline solution (sodium hydroxide), resulting in a yellow-brown color. Fetal hemoglobin resists the effect of alkali and stays pink. However, if the blood you use for the test is coffee-ground color (not red), it will be read falsely as adult blood.

Cadranel S, Scaillon M: Approach to gastrointestinal bleeding. In Guandalini S (ed): Textbook of Pediatric Gastroenterology and Nutrition. London, Taylor & Francis, 2004, pp 639–654.

13 What is another test that can help localize the source of GI bleeding?

The blood urea nitrogen (BUN)–to–creatinine ratio can help. A BUN–creatinine ratio > 30 indicates upper GI bleeding. In a study done at the Children’s Hospital of Los Angeles, the specificity was 100% (although the sensitivity was 39%). The BUN level is thought to rise after upper GI bleeding as a result of increased hepatic catabolism of the absorbed amino acid load from the intraluminal blood. Therefore, the bleeding must occur proximal to the ligament of Treitz. A BUN–creatinine ratio of 30 can occur with upper or lower GI bleeding.

Markel H, Oski JA, Oski FA, McMillan JA: The Portable Pediatrician. Philadelphia, Hanley & Belfus, 1992.

14 What are some common causes of upper GI bleeding in infants and children?

Squires RH: Gastrointestinal bleeding. In Altschuler SM, Liacouras CA (eds): Clinical Pediatric Gastroenterology. Philadelphia, Churchill Livingstone, 1998, pp 31–42.

Stevens MW, Henretig FM: Vomiting. In Fleisher GR, Ludwig S, Henretig FM (eds): Textbook of Pediatric Emergency Medicine, 5th ed. Philadelphia, Lippincott Williams & Wilkins, 2006, pp 681–689.

15 What are some common causes of lower GI bleeding in infants and children?

Squires RH: Gastrointestinal bleeding. In Altschuler SM, Liacouras CA (eds): Clinical Pediatric Gastroenterology. Philadelphia, Churchill Livingstone, 1998, pp 31–42.

Stevens MW, Henretig FM: Vomiting. In Fleisher GR, Ludwig S, Henretig FM (eds): Textbook of Pediatric Emergency Medicine, 5th ed. Philadelphia, Lippincott Williams & Wilkins, 2006, pp 681–689.

16 Distinguish between malrotation and volvulus

Malrotation is the incomplete or reverse rotation of the embryonic midgut about the superior mesenteric artery. The small bowel then hangs on a mesenteric stalk. Volvulus occurs when the midgut twists around the stalk, resulting in small bowel obstruction and vascular compromise due to compression of the mesenteric vessels. Midgut volvulus occurs in 70% of infants with malrotation.

Okada PJ, Hicks BA: Nontraumatic surgical emergencies. In Gausche-Hill M, Fuchs S, Yamamoto L (eds): APLS: The Pediatric Emergency Medicine Resource, 4th ed. Sudbury, MA, Jones and Bartlett Publishers, 2004, pp 367–371.

17 What are the clinical features of malrotation with volvulus?

An infant with malrotation and volvulus is usually less than 1 month of age. Symptoms include bilious vomiting, irritability, and abdominal pain. When volvulus is present, there are bloody or heme-positive stools. The infant can rapidly progress to a shocklike state. The physical examination reveals abdominal distention with dilated loops of bowel, lethargy, pallor, and possibly hypotension. Therapy includes fluid resuscitation, nasogastric tube, broad-spectrum antibiotics, and emergent surgery (Ladd’s procedure).

Okada PJ, Hicks BA: Nontraumatic surgical emergencies. In Gausche-Hill M, Fuchs S, Yamamoto L (eds): APLS: The Pediatric Emergency Medicine Resource, 4th ed. Sudbury, MA, Jones and Bartlett Publishers, 2004, pp 367–371.

18 What is the radiographic finding in an infant with malrotation and volvulus?

The abdominal radiographs may be normal (50–60% of patients) or show duodenal obstruction (double bubble). The upper GI study shows a displaced duodenal–jejunal junction (both to the right of the spine), with the jejunum on the right side of the abdomen. There may be a corkscrew appearance of contrast. A lower GI study shows a displaced cecum, usually in the right upper quadrant, or an abnormally oriented superior mesenteric artery.

Okada PJ, Hicks BA: Nontraumatic surgical emergencies. In Gausche-Hill M, Fuchs S, Yamamoto L (eds): APLS: The Pediatric Emergency Medicine Resource, 4th ed. Sudbury, MA, Jones and Bartlett Publishers, 2004, pp 367–371.

19 Is a “currant jelly” stool classic for intussusception?

Up to 75% of children with intussusception never have visible blood in the stool (although the stool is guaiac-positive). A currant jelly stool is a late finding because it implies that bowel necrosis has occurred. Intussusception generally occurs in children under 2 years of age, with a peak age range of 5–9 months. Classic symptoms occur in 10% of cases and include the sudden onset of severe, intermittent, crampy abdominal pain, with crying and drawing up of legs in episodes every 15 minutes. This is followed by vomiting and the passage of a “currant jelly” stool. There is also a “neurologic presentation,” which consists of lethargy followed by brief periods of irritability. Abdominal radiographs (Fig. 35-1) may show a soft tissue mass, a nascence of cecal gas and stool, a target sign, a meniscus or crescent sign, a paucity of bowel gas, or a bowel obstruction. Definitive diagnosis and treatment in >75% of cases are made by barium or air contrast enema (hydrostatic reduction). The most common location for the intussusception is ileocolic. Lead point is usually not present in younger children but is somewhat common in older children (e.g., Meckel’s diverticulum, duplication, vasculitis due to Henoch-Schönlein purpura).

Figure 35-1 Radiograph of intussusception.

Okada PJ, Hicks BA: Nontraumatic surgical emergencies. In Gausche-Hill M, Fuchs S, Yamamoto L (eds): APLS: The Pediatric Emergency Medicine Resource, 4th ed. Sudbury, MA, Jones & Bartlett Publishers, 2004, pp 376–381.

20 What is a Meckel’s diverticulum?

Meckel’s diverticulum is a remnant of the vitellointestinal or omphalomesenteric duct that may result in painless rectal bleeding. It is present in 2% of the population, is 2 inches long (or less), and is found within 2 feet of the ileocecal valve. It contains ectopic gastric mucosa in 60–90% of patients and in almost all of those who have painless rectal bleeding. (The gastric mucosa can result in an ulcer, which bleeds.) Diagnosis is by a Meckel’s scan (technetium 99m pertechnetate scan). Gastric mucosa concentrates the technetium 99. An intestinal duplication may also contain gastric mucosa and can cause GI bleeding or symptoms of obstruction or intussusception. A duplication occurs most commonly in the ileocecal region, but also is found in the distal esophagus, stomach, and duodenum.

Azizkhan RG: Meckel’s diverticulum. In Guandalini S (ed): Textbook of Pediatric Gastroenterology and Nutrition. London, Taylor & Francis, 2004, pp 729–738.

21 A child who has had surgical correction for Hirschsprung’s disease presents with fever, abdominal distention, and diarrhea. What is your concern?

This child probably has Hirschsprung’s enterocolitis and requires IV fluids, nasogastric drainage, broad-spectrum antibiotics, and decompression of the rectum or colon by rectal stimulation or irrigation. Enterocolitis is the most common cause of death in children with Hirschsprung’s disease. Other complications include persistent obstructive symptoms and fecal incontinence.

Dasgupta R, Langer JC: Hirschsprung disease. Curr Prob Surgery 41: 949–988, 2004.

22 True or false: Pain is worse after meals in younger children with ulcers

False. In most young children with ulcers, pain is not related to meals. In some older children and adolescents, pain may be exacerbated by acidic foods or spicy meals, as in adults. Symptoms in neonates include vomiting; infants may feed poorly or vomit; toddlers may have poorly localized abdominal pain or vomiting; adolescents may have epigastric pain. All age groups can have melena or upper GI bleeding.

Stevens MW, Henretig FM: Vomiting. In Fleisher GR, Ludwig S, Henretig FM (eds): Textbook of Pediatric Emergency Medicine, 5th ed. Philadelphia, Lippincott Williams & Wilkins, 2006, pp 681–689.

23 What is the relationship between Helicobacter pylori and gastritis/peptic ulcers in children?

Helicobacter pylori is a gram-negative, spiral-shaped bacterium present in over 50% of the population that causes gastritis and peptic ulcers. Although seroprevalence in the United States is 10%, the risk is higher for those who live with an infected family member, those in crowded living conditions, those who attend day care, those who have poor hygiene, American-born children of immigrant parents, and internationally adopted children. H. pylori colonizes and persists only in the gastric mucosa and causes gastritis and primarily duodenal ulcers. H. pylori infection has been associated with gastric adenocarcinoma and lymphoma, decades after infection.

Czinn SJ: Helicobacter pylori infection: Detection, investigation, and management. J Pediatr 146:S21–S26, 2005.

Gold BD, Colletti RB, Abbott M, et al: Helicobacter pylori infection in children: Recommendations for diagnosis and treatment. J Pediatr Gastroenterol Nutrition 31:490–497, 2000.

24 What are some therapies for H. pylori infection in children?

Eradication therapy is recommended for children with a definitive peptic ulcer and H. pylori on histology. Triple therapy is recommended and includes the following first-line therapies in a twice-daily fashion for 7–14 days:

One can substitute metronidazole, 20 mg/kg/d (up to 500 mg twice daily), for clarithromycin, or use clarithromycin, metronidazole, and omeprazole.

Czinn SJ: Helicobacter pylori infection: Detection, investigation, and management. J Pediatr 146:S21–S26, 2005.

Gold BD, Colletti RB, Abbott M, et al: Helicobacter pylori infection in children: Recommendations for diagnosis and treatment. J Pediatr Gastroenterol Nutrition 31:490–497, 2000.

25 Describe some of the anatomic and histologic differences between ulcerative colitis and Crohn’s disease

Brown JB, Li BUK: Inflammatory bowel disease. In Green TP, Franklin WH, Tanz RR (eds). Pediatrics: Just the Facts. New York, McGraw-Hill, 2005, pp 316–319.

Mamula P, Markowitz JE, Baldassano RN: Inflammatory bowel disease in early childhood and adolescence: Special considerations. Gastroenterol Clin North Am 32:967–995, 2003.

26 What are some of the extraintestinal features of ulcerative colitis and Crohn’s disease?

Since both can present with bloody diarrhea, abdominal pain, weight loss, and fever, extraintestinal manifestations may help determine which is more likely prior to endoscopy.

Brown JB, Li BUK: Inflammatory bowel disease. In Green TP, Franklin WH, Tanz RR (eds). Pediatrics: Just the Facts. New York, McGraw-Hill, 2005, pp 316–319.

Mamula P, Markowitz JE, Baldassano RN: Inflammatory bowel disease in early childhood and adolescence: Special considerations. Gastroenterol Clin North Am 32:967–995, 2003.

27 What is a food allergy?

This is an abnormal reaction after the ingestion of food. It can be non–immune-mediated (lactose intolerance, infectious [Salmonella], toxic [Clostridium botulinum]) or immune-mediated, including IgE-mediated (immediate hypersensitivity), non–IgE-mediated (food protein–induced enterocolitis, celiac disease), or mixed IgE and T cell (eosinophilic esophagitis).

Shah U, Walker WA: Food allergy. In Lifschitz CH (ed): Pediatric Gastroenterology and Nutrition in Clinical Practice. New York, Marcel Dekker, 2002, pp 601–613.

Spergel JM, Pawlowski NA: Food allergy: Mechanism, diagnosis and management in childhood. Pediatr Clin North Am 49:73–96, 2002.

28 What are some of the food allergy disorders of infancy and their treatment?

Food protein–induced enterocolitis syndrome occurs in the first few months of life and involves allergy mainly to milk protein and soy. The infant presents with vomiting, diarrhea, and irritability and can present in shock. Food protein–induced enteropathy presents in infancy with diarrhea and poor weight gain. Vomiting and malabsorption also occur. Milk sensitivity is the usual culprit, but soy, egg, wheat, and other food can cause this. Biopsy of the small intestine shows villous atrophy with cellular infiltration. These symptoms also improve when the agent is removed, but these reactions often resolve by 1 year of age.

In both of these cases, whole cow milk should be substituted with casein hydrolysate formulas (Nutramigen, Pregestimil, Alimentum). Even whey hydrolysate or soy protein formulas are not appropriate, as some children have allergies to these as well. An amino acid–based formula (Neocate, Vivonex) can also be used.

Shah U, Walker WA: Food allergy. In Lifschitz CH (ed): Pediatric Gastroenterology and Nutrition in Clinical Practice. New York, Marcel Dekker, 2002, pp 601–613.

Spergel JM, Pawlowski NA: Food allergy: Mechanism, diagnosis and management in childhood. Pediatr Clin North Am 49:73–96, 2002.

29 What is celiac disease?

This is a specific food protein–induced enteropathy due to gluten, a protein found in grains. The specific proteins are gliadin in wheat, secalines in rye, and hordeins in barley. Some patients may also have problems with oats. It is an HLA-associated condition. Presenting symptoms include weight loss/failure to thrive, chronic diarrhea, steatorrhea, and abdominal distention. Treatment is avoidance of these grains.

Shah U, Walker WA: Food allergy. In Lifschitz CH (ed): Pediatric Gastroenterology and Nutrition in Clinical Practice. New York, Marcel Dekker, 2002, pp 601–613.

Shamir R: Advances in celiac disease. Gastroenterol Clin North Am 32:931–947, 2003.

Spergel JM, Pawlowski NA: Food allergy: Mechanism, diagnosis and management in childhood. Pediatr Clin North Am 49:73–96, 2002.

30 List some of the malignant abdominal masses in children

Wilms’ tumor, neuroblastoma, hepatoblastoma, hepatocarcinoma, pelvic sarcoma, lymphoma, teratomas, and ovarian tumors.

Rheingold SR, Lange B: Oncologic emergencies. In Fleisher GR, Ludwig S, Henretig FM (eds): Textbook of Pediatric Emergency Medicine, 5th ed. Philadelphia, Lippincott Williams & Wilkins, 2006, pp 1239–1274.

31 What is the classic triad of findings associated with hemolytic uremic syndrome?

Acute hemolytic anemia, thrombocytopenia, and renal injury (oliguria, abnormal urinalysis, increasing BUN and creatinine levels). Although usually associated with bloody diarrhea, there are actually two phenotypes of hemolytic uremic syndrome (HUS). One is diarrhea-associated (D+ HUS or typical HUS), the other nondiarrheal (D−, or atypical HUS). D+ HUS is usually caused by Shiga toxins elaborated by E. coli O157:H7 or Shigella dysenteriae type 1.

Cronan K, Kost S: Renal and electrolyte abnormalities. In Fleisher GR, Ludwig S, Henretig FM (eds): Textbook of Pediatric Emergency Medicine, 5th ed. Philadelphia, Lippincott Williams & Wilkins, 2006, pp 873–919.

Wong CS, Jelacic S, Habeeb RL, et al: The risk of hemolytic-uremic syndrome after antibiotic treatment of Escherichia coli O157:H7 infections. N Engl J Med 342:1930–1936, 2000.

32 A child has diarrhea as a result of E. coli O157:H7. Should he receive antibiotics?

No, because there is an increased risk (adjusted relative risk, 17.2) of that child developing HUS. This is true for sulfa-containing drugs as well as β-lactams.

Wong CS, Jelacic S, Habeeb RL, et al: The risk of hemolytic-uremic syndrome after antibiotic treatment of Escherichia coli O157:H7 infections. N Engl J Med 342:1930–1936, 2000.

33 What laboratory tests should you order for a child you think has pancreatitis?

Serum amylase levels become elevated within 2–12 hours of symptoms of acute pancreatitis, peak at 12–72 hours, and often return to normal in 3–5 days. Since amylase is produced in the salivary glands and ovaries, an isolated serum amylase level does not necessarily reflect pancreatic origin. Serum lipase increases 4–8 hours after the onset of symptoms, peaks at 24 hours, and remains elevated for 8–14 days. A serum lipase level three times normal has better diagnostic accuracy for pancreatitis than serum amylase.

Azzam R, Li BUK: Pancreatic disorders. In Green TP, Franklin WH, Tanz RR (eds). Pediatrics: Just the Facts. New York, McGraw-Hill, 2005, pp 325–327.

Pietzak MM: Acute and chronic pancreatitis. In Guandalini S (ed): Textbook of Pediatric Gastroenterology and Nutrition. London, Taylor & Francis, 2004, pp 303–318.

34 What causes pancreatitis in children?

Acute pancreatitis in children is due to one of several causes:

Pietzak MM: Acute and chronic pancreatitis. In Guandalini S (ed): Textbook of Pediatric Gastroenterology and Nutrition. London, Taylor & Francis, 2004, pp 303–318.

35 What is cyclic vomiting syndrome?

This is a syndrome of vomiting in a cyclic pattern that is severe, recurring, and stereotypical. There is a high intensity of vomiting (6–12 times an hour) that occurs 1–2 times a month and lasts approximately 24 hours. The child is well between episodes. It is often precipitated by psychological stress, infection, exhaustion, a menstrual period, or certain foods (cheese, chocolate, caffeine, monosodium glutamate), and there is usually a strong family history of migraine headaches. Treatment includes IV fluids with 10% dextrose in 0.2 normal saline (D10.2NS), 10 mL/kg bolus, then give at 1.5 times maintenance, ondansetron and lorazepam (or chlorpromazine and diphenhydramine).

Sunku B, Li BUK: Cyclic vomiting syndrome. In Guandalini S (ed): Textbook of Pediatric Gastroenterology and Nutrition. London, Taylor & Francis, 2004, pp 289–302.

Li BUK, Misiewicz L: Cyclic vomiting syndrome: A brain-gut disorder. Gastroenterol Clin North Am 32:997–1019, 2003.

36 What are the criteria necessary to make the diagnosis of cyclic vomiting syndrome?

Li BU: New hope for children with cyclic vomiting syndrome. Contemp Pediatr 19:121, 2002.

37 What is the typical history of the GI symptoms associated with Henoch-Schönlein purpura?

GI symptoms normally include nausea, vomiting, and abdominal pain and can occasionally result in intussusception, GI hemorrhage, and, rarely, bowel necrosis. The GI symptoms usually develop within 8 days of the rash. However, it has been noted that GI symptoms, including abdominal pain, precede the rash in about 15–35% of cases, making the diagnosis of the condition more challenging.

Chang WL, Yang YH, Lin YT, Chiang BL: Gastrointestinal manifestations in Henoch-Schönlein purpura: A review of 261 patients. Acta Paediatr 93:1427–1431, 2004.

38 What causes the abdominal pain in Henoch-Schönlein purpura?

The pain is thought to be caused by submucosal hemorrhage as well as edema. Endoscopy may reveal purpura in the stomach, duodenum, terminal ileum, and colon.

39 What is the suggested imaging study in suspected intussusception associated with Henoch-Schönlein purpura?

Abdominal ultrasonography is recommended as opposed to air or barium contrast enema (typically ordered when intussusception is suspected in patients without Henoch-Schönlein purpura). Contrast enemas cannot make the diagnosis of ileoileal intussusception, which is typically seen in patients with Henoch-Schönlein purpura–related intussusception.