Ronald A. Furnival and Marissa A. Hendrickson
Vomiting is the coordinated action of the pharyngeal, esophageal, stomach, and diaphragmatic musculature to expel gastric contents, directed by the medullary vomiting center within the central nervous system. This center receives input from the chemoreceptor trigger zone in the floor of the fourth ventricle and from higher cortical centers that receive and process external stimuli. Although vomiting may provide a survival advantage by expelling ingested toxins, it frequently occurs with disorders from a variety of organ systems (1).
Infants and children with vomiting commonly present to the emergency department (ED) for diagnosis and treatment. For most pediatric patients, vomiting is associated with relatively minor self-limited conditions, but it may also be a manifestation of serious surgical or medical illness. In the ED, the first priority must be to determine whether clinical stabilization is immediately required and whether an emergent surgical or medical condition exists. If no evidence of serious illness is identified, the next priority becomes recognizing and initiating therapy for the less urgent clinical conditions associated with vomiting.
CLINICAL PRESENTATION
The initial ED history and physical examination should identify and address any evidence of systemic illness or toxicity. Persistent vomiting with severe dehydration or metabolic abnormalities may require treatment prior to establishing a definitive diagnosis. Because pediatric vomiting may be a nonspecific symptom associated with severe systemic illness (e.g., meningitis, sepsis, respiratory distress, drug overdose, closed head injury, ventriculoperitoneal shunt failure, etc.), the ED evaluation must consider or rule out these possible etiologies, based upon the initial history and physical examination.
The initial history must define whether the emesis is bilious or nonbilious. Bilious vomiting, containing dark green material from the biliary tract, generally indicates a mechanical or functional bowel obstruction below the ampulla of Vater. Nonbilious emesis implies either a more proximal obstruction in the duodenum or a functional disorder with no mechanical bowel obstruction (1). Yellow bile-stained emesis occasionally may occur with persistent vomiting and no bowel obstruction. This emesis is usually caused by a temporary reversal of gastric peristalsis. Fecal material in the emesis indicates a colonic obstruction, as in severe obstipation, Hirschsprung disease, or other large bowel disorders. Although studies have found that only 10% to 38% of infants and children presenting to the ED with bilious (either yellow or green) vomiting will ultimately be diagnosed with an emergent surgical condition, every child with bilious emesis must be assumed to have a bowel obstruction until proven otherwise (2–4).
The duration of vomiting, the number of episodes each day, and any additional gastrointestinal (GI) symptoms should be defined next, including abdominal pain, distention, anorexia, diarrhea, constipation, and presence of blood in the emesis or stools. The history should also note presence of systemic (fever, weight loss, nutritional status, hydration status), neurologic (headache, neck pain or stiffness, coordination or behavioral changes), genitourinary (dysuria, hematuria, change in urine output, vaginal discharge or bleeding), respiratory (cough, evidence of distress), or head and neck (otalgia, sore throat, dysphagia, nasal drainage) symptoms to further direct care and diagnostic evaluation. A past history of similar severe episodes of vomiting may lead to the diagnosis of a recurring condition, such as cyclic vomiting, an inborn error of metabolism, or malrotation with intermittent volvulus; a history of early morning vomiting should raise concerns for an intracranial mass lesion (1).
The physical examination should initially seek evidence of systemic toxicity, including respiratory or cardiovascular instability, altered mental status, or severe dehydration. A validated pediatric scoring tool for the clinical assessment of dehydration using a combination of four objective physical findings (dry mucous membranes, absent tears, abnormally lethargic or restless appearance, prolonged capillary refill) has proven to be helpful in the recognition of dehydration, with two of four findings present with 5% dehydration, and three or more present with more severe states of dehydration (5–7).
On abdominal examination, auscultation for bowel sounds prior to palpation may reveal diminished activity with ileus arising from surgical or medical illness, or increased activity (borborygmi) with partial bowel obstruction or a diarrheal disorder. Next, palpation for abdominal tenderness, distention, mass, or enlargement of the liver or spleen should be performed. Gentle one- or two-finger percussion, rather than the less accurate gross abdominal wall movement with the compression-rebound technique, may demonstrate peritoneal findings associated with surgical conditions such as appendicitis. Finally, a thorough general evaluation for nonabdominal conditions associated with vomiting, including the head and neck, pulmonary, genitourinary, and neurologic examination, may identify the etiology and direct or obviate further diagnostic workup.
DIFFERENTIAL DIAGNOSIS
While viral gastroenteritis is one of the most common causes of vomiting for infants and children of all ages, the differential diagnosis for vomiting varies according to age at presentation. Table 223.1 outlines an age-based differential diagnosis for surgical and medical etiologies of pediatric vomiting.
TABLE 223.1
Age-Based Differential Diagnosis for Vomiting
For the infant from birth to 2 months of age, the most common condition associated with vomiting is gastroesophageal reflux, often resulting from overfeeding; it typically occurs within 30 to 60 minutes of feeding in an otherwise healthy-appearing infant. Occult gastroesophageal reflux may present as positional fussiness, persistent cough and congestion, or truncal arching (Sandifer syndrome) that may mimic tonic seizure activity. Reflux precautions, including formula thickened with rice cereal, small frequent feedings, and upright positioning for 30 minutes after feedings, will effectively treat the majority of infants. Persistent reflux may require medical therapy (8).
Pyloric stenosis is the most common surgical condition that must be differentiated from gastroesophageal reflux in vomiting infants. Most affected infants present at 3 to 4 weeks of age, with a history of 1 to 2 weeks of progressive forceful “projectile” nonbilious vomiting. With more advanced disease, there may be weight loss from severe dehydration. While palpation of the hypertrophied pylorus or “olive” is diagnostic, the physical examination is often nonspecific, and an ultrasound is generally required for definitive diagnosis in younger infants (9,10). ED treatment includes prompt evaluation for electrolyte disturbances (the classic presentation with hypochloremic metabolic alkalosis has become increasingly rare) and intravenous (IV) fluid rehydration, with surgical referral for suspected cases (9).
Other emergent surgical causes of vomiting in the first 2 months of life include congenital GI anomalies (intestinal stenosis or duplications, duodenal or antral webs, annular pancreas, etc.), incarcerated inguinal hernia, malrotation with volvulus, and Hirschsprung disease. Most UGI congenital anomalies present within the first few days of life and are infrequently seen in the ED setting. An inguinal hernia may be noted on examination of the diaper area, with the presence of an inguinal, scrotal, or labial mass. Steady and gentle pressure at the external inguinal ring and on the mass can successfully reduce the majority of hernias. However, some patients may require sedation and surgical consultation if the initial ED attempt is unsuccessful.
The young infant presenting to the ED with bilious emesis (even one episode) must, without exception, be assumed to have GI malrotation with volvulus until proven otherwise. Eighty-five percent of patients with volvulus present in the first year of life, and 60% of patients present within the first month of life. The abdominal examination may be normal in up to 75% of cases, but diminished bowel sounds, distention, a palpable mass, or tenderness may be noted in 10% to 25% of infants with volvulus (3). Hypovolemic shock from prolonged intestinal ischemia is uncommon at presentation, but must be considered in the moribund infant. Immediate evaluation with a UGI series (a contrast enema may miss the diagnosis in up to 20% of patients) is required for all suspected cases, with emergent surgical consultation and laparotomy for any symptomatic patient with an identified malrotation (1,3,11).
Hirschsprung disease, or aganglionosis, is a fairly common cause of intestinal obstruction in newborns, infants, or young children. It occurs in 1 in 5,000 live births, and more than 80% of cases are diagnosed within the first year of life. Up to 90% of infants with Hirschsprung disease have a history of failure to pass meconium in the first 24 hours of life, making this an important historical question for any child presenting with abdominal pain. Hirschsprung is due to a congenital absence of ganglion cells in the colonic submucosa, resulting in uncoordinated intestinal contractions which manifest clinically as chronic constipation, abdominal distention, and vomiting. Abdominal radiographs may demonstrate dilated proximal bowel loops with air-fluid levels; a contrast enema may be diagnostic in more than 80% of cases. ED treatment consists of IV fluid resuscitation, nasogastric (NG) decompression, broad-spectrum antibiotics (with anaerobic coverage), and surgical consultation for confirmatory biopsy and corrective surgery (12). Even after corrective surgery, toxic megacolon or enterocolitis remains a significant concern, occurring in more than one-third of Hirschsprung patients because of retained aganglionic segments of bowel. Enterocolitis may present as abdominal distention, foul watery diarrhea, lethargy, or systemic toxicity, and must be recognized and treated early with aggressive supportive care, including broad-spectrum antibiotics and rectal irrigation (12).
Many other medical conditions may cause vomiting in young infants. Infections such as sepsis, meningitis, encephalitis, hepatitis, pharyngitis, stomatitis, or otitis media may present with vomiting as an initial symptom. Gastroenteritis is common year-round, with seasonal peaks during summer and winter viral outbreaks. Urinary tract infection is the most common bacterial source for a fever in infants with a normal physical examination, and may present with vomiting and no diarrhea (13). Respiratory distress from pertussis, pneumonia, asthma, bronchiolitis, or aspiration in the developmentally impaired patient may also be noticed only after the infant has been vomiting.
Intracranial pathology, from occult closed head injury, abuse, hydrocephalus, or hemorrhage may present with neurologic findings and associated vomiting. Victims of nonaccidental trauma involving occult head trauma or abdominal trauma may present with vomiting. Only with careful history taking and consideration of abuse as an etiology will these cases be detected (see Chapter 290). Patients with indwelling ventricular peritoneal shunts (see Chapter 291) may present with vomiting as their only sign of increasing intracranial pressure (ICP) with shunt failure.
Finally, metabolic conditions such as inborn errors of metabolism, renal tubular acidosis, and congenital adrenal hyperplasia may present as vomiting with metabolic acidosis, hypoglycemia, hyperammonemia, or hyperkalemia in combination with hyponatremia (14,15). While a number of the conditions outlined previously may also affect the older infant or child, gastroesophageal reflux, congenital anomalies, and inborn metabolic disorders become less likely with increasing age.
Two common surgical disorders to consider in the older infant or child with vomiting are appendicitis and intussusception. While only 10% of appendicitis occurs in children younger than 10 years of age, and only 1% in infants younger than 2 years, it remains the most frequent indication for emergent pediatric surgery. The “classic” findings of right lower quadrant abdominal pain, vomiting, and fever are uncommon in younger patients, who may have an atypical history of diarrhea or respiratory distress, evidence of generalized sepsis, or atypical laboratory findings at presentation (16). Because of the nonspecific nature of such symptoms and perhaps a more rapid progression to perforation, appendicitis in the child younger than 4 years of age is often associated with an 80% perforation rate at the time of diagnosis and a significant mortality risk among younger infants. Older children may be more likely to have the classic presentation of appendicitis, and may be appropriate for surgical consultation and clinical diagnosis.
While contrast pelvic computed tomography (CT) scan has been quite accurate for the diagnosis of pediatric appendicitis, recent research has attempted to improve appendicitis diagnostic accuracy, while limiting CT scan utilization and its associated radiation risk. A multicenter-validated prediction rule using an absolute neutrophil count ≤6.75 × 103 µL with either no maximal tenderness in the right lower abdominal quadrant, or absence of pain with walking or jumping, was able to identify children at low risk of appendicitis with 98% sensitivity, patients who may be appropriate for further clinical observation (17). If imaging is utilized for the diagnosis of appendicitis, a staged approach using US, followed by CT scan if negative or equivocal, has been found to be both very sensitive for the diagnosis, and cost-effective, while limiting radiation exposure (18,19).
Intussusception, from a spontaneous invagination of the intestine upon itself, compromises the vascular supply to the inner segment or intussusceptum. Approximately 95% of intussusception is ileocolic, beginning at the ileocecal valve; the remaining 5% are ileoileal or occur within the colon or sigmoid. Sixty-five percent of intussusception occurs in infants younger than 1 year of age, most frequently (45%) between 5 and 9 months of age (20). The typical infant presents with sudden onset of intermittent severe abdominal pain and vomiting and may appear well between episodes. Bilious vomiting, lethargy, passage of bloody mucus or “currant-jelly” stool, peritonitis, or evidence of cardiovascular compromise are often late findings that indicate more advanced intestinal ischemia, which may require surgical resection (21). The abdominal examination may identify a palpable mass but is usually normal, often with only a positive stool guaiac test to confirm the clinical suspicion for intussusception; abdominal radiographs are generally normal or nonspecific (22). Ultrasound or air-contrast enema is diagnostic for nearly 100% of cases. Air-contrast enema allows therapeutic reduction of the intussusception, and is associated with successful reduction in up to 90% of pediatric cases (23).
In older infants and children, vomiting may be due to a number of medical conditions, including endocrinologic disorders such as new-onset type 1 diabetes, which may present as diabetic ketoacidosis, or renal and adrenal insufficiency. Henoch–Schönlein purpura (HSP), with its characteristic vasculitic lesions concentrated on the lower extremities, may cause abdominal pain and vomiting associated with HSP’s increased risk for intussusception.
A number of other conditions, both common and uncommon, may also need to be considered. In accidental drug ingestion in the exploring toddler or intentional overdose in the adolescent, vomiting may be associated with toxin-specific findings. Pancreatitis, cholecystitis, inflammatory bowel disease, and nephrolithiasis, most often seen in older patients, may also present with frequent vomiting. Migraine, cyclic vomiting, and some seizure variants may cause recurrent vomiting episodes (24). Pregnancy (intrauterine and ectopic), ovarian cysts, torsion, and pelvic inflammatory disease must be considered in the differential of the vomiting adolescent female.
DIAGNOSTIC APPROACH
The initial ED therapy for the vomiting infant or child must focus on identifying and managing any evidence of systemic toxicity. Patients with clinical evidence or concern for increased ICP or occult abdominal injury should be stabilized and imaged emergently. Most well-appearing or mildly ill-appearing children without severe abdominal pain, bilious vomiting, or evidence of medical or surgical emergency can be managed with a trial of oral hydration with clear liquids, facilitated with oral ondansetron. However, in children with evidence of clinical instability, prompt IV access should be established, with fluid administration of 20 mL/kg boluses of isotonic normal saline or lactated Ringers solution, and repeated boluses as needed. Analgesics should be administered early in the child being evaluated for appendicitis or other painful conditions; well-designed prospective pediatric studies have found no adverse effects of ED pain control on diagnostic accuracy or clinical outcomes (25). Surgical consultation should be arranged for all patients with suspected surgical conditions, evidence of peritonitis, or unstable trauma prior to reaching a definitive diagnosis.
Initial diagnostic laboratory studies generally include serum electrolytes, glucose, and renal function tests when there is clinical evidence of moderate to severe dehydration. A bedside glucose measurement should be obtained in unstable patients with altered mental status or in whom undiagnosed diabetes is in the differential diagnosis. In the mildly dehydrated child the bedside glucose may be the only test needed. Additional tests may also be indicated for more severely ill children including a complete blood count (CBC) with a type and cross-match for surgical patients, liver function tests, lipase test for undiagnosed pancreatitis or gall bladder disease, and a urinalysis and urine culture for the febrile patient with a possible urinary tract infection.
After initial stabilization, diagnostic imaging may be necessary to identify the cause of vomiting. A chest x-ray should be considered in the patient with respiratory symptoms and may lead to the diagnosis of pneumonia. If the infant or child is suspected of having bowel obstruction, ileus, or mass, or with evidence of peritonitis, flat and upright abdominal x-rays may confirm the diagnosis and direct further care. For the young infant with bilious vomiting, the initial test of choice is unquestionably the UGI series, which is more sensitive for the diagnosis of malrotation than contrast enema studies. However, confirmatory studies must not delay an emergent surgical consultation in this situation. The contrast enema may be both diagnostic and therapeutic for the older infant or toddler with a suspected intussusception, although ultrasound is often the preferred initial diagnostic test. A contrast enema may also diagnose Hirschsprung disease in the infant with chronic constipation, demonstrating a funnel-shaped transition zone at the border between the normal and abnormal bowel segments. Ultrasound is often helpful in diagnosing pyloric stenosis, appendicitis, intussusception, ureteropelvic junction obstruction, and gynecologic disorders. Appendicitis may be diagnosed by ultrasound or a pelvic CT scan, though a staged approach with an initial US is recommended to minimize the radiation exposure associated with CT (18,19). CT scan is, however, the test of choice for the evaluation of abdominal masses, nephrolithiasis, abdominal trauma, and intracranial pathology.
CRITICAL INTERVENTIONS
• Address clinical instability prior to efforts at definitive diagnosis.
• Check a bedside serum glucose in the infant or child with altered mental status or other evidence of systemic toxicity.
• Give stress-dose corticosteroids (hydrocortisone 25–100 mg IV bolus) to the ill-appearing steroid-dependent patient as soon as possible.
• Consider bilious vomiting or evidence of peritonitis to be caused by an emergent surgical condition until proven otherwise.
DISPOSITION
For the vomiting infant or child with a self-limited condition, no evidence of serious systemic illness, and only mild or moderate dehydration, ED oral hydration with continued outpatient oral rehydration is appropriate, along with defined discharge instructions and a clear follow-up plan. IV fluid rehydration should be utilized for the vomiting patient who cannot tolerate oral fluids, with demonstrated electrolyte abnormalities, or with more severe illness. Recent well-designed prospective pediatric studies have demonstrated a benefit from the administration of oral or IV ondansetron with ED rehydration, noting a significant reduction in continued vomiting, improved tolerance of oral fluid challenges, and reduced hospital admission rates (26–28). While two 20 mL/kg IV isotonic fluid boluses may improve most mildly dehydrated patients enough to make them safe for discharge, those with persistent vomiting, and significant serum electrolyte or glucose abnormalities may benefit from continued inpatient rehydration and observation.
Common Pitfalls
• Overzealous use of laboratory studies and IV fluids in well-appearing children with vomiting; many can be managed with oral hydration and oral ondansetron as needed.
• Forgetting to assess for hypoglycemia in a vomiting infant or child. A rapid glucose test should be checked with the first blood draw.
• Failing to aggressively evaluate and treat the young infant with bilious emesis, even if physical examination and laboratory studies appear normal. Do not miss the diagnosis of malrotation.
• Overlooking subtle presentations of occult injury in patients with nonaccidental trauma, accidental or intentional ingestions, and ventriculoperitoneal shunt failures.
REFERENCES
1. Chandran L, Chitkara M. Vomiting in children: Reassurance, red flag, or referral? Pediatr Rev. 2008;29(6):183–192.
2. Godbole P, Stringer MD. Bilious vomiting in the newborn: How often is it pathologic? J Pediatr Surg. 2002;37(6):909–911.
3. Malhotra A, Lakkundi A, Carse E. Bilious vomiting in the newborn: 6 years data from a Level III Centre. J Paediatr Child Health. 2010;46(5):259–261.
4. Sadow KB, Atabaki SM, Johns CM, et al. Bilious emesis in the pediatric emergency department: Etiology and outcome. Clin Pediatr (Phila). 2002;41(7):475–479.
5. Bailey B, Gravel J, Goldman RD, et al. External validation of the clinical dehydration scale for children with acute gastroenteritis. Acad Emerg Med. 2010;17(6):583–588.
6. Goldman RD, Friedman JN, Parkin PC. Validation of the clinical dehydration scale for children with acute gastroenteritis. Pediatrics. 2008;122(3):545–549.
7. Gorelick MH, Shaw KN, Murphy KO. Validity and reliability of clinical signs in the diagnosis of dehydration in children. Pediatrics. 1997;99(5):E6.
8. Horvath A, Dziechciarz P, Szajewska H. The effect of thickened-feed interventions on gastroesophageal reflux in infants: Systematic review and meta-analysis of randomized, controlled trials. Pediatrics.2008;122(6):e1268–e1277.
9. Glatstein M, Carbell G, Boddu SK, et al. The changing clinical presentation of hypertrophic pyloric stenosis: The experience of a large, tertiary care pediatric hospital. Clin Pediatr (Phila). 2011;50(3):192–195.
10. Iqbal CW, Rivard DC, Mortellaro VE, et al. Evaluation of ultrasonographic parameters in the diagnosis of pyloric stenosis relative to patient age and size. J Pediatr Surg. 2012;47(8):1542–1547.
11. Lampl B, Levin TL, Berdon WE, et al. Malrotation and midgut volvulus: A historical review and current controversies in diagnosis and management. Pediatr Radiol. 2009;39(4):359–366.
12. Doodnath R, Puri P. A systematic review and meta-analysis of Hirschsprung’s disease presenting after childhood. Pediatr Surg Int. 2010;26(11):1107–1110.
13. Shaw KN, Gorelick M, McGowan KL, et al. Prevalence of urinary tract infection in febrile young children in the emergency department. Pediatrics. 1998;102(2):e16.
14. Kamboj M. Clinical approach to the diagnoses of inborn errors of metabolism. Pediatr Clin North Am. 2008;55(5):1113–1127, viii.
15. Zand DJ, Brown KM, Lichter-Konecki U, et al. Effectiveness of a clinical pathway for the emergency treatment of patients with inborn errors of metabolism. Pediatrics. 2008;122(6):1191–1195.
16. Becker T, Kharbanda A, Bachur R. Atypical clinical features of pediatric appendicitis. Acad Emerg Med. 2007;14(2):124–129.
17. Kharbanda AB, Dudley NC, Bajaj L, et al. Validation and refinement of a prediction rule to identify children at low risk for acute appendicitis. Arch Pediatr Adolesc Med. 2012;166(8):738–744.
18. Krishnamoorthi R, Ramarajan N, Wang NE, et al. Effectiveness of a staged US and CT protocol for the diagnosis of pediatric appendicitis: Reducing radiation exposure in the age of ALARA. Radiology.2011;259(1):231–239.
19. Wan MJ, Krahn M, Ungar WJ, et al. Acute appendicitis in young children: Cost-effectiveness of US versus CT in diagnosis–a Markov decision analytic model. Radiology. 2009;250(2):378–386.
20. Weihmiller SN, Buonomo C, Bachur R. Risk stratification of children being evaluated for intussusception. Pediatrics. 2011;127(2):e296–e303.
21. Jen HC, Shew SB. The impact of hospital type and experience on the operative utilization in pediatric intussusception: A nationwide study. J Pediatr Surg. 2009;44(1):241–246.
22. Morrison J, Lucas N, Gravel J. The role of abdominal radiography in the diagnosis of intussusception when interpreted by pediatric emergency physicians. J Pediatr. 2009;155(4):556–559.
23. Bucher BT, Hall BL, Warner BW, et al. Intussusception in children: Cost-effectiveness of ultrasound vs diagnostic contrast enema. J Pediatr Surg. 2011;46(6):1099–1105.
24. Li BU, Lefevre F, Chelimsky GG, et al. North American Society for Pediatric Gastroenterology, Hepatology, and Nutrition consensus statement on the diagnosis and management of cyclic vomiting syndrome. J Pediatr Gastroenterol Nutr. 2008;47(3):379–393.
25. Bailey B, Bergeron S, Gravel J, et al. Efficacy and impact of intravenous morphine before surgical consultation in children with right lower quadrant pain suggestive of appendicitis: A randomized controlled trial. Ann Emerg Med.2007;50(4):371–378.
26. DeCamp LR, Byerley JS, Doshi N, et al. Use of antiemetic agents in acute gastroenteritis: A systematic review and meta-analysis. Arch Pediatr Adolesc Med. 2008; 162(9):858–865.
27. Fedorowicz Z, Jagannath VA, Carter B. Antiemetics for reducing vomiting related to acute gastroenteritis in children and adolescents. Cochrane Database Syst Rev. 2011;(9):CD005506.
28. Roslund G, Hepps TS, McQuillen KK. The role of oral ondansetron in children with vomiting as a result of acute gastritis/gastroenteritis who have failed oral rehydration therapy: A randomized controlled trial. Ann Emerg Med.2008;52(1):22–29 e6.