George Gershman, MD
A 10-month-old previously healthy infant was brought to the emergency department by his mother, who reported the sudden onset of green emesis and abdominal pain over the last 4 hours. Vomiting was not associated with meals. The mother denied recent illness, travel, or sick contacts. The patient’s past medical history is unremarkable. His birth weight was 3,200 g (7.05 lb), and his current weight is 9,080 g (20.0 lb). The physical examination is significant for distended abdomen tender to palpation.
1. What is the mechanism of vomiting?
2. What are the common causes of vomiting in newborns and infants?
3. What are the common causes of vomiting in older children?
4. What is the significance of bilious vomiting?
5. What are the unique features of vomiting related to increased intracranial pressure?
6. What are some strategies for the management of vomiting in older children?
Vomiting is a common symptom in infants and children and led Thomas Phaire to write, “Many tymes the stomake of ye child is so feble that it cannot retayne eyther meate or drynke…” (The Boke of Chyldren, 1544). Vomiting is defined as the forceful ejection of the stomach contents through the mouth. The mechanism involves a series of complex, neurologically coordinated events under the control of the central nervous system (CNS). Vomiting is often accompanied by autonomic signs such as pallor, diaphoresis, hypersalivation, listlessness, and tachycardia. Nausea and vomiting are common symptoms in infants and children and may be associated with gastrointestinal (GI) illnesses, other acute or chronic disorders, and medications.
In contrast, regurgitation (commonly called “spitting up” by parents) is the effortless bringing up of 1 or 2 mouthfuls of food without distress or discomfort. This is a frequent symptom of gastroesophageal reflux in infants (see Chapter 121). Rumination, a form of autostimulation, is the voluntary induction of regurgitation. It is most often noted in infants between the ages of 3 and 6 months. Rumination occurs in infants with developmental delays or with a disturbed mother-infant relationship. Rumination should be considered in infants from deprived environments (eg, neglectful homes).
Fifty percent of infants have spitting up or vomiting as an isolated symptom, and less than 5% of these infants have significant underlying disease. Vomiting occurs less frequently in older children, who often experience acute, self-limited illnesses, such as gastroenteritis.
Vomiting is categorized by its color (bilious or non-bilious) and temporal pattern (ie, acute, chronic, or cyclic [episodic]). The vomitus is considered bilious if it has a green or bright yellow color, indicative of large amounts of bile in the stomach and usually associated with intestinal obstruction. When vomiting occurs suddenly in a previously healthy child, it is acute. Most frequently, vomiting is related to acute gastroenteritis, urinary tract or other extraintestinal infections, or toxic ingestion. Acute vomiting may be indicative of a surgical condition, such as appendicitis, intestinal obstruction, or other acute condition. Chronic vomiting consists of a low-frequency (ie, once or twice daily) vomiting that never leads to dehydration. Chronic conditions such as peptic ulcer disease, Crohn disease, and cow’s milk protein allergy can be associated with chronic vomiting. Children with cyclic vomiting experience intense, unremitting nausea and paroxysmal vomiting lasting hours to days, often leading to dehydration.
Infants and children may present with vomiting as an isolated symptom or in association with other symptoms, including faintness, diaphoresis, sweating, pallor, tachycardia, fever, anorexia, abdominal pain, and diarrhea (Box 120.1). When vomiting has persisted over a period, weight loss or failure to thrive (FTT) may occur. Neurologic symptoms, including headache and gait disturbances, may be noted in children with CNS problems. Other neurologic symptoms of altered muscle tone, lethargy, seizures, or coma in young infants suggest inborn errors of metabolism.
Vomiting is a reflex reaction that occurs in response to numerous stimuli, such as enteric infections, toxins, drugs, chemotherapy, and radiation. The final common pathway involves expulsion of food from the relaxed stomach into the mouth due to coordinated contraction of the abdominal wall, respiratory muscles, increased intra-abdominal and thoracic pressure, and relaxation of the lower and upper esophageal sphincters.
Box 120.1. Diagnosis of Vomiting in the Pediatric Patient
Anything that delays gastric emptying may be associated with vomiting. Gastric emptying may be delayed by a high-fat meal, swallowed mucus (eg, maternal mucus after birth, nasal mucus with an upper respiratory infection), fever, infection, and malnutrition. Delayed gastric emptying may develop with long-standing diabetes mellitus.
Vomiting can be divided into 3 phases: nausea, retching, and emesis. However, nausea may occur without retching and vomiting, and retching may occur without vomiting.
Nausea is a significant and difficult-to-define discomfort related to the sensation of a need to vomit. It can be produced by various stimuli (eg, bacterial toxins, drugs, intestinal distention, visceral pain, unpleasant memories, labyrinthine stimulation, noxious odors, visual stimulations, unpleasant taste, increased cerebral pressure). Peripheral receptors in the stomach and the small and large intestines detect emetic stimuli, distention and contractions are recognized by mechanoreceptors, and toxins are sensed by chemoreceptors. Emetic stimuli may also originate from the obstructed or inflamed bile ducts, peritoneal inflammation, mesenteric vascular occlusion, pharynx, and heart. Vagal pathways mediate emetic responses to a variety of peripheral stimuli. Most afferent vagal fibers project to the nucleus tractus solitarius and some to the area postrema or dorsal vagal motor nucleus. The serotonergic pathway plays the central role in nausea induced by peripheral stimuli.
The area postrema on the dorsal surface of the medulla close to the fourth ventricle is considered the chemoreceptor trigger zone to a variety of neurochemical stimuli. Bacterial toxins, drugs, toxic products of metabolic disorders, and radiation therapy may induce nausea by stimulation of numerous central receptors: dopamine D2, muscarinic M1, histaminergic H1, serotonergic 5-HT3, and vaso-pressinergic subtypes located in the area postrema. However, afferent excitation of multiple brain sites, including the nucleus tractus solitarius, dorsal vagal and phrenic nuclei, medullary nuclei controlling respiration, hypothalamus, and amygdala, is responsible for coordinated activities of various organs and muscles and the induction of retching and emesis.
Retching is the second phase of vomiting. It is produced by concurrent contractions of inspiratory thoracic, diaphragmatic, and abdominal muscles against the closed glottis. The generated high positive intra-abdominal pressure forces gastric contents into the esophagus and herniates the gastric cardia into the thorax. At this phase, the high negative thoracic pressure prevents emesis of gastric fluids.
Emesis is the final stage of vomiting. Synchronous contractions of the inspiratory and expiratory muscles generate high positive intrathoracic pressure sufficient to produce expulsion of gastric contents into the mouth. Oral propulsion of the vomitus is facilitated by the elevation of the hyoid bone and larynx. Airways are protected from aspiration by glottis closure. Elevation of the soft palate prevents passage of the vomitus into the nasal cavities. Hyperventilation may occur before emesis. During vomiting, breathing is suppressed.
With emesis, retrograde giant contractions originate from the middle of the small intestine. Intestinal contents move into the stomach, causing duodenogastric reflux. Within the stomach, the fundus remains flaccid, but the antrum and pylorus contract. Relaxation of the lower esophageal sphincter also occurs.
In children with pyloric stenosis, duodenogastric reflux is prevented by hypertrophy of the pylorus. Projectile vomiting is facilitated by giant, often-visible contractions of the antrum and relaxation of the proximal stomach and low esophageal sphincter. Nausea is not associated with vomiting related to pyloric stenosis, and affected infants are frequently eager to eat immediately after vomiting.
Vomiting induced by increased intracranial pressure (ICP) is also not associated with nausea. In addition, such vomiting frequently occurs first thing in the morning on awaking and on an empty stomach. Regurgitation is a return of undigested food back up the esophagus to the mouth without the force and displeasure associated with vomiting. It could be manifested by visible spitting up after feeding or could be silent. Clinical evidence of regurgitation is not always associated with gastroesophageal reflux disease.
Vomiting can be a manifestation of GI, renal, metabolic, allergic, and CNS disorders, and the age of the patient influences the differential diagnosis and management. Some conditions respond to medical management, and others mandate surgical intervention (Box 120.2). The green color of the vomitus, referred to as bilious vomiting, is a serious sign, usually indicative of intestinal obstruction distal to the major duodenal papilla and of the need for surgical intervention. Bilious vomiting can also occur in children with pseudo-obstruction or acute pancreatitis and other conditions associated with paralytic ileus.
The presence of blood in the vomitus is another ominous sign and is discussed in Chapter 122.
The most common cause of vomiting is acute viral or bacterial gastroenteritis. Acute gastroenteritis is discussed in greater detail in Chapter 123. In cases that are not related to acute gastroenteritis, considering the age of the patient is the best approach to the differential diagnosis of vomiting.
Newborns and Infants
Vomiting in neonates may be associated with the ingestion of irritants such as maternal blood or mucus. Either of these substances delays gastric emptying. Structural anomalies of the GI tract may also cause vomiting in neonates. The onset of symptoms is directly related to the level of obstruction—the higher the structural obstruction, the earlier the onset of vomiting. Lesions of the esophagus, such as esophageal atresia, may be evident in the delivery room, with an unsuccessful attempt to pass a nasogastric tube. Lower GI lesions, such as ileal atresia, may not present for several days. These lesions require surgical intervention. Infants with atretic lesions may also have a history of polyhydramnios or a single umbilical artery.
Box 120.2. Differential Diagnosis of Vomiting in Infancy
•Ingestion of maternal blood or mucus
•Atresia/stenosis of gastrointestinal tract
•Inborn errors of metabolism
•Congenital adrenal hyperplasia
•Infections (eg, otitis media, urinary tract)
•Congenital megacolon (Hirschsprung disease)