Vomiting is the forceful retrograde expulsion of gastric contents through the mouth consequent to the coordinated contraction of diaphragm, abdominal, and respiratory muscles. It is associated with a characteristic autonomic response, including pallor, lethargy, hypersalivation, and tachycardia. This differentiates vomiting from regurgitation, which is an effortless involuntary reflux of undigested gastric contents and is not associated with abdominal/diaphragmatic contractions or autonomic responses. Nausea is the subjective unpleasant sensation of impending vomiting that precedes but is not always associated with vomiting. Emesis is a term that can be used to describe any expulsion of gastric contents, and is useful to the physician when describing symptoms that have not yet been fit into the more exact categories of vomiting or regurgitation. Rumination is voluntary reflux of gastric contents within the first hour after eating and is associated with chewing and reswallowing of undigested food. Retching or “dry heaves” is the activated emetic reflux without vomiting, due to vomiting motion against a closed glottis (Table 2–1). Vomiting should also be differentiated from coughing or spitting of mucus from the lungs.

Vomiting is a non-specific symptom caused by disorders affecting a wide range of organs. It can represent a mild self-limited illness (gastroenteritis), or occur as the result of severe life-threatening conditions (midgut volvulus). Vomiting is a common complaint among children who visit the pediatrician and the emergency department. Primary etiologies originate from the gastrointestinal tract, and are further divided into emergent disorders such as intussception and non-emergent causes such as viral gastroenteritis. Secondary causes involve etiologies that originate outside the gastrointestinal tract (Figure 2–1). Many of the secondary causes need immediate intervention, including cerebellar tumors, acute hydronephrosis from uretero-pelvic junction (UPJ) obstruction, and adrenal failure. In this chapter, we discuss a practical approach to a child who presents with vomiting.

Understanding the different neuroendocrine pathways and the neurotransmitters that mediate vomiting is useful in understanding the treatment of this symptom. Stimulation of the brain stem vomiting center is the final common result of many possible initiating events. The vomiting center is a complex of central nervous system nuclei, including the nucleus tractus solitarus (NTS), the parvicellular reticular formation, and the Bötzinger complex situated in the medulla oblongata.1 The vomiting center is stimulated through four access points:

• area postrema (chemoreceptor trigger zone (CTZ));
  
• hypothalamus;
  
• vestibular region;
  
• gastrointestinal tract.

The area postrema is a circumventricular organ located in the floor of fourth ventricle and is located outside the blood brain barrier, allowing it to sense circulating substances easily. This area, also known as the CTZ, has numerous D2, 5HT3, opiod, ACh, and substance P chemoreceptors that when stimulated by uremic toxins and emetic drugs (apomorphine) lead to vomiting.

The hypothalamus is stimulated by anxiety, stress, fear, and odors, leading to the release of GABA and corticotrophin-releasing factor that in turn leads to activation of vomiting center.

When activated by motion or inflammation (labyrinthitis), the eighth cranial nerve stimulates the vomiting center through the vestibular system by releasing acetylcholine and histamine.

Mucosal irritation (toxins or food poisoning) or distension of the gastrointestinal tract leads to stimulation of vomiting center via the vagal (5HT3) and enteric nervous system afferents.

Vomiting is a highly coordinated sequence of physiologic events as shown in Figure 2–2. Stimulation of vomiting center initiates a programmed emetic response that causes descent of the diaphragm and contraction of the intercostal muscles against the closed glottis. Finally, increase in intra-abdominal pressure from the contraction of abdominal muscles and elevation of diaphragm results in forceful expulsion of gastric contents into lower esophagus, and beyond.

The diagnostic approach to a patient begins by defining the symptoms and addressing the following questions:

• Is the child adequately hydrated?
  
• Is the emesis vomiting or regurgitation?
  
• What is the temporal pattern of vomiting?
  
• Are there any red flag symptoms or signs that require further evaluation?
  
• Are there any associated symptoms and signs?

The initial encounter with the patient should focus on assessing the degree of dehydration and managing the patient accordingly. Dehydration is classified as mild, moderate, or severe based on the child’s appearance, urine output, skin turgor, mucous membranes, tears, capillary refill time, heart rate, and blood pressure.

Once the patient is stable, a detailed history and examination will often differentiate vomiting from regurgitation as shown in Table 2–2.2 This difference is key to the identification of gastroesophageal reflux (regurgitation) and especially critical preoperatively identifying those at risk for post-Nissen retching syndrome.3 Once the diagnosis of vomiting is established, the long list of differential diagnosis outlined in Table 2–3 can be narrowed down by obtaining the age and temporal pattern of vomiting (acute, chronic, or cyclic). Further questions should be elicited carefully to look for red flag symptoms and signs such as weight loss, bilious or bloody emesis, etc., as shown in Table 2–4. Other associated symptoms and signs also provide vital information such as contents of vomitus, dysphagia, and the relationship to meals (Table 2–5). The two most important parameters that are helpful in narrowing the differential diagnosis of vomiting are age of the patient and the pattern of vomiting.