1. 
   

   What key clinical entities must be considered in the initial assessment of a hospitalized patient with acute nausea and vomiting?

   
   
2. 
   

   What is the clinical diagnostic approach to the inpatient with nausea and vomiting?

   
   
3. 
   

   How should patients with nausea and vomiting in the hospital setting be treated?

Nausea and vomiting are common and uncomfortable symptoms with a large number of underlying causes. Nausea is a subjective sensation, usually experienced in the epigastrium or throat when vomiting is imminent (although vomiting may or may not occur). Nausea may be followed by retching, which is repetitive active contraction of the abdominal musculature. Retching may occur in isolation without the forceful expulsion of gastric contents. In contrast, vomiting is a highly physical event that results in the evacuation of gastric contents. This should be distinguished from regurgitation, which is the effortless reflux of gastric or esophageal contents to the hypopharynx.

Pathophysiology

Studies have suggested that the act of vomiting is controlled by a central neurologic center. Borison and colleagues have studied the mechanism of vomiting in cats and found that vomiting can be induced by electrical stimulation of a “vomiting center” located in the dorsal portion of the medulla. These studies, however, have not yet been repeated in human subjects. Experimental studies have also suggested that a chemoreceptor trigger zone (CTZ) activates the vomiting center when stimulated.

Emetic stimuli can cause vomiting by one of two mechanisms. One mechanism is by activation of afferent vagal and sympathetic neural pathways within the gastrointestinal tract that act directly on the vomiting center. Ablation of these pathways in experimental animals prevents vomiting induced by copper sulfate, which is known to cause vomiting. The second mechanism by which emetic stimuli can cause vomiting is via the CTZ. Unlike the vomiting center, the CTZ is not responsive to electrical stimuli, but only to chemical stimuli from the circulation that crosses the blood–brain barrier. These stimuli include drugs, uremia, diabetic ketoacidosis (DKA), and toxins derived from gram-positive bacteria. The exact neurotransmitters that are involved are not known, but there is strong evidence that both dopamine and serotonin may mediate vomiting.

Regardless of the emetic stimulus or the mechanism by which the vomiting center is activated, the act of vomiting is initiated from the vomiting center. The efferent pathways are primarily somatic and involve the vagus, phrenic, and spinal nerves that supply the abdominal musculature.

Approach to Nausea and Vomiting

Three steps should be considered in approaching nausea and vomiting:

1. 
   

   What is the etiology?

   
   
2. 
   

   What are the consequences and/or complications that need to identified and corrected?

   
   
3. 
   

   What therapy can be provided?

There are a vast number of causes of nausea and vomiting (Tables 95-1 and 95-2). The differential diagnosis can be approached with a careful history and physical examination. The acuity of symptoms should first be addressed. Acute nausea and vomiting are usually associated with acute infection (especially of the gastrointestinal tract), ingestion of toxins, gastrointestinal obstruction or ischemia, new medication, pregnancy, or head trauma/increased intracranial pressure. Chronic nausea and vomiting, which are usually defined as the persistence of symptoms for more than 1 month, suggest partial mechanical obstruction, intracranial pathology, motility disturbance as in gastroparesis, metabolic or endocrine etiology, or a psychologic disturbance.