INTRODUCTION

Nausea, the unpleasant sensation of being about to vomit, can occur alone or can accompany vomiting (the forceful expulsion of gastric contents), dyspepsia, or other gastrointestinal symptoms. Retching differs from vomiting in the absence of expulsion of gastric content. In addition, patients may confuse vomiting with regurgitation, which is the return of esophageal contents to the hypopharynx with little effort [1]. (See "Clinical manifestations and diagnosis of gastroesophageal reflux in adults".)

The recommendations made in this topic are generally consistent with the American Gastroenterological Association (AGA) guidelines for nausea and vomiting [2]. The pathophysiology of nausea and vomiting and the overall approach to the patient with these symptoms will be reviewed here. The prevention and treatment of chemotherapy-induced nausea and vomiting and characteristics of antiemetic drugs are discussed separately. (See "Prevention and treatment of chemotherapy-induced nausea and vomiting" and "Characteristics of antiemetic drugs".)

PATHOPHYSIOLOGY

Normal function of the upper gastrointestinal tract involves an interaction between the gut and the central nervous system. The motor function of the gut is controlled at three main levels: the parasympathetic and sympathetic nervous systems; enteric brain neurons; and smooth muscle cells (figure 1). A discussion of the anatomy and physiology of gastric motor function is discussed separately. (See "Pathogenesis of delayed gastric emptying".)

Nausea — Studies that produce motion sickness in humans indicate how some of the physiologic interactions can cause nausea [3,4]. In one report, for example, gastric myoelectrical activity and endogenous neuroendocrine responses were compared in subjects with and without motion sickness elicited by vection (induced by rotating a drum with black and white vertical stripes around seated stationary subjects) [3]. Thirteen subjects developed tachygastria (an increase in gastric slow wave rhythm) and motion sickness during vection, while nine maintained normal gastric rhythms and remained symptom-free. Nausea followed within minutes of and was proportional to the degree of tachygastria. Anticipatory increases in plasma cortisol and beta endorphin occurred in subjects who developed nausea and gastric tachyarrhythmias; endogenous epinephrine and norepinephrine concentrations were also increased in these subjects.

Vomiting — Vomiting is a reflex that allows an animal to rid itself of ingested toxins or poisons. It can be activated by humoral or neuronal stimuli, or both [5]. Multiple afferent and efferent pathways exist which induce vomiting; the following are the major components of these pathways: