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Pathophysiology of nausea and vomiting. Vomiting is caused by noxious stimulation of the vomiting center directly or indirectly via 1 or more of 4 additional sites: the gastrointestinal (GI) tract, the vestibular system, the chemoreceptor trigger zone, and higher centers in the cortex and thalamus. Once receptors are activated, neural pathways lead to the vomiting center, where emesis is initiated. Neural traffic originating in the GI tract travels along afferent fibers of cranial nerves IX (glossopharyngeal) and X (vagal). Antiemetic targets for drug interventions are predicated on their ability to block the illustrated receptor sites. Receptors illustrated along with their conventional ligands are as follows: H₁ histamine, M₁ acetylcholine, 5-HT₃ serotonin, DA₂ dopamine, NK₁ (neurokinin) substance P, and mu/kappa opioids. Transmitter mediators in the cerebral cortex and thalamus are poorly understood, although cortical cannabinoid (CB₁) pathways have been characterized.

Selection criterion and breakdown of study cases. Of the 791 patients who underwent general anesthesia with total intravenous anesthesia (TIVA) using propofol, fentanyl, and remifentanil, 761 patients without any of the exclusion criteria were enrolled. A total of 121 patients had postoperative nausea and vomiting (PONV), whereas 640 did not.

Risk factors for postoperative nausea and vomiting (PONV; 0–24 h) after intubated general anesthesia using total intravenous anesthesia (TIVA). Arrows illustrate factors with increased PONV risk. Arrow thickness illustrates size of the factor's adjusted odds ratio (OR) per study data. The strongest PONV risk factor was bimaxillary osteotomy (OR 5.69) followed by female sex (OR 2.73) and sagittal split ramus osteotomy (SSRO; OR 2.28). Factors lacking arrows were not significantly associated with PONV.