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Postoperative nausea and vomiting is a serious problem that is a major concern for anesthesiologists.[269] [270] The etiology, treatment, and prevention of postoperative nausea and vomiting have been investigated extensively ( Fig. 11-10 ).[271] The intraoperative use of opioids is a well-known risk factor for postoperative nausea and vomiting. Opioids stimulate the chemoreceptor trigger zone in the area postrema of the medulla possibly through δ-receptors, leading to nausea and vomiting. Alfentanil, compared with approximately equipotent doses of fentanyl and sufentanil, is associated with a lower incidence of postoperative nausea and vomiting.[272]
The use of propofol in balanced or total intravenous anesthesia (TIVA) significantly reduces the incidence of opioid-induced nausea and vomiting. [273] The incidence of postoperative nausea and vomiting can be as low as 5% to 20% after propofol-alfentanil anesthesia.
When opioids are employed, antiemetic prophylaxis should be considered, which includes drugs with anticholinergic activity, butyrophenones, dopamine antagonists, serotonin antagonists and acupressure. Ondansetron, a serotonin type 3 receptor antagonist, was proved to be effective for postoperative opioid-induced nausea and vomiting.[274] Cannabinoid receptor agonists have been demonstrated to be effective antiemetics in some clinical settings. Animal experiments have shown that the cannabinoid agonists suppress opioid-induced retching and vomiting by activation of the cannabinoid CB1 receptor.[275]
Figure 11-10
The chemoreceptor trigger zone and the emetic center
with the agonist and antagonist sites of action of various anesthetic-related agents
and stimuli. (From Watcha MF, White PF: Postoperative nausea and vomiting.
Its etiology, treatment, and prevention. Anesthesiology 77:162–184, 1992.)
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