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Postoperative nausea and vomiting (PONV) is the most common complication associated with anesthesia and surgery, occurring in approximately one-third of all patients and up to 70% of “high-risk” patients.1 PONV is a cause of great distress for patients, and in addition to creating a highly unpleasant experience of discomfort, it can lead to a variety of unintended consequences such as delayed discharge, wound dehiscence, dehydration, tearing of sutures, and potential pulmonary aspiration, all of which serve to greatly increase medical costs.2 Understanding the various mechanisms involved in PONV is critical for optimizing the prophylaxis and treatment of this unwanted side effect of anesthesia.
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There are numerous risk factors associated with the development of PONV, and these can be divided into patient specific risk factors, anesthesia-related factors, and surgery-related factors (Table 15–1). By careful evaluation of an individual's risk factors for the development of PONV, those who will most likely benefit from prophylactic antiemetic therapy can be more easily identified.
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PHYSIOLOGIC MECHANISM OF EMESIS
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The physiologic process of vomiting (emesis) involves a series of autonomic changes that operate in the brainstem at the level of the medulla oblongata. Within this region of the hindbrain, various afferent sources of emetic input are received by the area postrema, known as the chemoreceptor trigger zone (CTZ), and the vomiting center located in the nucleus tractus solitarius (NTS).3 The signals received by the CTZ and the vomiting center are mediated primarily by major neurotransmitter receptor systems. The major neurotransmitters and receptors that supply signals to the CTZ and vomiting center are serotonin (5-HT3), dopamine (D2), histamine (H1), muscarinic acetylcholine, and neurokinin (Figure 15–1). Pharmacologic antiemetic agents that work to block the neurotransmitters involved in the development of emesis have long been the mainstay of prophylaxis and treatment of PONV.
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ANTIEMETIC PHARMACOLOGIC THERAPY