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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.
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.
The inflammatory process. Normally, small arterioles deliver blood to capillaries, which are then drained by venules. Vasoactive autacoids trigger the vascular phase, causing arterioles to dilate and endothelial cells to shrink, making capillaries and venules more permeable. Hyperemia produces the cardinal signs of redness and heat. Permeability allows extravasation of plasma leading to swelling and pain. Chemotactic autacoids target leukocytes (WBCs), which adhere to endothelium (margination), squeeze through the openings (diapedesis) and migrate out into the tissues (emigration). Nonsteroidal anti-inflammatory drugs (NSAIDS) inhibit the vascular phase, and the glucocorticoids inhibit both phases.
The hypothalamic-pituitary-adrenal (HPA) axis. 2 In this figure, solid arrows represent stimulation and dashed arrows indicate inhibition. The hypothalamus secretes corticotropin-releasing factor (CRF), which stimulates the pituitary to secrete corticotropin (formerly called adrenocorticotropic hormone). Corticotropin stimulates the adrenal cortex to synthesize and secrete cortisol. Provided serum concentrations are adequate, cortisol performs vital physiological functions and inhibits further activity of the HPA axis. Serum cortisol levels peak at ∼8:00 am and gradually decline over 12–16 hours. As cortisol is consumed, its serum levels diminish and inhibition of the axis wanes. This allows production of cortisol to commence again. This pattern of function is called circadian or diurnal rhythm and occurs at a normal basal rate unless the axis is excited by other factors such as hypoglycemia, trauma, or stress. Glucocorticoids produce an impressive number of physiological effects. When supraphysiologic doses are administered, the subsequent pharmacological effects consist essentially of exaggerated physiologic effects. These doses will also impart a negative feedback on the axis that eventually leads to adrenal atrophy following sustained use.
Molecular structures of selected glucocorticoids. Prednisone is inactive as the parent drug and is converted to prednisolone following administration. Methylprednisolone differs only in a mere methyl substitution. Betamethasone and dexamethasone are optical isomers differing only in the orientation of the methyl group indicated by the asterisk. Triamcinolone is similar in structure and like other agents can be created for sustained activity as a repository formulation by adding slowly absorbed groupings such as acetates or the acetonide illustrated here by the shaded grouping.
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.