Common occurrence following anesthesia leading to patient dissatisfaction and discomfort.
#2 M/C postoperative complaint (after pain)
Surgical risk factors:
Type and location of surgery play a role as well, and ocular and tympanic surgery, intracranial, abdominal, and gynecological surgeries pose an increased risk for PONV.
Anaesthesia risk factors:
Volatile anesthetics (inhalational anesthesia agents) Etomidate use (IV anaesthetic) Nitrous oxide Postoperative opioid use
Model of the phases and stimuli that contribute to postoperative and postdischarge nausea and vomiting (PONV and PDNV). Both inhalational anesthesia and intravenous opioids (e.g., fentanyl) can contribute to PONV, which is defined by most authors as nausea and vomiting experienced in the post-anesthesia care unit (PACU) or in-patient stay in the hospital. PDNV appears to be the result of opioid analgesic usage. Although not well understood, surgery-related effects on gastrointestinal motility (e.g., postoperative ileus) and GI inflammation might also contribute to nausea and vomiting. Patients can also develop tolerance to opioid-induced nausea and vomiting. This model is dependent on the type of surgery and may be shorter or longer periods of PONV and PDNV. | Horn, C. C., Wallisch, W. J., Homanics, G. E., & Williams, J. P. (2014). Pathophysiological and neurochemical mechanisms of postoperative nausea and vomiting. European journal of pharmacology, 722, 55–66. https://doi.org/10.1016/j.ejphar.2013.10.037
Patient risk factors:
Vicious cycle can occur where vomiting worsens the comorbidity that may be causing the PONV in the first place.
Highest risk patients are young to middle-aged, non-smoking females with a history of PONV or motion sickness (all are independent risk factors) Perioperative complications/comorbidities: Dehydration, aspiration, electrolyte changes, etc
Source of PONV is multifactorial and believed to be from the chemoreceptor trigger zone in the brainstem, from opiate-induced, direct effects on the gastrointestinal (GI) tract and other anesthetics as well as in the vestibular system through movement and from the sensitization of this system by agents commonly used in anesthesiology.
Neural pathways and pharmacology of postoperative nausea and vomiting (PONV): A) Brain pathways stimulated by inhalational anesthesia and opioids. Stimulation of three sensory pathways produce the vomiting reflex, including the vestibular nuclei (Vnu), area postrema (AP), and vagal afferent fibers from the gastrointestinal (GI) tract. These inputs project to the nucleus of the solitary tract (NTS), which potentially has output pathways to local brainstem areas to produce the vomiting reflex and projections to the mid- and forebrain for the perception of nausea. Although opioids act directly on brainstem, they could also influence vagal afferent signaling by altering GI motility. Inhalational anesthesic agents could enhance 5-HT3 signals at peripheral and central sites to produces emesis or nausea. Brain pathways potentially involved in nausea include the parabrachial nucleus (PB), thalamus (Thal), amygdala (Amy), insular cortex (IC), anterior cingulate cortex (ACC), and somatosensory/viscerosensory cortex (SC). B) Neuropharmacological targets associated with PONV. Opioids have emetic and antiemetic effects in animals and potentially humans too; at low doses morphine produces emesis, but at high doses it acts as an antiemetic. These actions are potentially the result of stimulation of different sites within the emetic neural circuitry, separated by the blood-brain barrier. As concentrations of opioids increase in the systemic circulation or if the specific opioid drug is more lipid soluble (e.g., fentanyl), there is a greater antiemetic effect via μ opioid receptors inside the blood-brain barrier (e.g., NTS), counterbalancing the emetic action of opioids on μ opioid receptors in the AP. Other sites of antiemetic actions include serotonin type 3 (5-HT3) receptors in the AP, NTS, and gut vagal afferent fibers (a potential target for inhalational anesthetic agents); dopamine type 2 (D2) receptors in the AP; tachykinin 1 (NK1) receptors in the NTS and other hindbrain nuclei; and histamine 1(H1) and muscarinic 3 or 5 (M3/5) receptors in the Vnu. | Horn, C. C., Wallisch, W. J., Homanics, G. E., & Williams, J. P. (2014). Pathophysiological and neurochemical mechanisms of postoperative nausea and vomiting. European journal of pharmacology, 722, 55–66. https://doi.org/10.1016/j.ejphar.2013.10.037
The treatment of PONV is most effective with a combination of agents and prevention is more effective than initiating therapy after the onset of symptoms.
Doses and Side Effects of Antiemetics | Moon Y. E. (2014). Postoperative nausea and vomiting. Korean journal of anesthesiology, 67(3), 164–170. https://doi.org/10.4097/kjae.2014.67.3.164