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Nausea, Vomiting, and Hiccups: a Review of Mechanisms and Treatment

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Nausea, Vomiting, and Hiccups: a Review of Mechanisms and Treatment CONTINUING EDUCATION Nausea, Vomiting, and Hiccups: A Review of Mechanisms and Treatment Daniel E. Becker, DDS Associate Director of Education, General Dental Practice Residency, Miami Valley Hospital Dayton, Ohio Nausea,vomiting, and hiccups are troubling complications associated with sedation and general anesthesia.This article will review the basic pathophysiology of these events and current recommendations for their prevention and management. Key Words: Nausea; Vomiting; PONV; Hiccups; Anesthetic complications; Antiemetics. ausea and vomiting is one of the most common expulsion of vomitus (ie, dry heaves). The term nausea N postoperative complaints from patients follow- referstoasubjectivefeelingoftheneedtovomit.The ing general anesthesia, second only to pain. Its occur- nauseated patient does not necessarily vomit or retch. rence is miserable for the patient and both troubling Nausea should be distinguished from dyspepsia (upset and perplexing to the provider. It is not surprising that stomach), which encompasses epigastric burning, a staggering number of publications have been dedi- gnawing discomfort, bloating, or pain. It is not uncom- cated to the prevention and management of this com- mon for nausea to accompany dyspepsia, but they are plication. Unfortunately, its pathophysiology is incom- distinct events. pletely understood, and the many contributing factors Thevomitingcenterliesinthemedullaoblongata have rendered the majority of these publications in- and comprises the reticular formation and the nucleus conclusive. In many cases, this has spawned miscon- of the tractus solitarius. When activated, motor path- ceptions and anecdotes that are not scientifically waysdescendfromthiscenterandtriggervomiting. grounded.This continuing education article summariz- These efferent pathways travel within the 5th, 7th, es current thinking and guidelines on the subject and 9th, 10th, and 12th cranial nerves to the upper gastro- also addresses the issue of hiccups, a less frequent but intestinal tract, within vagal and sympathetic nerves to nevertheless troubling complication. the lower tract, and within spinal nerves to the dia- phragm and abdominal muscles.1 The vomiting center can be activated directly by irritants or indirectly fol- DEFINITIONS AND PHYSIOLOGY lowing input from 4 principal areas: gastrointestinal tract, cerebral cortex and thalamus, vestibular region, Postoperative nausea and vomiting (PONV) is the con- and chemoreceptor trigger zone (CRTZ).The CRTZ is ventional title for this complication, and PONV has be- closest in proximity, lying between the medulla and come the official medical subject heading in the Na- the floor of the fourth ventricle. Unlike other brain tional Library of Medicine. However, this label should centers, it is not protected by the blood-brain barrier. not detract from the fact that nausea and vomiting are This is to say that the endothelium of its capillaries is distinct entities that may occur at any point during or not tightly joined or surrounded by glial cells and is after a clinical procedure.Vomiting or emesis, which is permeated easily by irritants regardless of their lipid the actual oral expulsion of gastrointestinal contents, solubility or molecular size. The components of this istheresultofcontractionsofthegutandthethoraco- vomiting network are illustrated in Figure 1, along with abdominal wall musculature. This contrasts with regur- principal receptors and ligands that provide activation. gitation, which is the effortless passage of gastric con- Before vomiting occurs, there may be a period of an- tents into the mouth. Retching is the term used to de- tiperistalsis, in which rhythmic contractions occur up scribe the muscular events of vomiting without the digestive tract instead of downward. This may commence as far down as the ileum, with the antiperi- Address correspondence to Dr Daniel E. Becker at debecker@ staltic wave pushing contents of the lower small intes- mvh.org. tine contents upward into the duodenum and stomach Anesth Prog 57:150^157 2010 ISSN 0003-3006/10 E 2010 by the American Dental Society of Anesthesiology SSDI 0003-3006(000) 150 Anesth Prog 57:150^157 2010 Becker 151 explanation has been offered for the increased inci- dence in female patients, but this increased risk per- sists throughout life, even following menopause, which obviates any role for estrogen as a factor. It is speculat- ed that smokers may have developed some tolerance because of the chronic emetogenic influence of nico- tine, which is lacking in the nonsmoker. A history of motion sickness suggests a more susceptible vestibular component. Nevertheless, it is surprising that none of these factors is a reliable predictor independently. For example, a prior history of PONV would intuitively suggest high risk, but female gender is actually a stron- ger independent predictor.2 Thenatureandextentofthesurgicalprocedure have been studied extensively. The most commonly cited procedures and their possible mechanisms are as follows: tympanoplasty (vestibular stimulation), Figure 1. Pathophysiology of nausea and vomiting. Vomit- ing is caused by noxious stimulation of the vomiting center ENT and oral surgery (swallowed blood), breast sur- directly or indirectly via 1 or more of 4 additional sites: the gery (anxiety and emotional load), laparoscopy (peri- gastrointestinal (GI) tract, the vestibular system, the chemo- toneal irritation), and abdominal and hysterectomy receptor trigger zone, and higher centers in the cortex and (GI and vagal stimulation). With the exception of stra- thalamus. Once receptors are activated, neural pathways bismus surgery in children, no surgical procedure is a lead to the vomiting center, where emesis is initiated. Neural traffic originating in the GI tract travels along afferent fibers sound independent predictor. PONV in these cases ofcranialnervesIX(glossopharyngeal)andX(vagal).Anti- more likely reflects prolonged exposure to emetogenic emetic targets for drug interventions are predicated on their anesthetics and underlying patient-related factors.3 ability to block the illustrated receptor sites. Receptors illus- Emetogenic agents have the strongest evidence for trated along with their conventional ligands are as follows: risk of PONV. Patient and surgical risk factors likely H1 histamine, M1 acetylcholine, 5-HT3 serotonin, DA2 dopa- mine, NK1 (neurokinin) substance P, and mu/kappa opioids. play a role in the susceptibility to these agents. Transmitter mediators in the cerebral cortex and thalamus Opioids have well-established emetogenic effects. The are poorly understood, although cortical cannabinoid (CB1) degree of risk is predicated on the total dose adminis- pathways have been characterized. tered, not on the particular agent or whether it is ad- ministered intraoperatively or postoperatively.3 Fur- within a few minutes. Then, distention within these thermore it occurs more frequently following ambula- upper portions of the gastrointestinal tract generates tion, which suggests a vestibular component in its afferent impulses to the vomiting center, where the ac- pathogenesis. Inhalation anesthetics are also well-es- tual act of vomiting is initiated.1 For this reason, an tablished emetogenics, with the volatile agents more empty stomach does not preclude the expulsion of so than nitrous oxide.4^6 Their degree of risk is direct- vomitus. At the onset of vomiting, intrinsic contrac- ly related to duration of exposure. Propofol is com- tions occur in both the duodenum and the stomach, monly regarded as an antiemetic, but whether nonsed- the lower esophageal sphincter relaxes, and vomitus ative doses actually impart an antiemetic influence is moves from the stomach into the esophagus. Next, equivocal.7, 8 At sedative doses, however, both propo- the inspiratory and abdominal muscles contract and fol and midazolam appear to increase threshold for expel the vomitus into the mouth. postoperative nausea.9 Nevertheless, there is little doubt that propofol is far less emetogenic than the in- halation agents.4,10 FACTORS CONTRIBUTING TO PONV PONV is multifactorial in its origin. In addition to well- ANTIEMETIC DRUGS established emetogenic agents such as opioids and in- halation anesthetics, a large number of factors appear The efficacy of antiemetic drugs is predicated on their to render patients more susceptible. Patient-related ability to act as antagonists at receptor sites within the factors with the most established significance include vomiting center and associated regions (Figure 1). female gender, nonsmoking history, anxiety and prior From an empiric standpoint, those that block acetyl- history of PONV, motion sickness, and migraine. No choline and histamine appear most useful when ves- 152 Nausea, Vomiting, and Hiccups Anesth Prog 57:150^157 2010 Ta b l e 1. Relative Actions of Selected Antiemetic Drugs*11 Dose (mg)À Relative Antagonist Activity Product IV/PO Muscarinic Histaminic Dopamine Serotonin Scopolamine (1.5 mg transdermal patch) ++++ + 00 Diphenhydramine 25^50/25^50 ++ ++++ 00 Hydroxyzine NA/25^100 ++ ++++ 00 Promethazine` 12.5^25/25 ++ ++++ ++ 0 Prochlorperazine` 2.5^10/5^10 ++ ++ ++++ + Droperidol 0.625/NA 0 + ++++ + Metocloprami de 10^20/10^20 0 0 +++ ++ Ondansetron 1^4§/16 0 0 0 ++++ * Designations of 0-++++ reflect relative activity as antagonists. Actions based on low activity (+) are less likely to be achieved with conventional doses. NA indicates not available. À Doses derived from Access Medicine Drug Monographs, McGraw-Hill, 2010. ` Available
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