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Table of Contents
Year : 2017  |  Volume : 33  |  Issue : 4  |  Page : 427-428

Postoperative nausea and vomiting: The achilles heel of anesthesiologists

1 Department of Anesthesiology and Pain Medicine, University of Cincinnati Medical Center, Cincinnati, Ohio, USA
2 Department of Anesthesia, University of Iowa Hospitals and Clinics, Iowa City, Iowa, USA
3 Pain Fellowship Program, Department of Anesthesiology and Pain Medicine, University of Cincinnati Medical Center, Cincinnati, Ohio, USA

Date of Web Publication9-Jan-2018

Correspondence Address:
Shuchita Garg
Clinical Assistant professor, Department of Anesthesiology and Pain Medicine, University of Cincinnati Medical Center, Cincinnati, Ohio 45219
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/joacp.JOACP_321_17

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How to cite this article:
Garg S, Subramani S, Sachdeva H. Postoperative nausea and vomiting: The achilles heel of anesthesiologists. J Anaesthesiol Clin Pharmacol 2017;33:427-8

How to cite this URL:
Garg S, Subramani S, Sachdeva H. Postoperative nausea and vomiting: The achilles heel of anesthesiologists. J Anaesthesiol Clin Pharmacol [serial online] 2017 [cited 2020 Nov 26];33:427-8. Available from:

We are more often fooled by things we think we know than things we do not… Claude Bernard

Postoperative nausea and vomiting (PONV) has been the Achilles heel of anesthesiologists since over a century now. From being described as the big “little problem” in 1991,[1] it has now progressed into a chronic, “gnawing itch,” that does not want to go away soon. Despite predisposing factors not exactly being under control of the anesthesiologists, PONV is often blamed on anesthesia, and since ages has been denigrating anesthesiologists.

The prevailing incidence of PONV remains displeasingly high.[2] Unfortunately, 10% of the patients with no risk factors will experience PONV. If patients have three or more risk factors (female gender, history of PONV/smoking/motion sickness, use of opioids postoperatively), the incidence dramatically surges to 61% and 79%, respectively.[3] Almost thirty years ago, Macario had patients rank their most feared expectations from anesthesia.[4] The patients appraised from most undesirable to least undesirable (in order): vomiting, gagging on the tracheal tube, incisional pain, nausea, recall without pain, residual weakness, shivering, sore throat, and somnolence. It is not surprising that patients are ready to pay anywhere between US $56 to US $100 (approximately 3500–6500 INR) for a hypothetical ideal antiemetic.[5] PONV incurs augmented medical costs, morbidity, delayed recovery/discharge, and readmissions. Thus, it behooves those involved with anesthetic care to understand, preempt, and formulate personalized plans to deal with this distressing complication.

There have been multitudes of research, and journals are inundated with an exponential number of manuscripts claiming eureka moments pertaining to the remedy of PONV. Regrettably, most manuscripts are corrupted due to flawed methodology. Future researchers are advised to steer clear of typical yet avoidable mistakes. Preferably they should address original/pertinent hypothesis, instead of continually inspecting predictable antiemetics, whose efficacy have already been established by meta-analysis. Emphasis must be made on choosing a power analysis driven representative sample size. Instead of using doubtful risk factors, groups should be compared with recognized risk scores for predicting PONV.[6] Even though nausea and vomiting have been considered sequential, existing data differentiates their pathophysiology, implying that specific risk factors be used for each.[7],[8] The main outcome/endpoint must be well defined. Symptoms such as retching, nausea, vomiting, and specific rescue intervention(s), should be reported (with the exact incidences) separately. It is recommended to utilize the various established predictive models for PONV.[8],[9],[10],[11],[12],[13] The observation period should last for at least 24 hours post-surgical procedure, encompassing preferably early, intermediate, or delayed postoperative period. Finally, causes of potential bias, problems related with multiplicity of analysis and outcomes, and inherent limitations related with data interpretation, should be factored in before justifying a conclusion.

A critical role in the central mechanism of vomiting is played by area postrema, a highly vascularized structure located on the dorsal surface of the medulla oblongata at the caudal end of the fourth ventricle. It is very sensitive in detecting emetic stimuli/agents in blood and cerebrospinal fluid as it lacks a blood–brain barrier. Various neurotransmitter receptor systems [dopaminergic (D2), cholinergic (muscarinic), histaminergic (H1) serotonergic (5-HT3)] and neurokinin NK1 systems have been conjectured to be responsible for nausea and vomiting. Their corresponding receptors have been the targets for antiemetic pharmacological research. Extrapolation of success in treating chemotherapy-induced nausea vomiting (CINV) into anesthesia has for long been the route taken to find a remedy for PONV. Weak and narrow spectrum antiemetic properties of 5-HT1A receptor agonists encouraged the neuropharmacological quest to investigate the role of neurotransmitter systems other than the serotonergic system to make available a highly effective broad-spectrum antiemetic. Initial studies reported the emetic action of the tachykinin, substance P (SP).[14] It was observed that depletion of SP in the central emetic pathway could potentially lead to antiemesis.[15] This was followed by research evaluating the efficacy of potent, highly selective nonpeptide NK1 receptor antagonists.

Okafor et al. reviewed the potential of one of the new entrant “neurokinin-1 antagonist” in this issue.[16] This opens new avenues for plausible manipulation of the central emetic pathway to develop a “road map” for optimal dosage for prevention, as well as rescue protocol for both adult and pediatric population scheduled for anesthesia. This also throws up a prospect for multicenter collaboration on accumulating and analyzing outcome data. It should perhaps generate interest in exploring pharmacodynamic/pharmacokinetics of commonly used anesthetic agents' interaction with SP in the area postrema. Other areas of possible research for anesthesiologists may involve the practicality of NK1 receptor antagonists in pain management, bronchospasm, preoperative anxiety, and stroke.

It is the appropriate requirement of the time to take up the challenge of designing and development of novel modalities of antiemetic drugs and yet keep it economical to ensure effectiveness and beneficial outcomes. The race is heating up between 5-HT3 antagonist (latest being long acting palonosetron), NK1 receptor antagonists, and other nonpharmacological (ginger/acupuncture) therapies to find an effective cure for the relentless itch that needs to be exterminated.

  References Top

Kapur PA. The big “little problem”. Anesth Analg 1991;73:243-5.  Back to cited text no. 1
Smith HS, Smith EJ, Smith BR. Postoperative nausea and vomiting. Ann Palliat Med 2012;1:94-102.  Back to cited text no. 2
Roberts SM, Bezinover DS, Janicki PK. Reappraisal of the role of dolasetron in prevention and treatment of nausea and vomiting associated with surgery or chemotherapy. Cancer Manag Res 2012;4:67-73.  Back to cited text no. 3
Macario A, Weinger M, Carney S, Kim A. Which clinical anesthesia outcomes are important to avoid? The perspective of patients. Anesth Analg 1999;89:652-8.  Back to cited text no. 4
Gan T, Sloan F, Dear Gde L, El-Moalem HE, Lubarsky DA. How much are patients willing to pay to avoid postoperative nausea and vomiting? Anesth Analg 2001;92:393-400.  Back to cited text no. 5
Apfel CC, Kranke P, Eberhart LH, Roos A, Roewer N. Comparison of predictive models for postoperative nausea and vomiting. Br J Anaesth 2002;88:234-40.  Back to cited text no. 6
Eberhart LH, Morin AM, Guber D, Kretz FJ, Schäuffelen A, Treiber H, et al. Applicability of risk scores for postoperative nausea and vomiting in adults to paediatric patients. Br J Anaesth 2004;93:386-92.  Back to cited text no. 7
Stadler M, Bardiau F, Seidel L, Albert A, Boogaerts JG. Difference in risk factors for postoperative nausea and vomiting. Anesthesiology 2003;98:46-52.  Back to cited text no. 8
Apfel CC, Läärä E, Koivuranta M, Greim CA, Roewer N. A simplified risk score for predicting postoperative nausea and vomiting. Anesthesiology 1999;91:693-700.  Back to cited text no. 9
Palazzo M, Evans R. Logistic regression analysis of fixed patient factors for postoperative sickness: A model for risk assessment. Br J Anaesth 1993;70:135-40.  Back to cited text no. 10
Sinclair DR, Chung F, Mezei G. Can postoperative nausea and vomiting be predicted? Anesthesiology 1999;91:109-18.  Back to cited text no. 11
Apfel CC, Kranke P, Eberhart LH, Roos A, Roewer N. Comparison of predictive models for postoperative nausea and vomiting. Br J Anaesth 2002;88:234-40.  Back to cited text no. 12
Sarin P, Urman RD, Ohno-Machado L. An improved model for predicting postoperative nausea and vomiting in ambulatory surgery patients using physician-modifiable risk factors. J Am Med Inform Assoc 2012;19:995-1002.  Back to cited text no. 13
Carpenter DO, Briggs DB, Strominger N. Peptide-induced emesis in dogs. Behav Brain Res 1984;11:277-81.  Back to cited text no. 14
Andrews PLR, Bhandari P. Resinferatoxin, an ultrapotent capsaicin analogue, has anti-emetic properties in the ferret. Neuropharmacology 1993;32:799-806.  Back to cited text no. 15
Okafor D, Kaye AD, Kaye RJ, Urman RD. The role of neurokinin-1 (substance P) antagonists in the prevention of postoperative nausea and vomiting. J Anaesthesiol Clin Pharmacol 2017;33: 441-5.  Back to cited text no. 16
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