Next Article in Journal
Hyperspectral Ophthalmoscope Images for the Diagnosis of Diabetic Retinopathy Stage
Next Article in Special Issue
Frontiers of Robotic Colonoscopy: A Comprehensive Review of Robotic Colonoscopes and Technologies
Previous Article in Journal
Gender, Albuminuria and Chronic Kidney Disease Progression in Treated Diabetic Kidney Disease
Previous Article in Special Issue
Endoscopic Submucosal Dissection of Papillary Gastric Adenocarcinoma; Systematic Review
 
 
Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
Journals
JCM
Volume 9
Issue 6
10.3390/jcm9061612
jcm-logo
Submit to this Journal Review for this Journal Propose a Special Issue
► Article Menu

Article Menu

share Share announcement Help format_quote Cite question_answer Discuss in SciProfiles thumb_up
...
Endorse textsms
...
Comment
first_page
settings
Order Article Reprints
Font Type:
Arial Georgia Verdana
Font Size:
Aa Aa Aa
Line Spacing:
Column Width:
Background:
Article

Effect of Body Mass Index on Postoperative Nausea and Vomiting: Propensity Analysis

by
Jong Ho Kim
1,2,†,
Mingi Hong
2,†,
Young Joon Kim
1,
Ho Seok Lee
1,2,
Young Suk Kwon
1,2,* and
Jae Jun Lee
1,2,*
1
Department of Anesthesiology and Pain Medicine, Chuncheon Sacred Heart Hospital, College of Medicine, Hallym University, Chuncheon 24253, Korea
2
Institute of New Frontier Research Team, Hallym University, Chuncheon 24253, Korea
*
Authors to whom correspondence should be addressed.
†
These authors contributed equally to this work.
J. Clin. Med. 2020, 9(6), 1612; https://doi.org/10.3390/jcm9061612
Submission received: 13 April 2020 / Revised: 22 May 2020 / Accepted: 24 May 2020 / Published: 26 May 2020
(This article belongs to the Special Issue Gastrointestinal Disorders: Diagnosis, Treatments and Clinical Features)
Browse Figures
Review Reports Versions Notes

Abstract

:
The impact of body mass index (BMI) on postoperative nausea and vomiting (PONV) is controversial, and few studies have focused on their relationship. We investigated the effects of BMI on PONV, taking into account other PONV risk factors. We analyzed adults over the age of 18 years who received general anesthesia between 2015 and 2019, using propensity score matching. Before propensity score matching, odds ratios (ORs) for PONV were lower for overweight (OR, 0.91; 95% confidence interval (CI), 0.87–0.96; p < 0.0001) or obese patients (OR, 0.77; 95% CI, 0.71–0.84; p < 0.0001) than for normal-BMI patients. After matching, the ORs for PONV of overweight (OR, 0.89; 95% CI, 0.80–0.98; p = 0.016) and obese patients (OR, 0.71; 95% CI, 0.63–0.79; p < 0.0001) were low. However, the ORs of underweight patients did not differ from those of normal-BMI patients, irrespective of matching. Therefore, the incidence of PONV may be lower among adults with a higher-than-normal BMI.

1. Introduction

Postoperative nausea and vomiting (PONV) are common complications of anesthesia [1] that occur in 30% of hospitalized patients; moreover, their incidences are significantly greater in high-risk patients [2]. In previous studies, vomiting was the most undesirable outcome of patients after surgery, and nausea was the fourth most undesirable outcome [3]. PONV is usually non-fatal [4] but, in rare cases, can cause serious pathological conditions such as dehydration, electrolyte imbalance, suture tension and dislocation, venous hypertension and bleeding, aspiration of gastric contents, esophageal rupture, and life-threatening airway damage [5,6,7].
Several studies have identified factors that alleviate or exacerbate PONV [2,5,6,8,9,10]. However, whether obesity is a risk factor for PONV is controversial. A relatively high body mass index (BMI) may promote PONV [8,11], but the opposite effect has also been reported [12,13,14]. Others have found that BMI is not a risk factor for PONV [15,16].
Many previous PONV studies were retrospective observational studies [12,13,17,18,19]. As observational studies conduct research in specific groups without random assignment, they are slightly more realistic representations of the clinical situation, and statistical controls can be applied for specific confounding variables. However, observational studies cannot avoid selection bias. It is fundamentally impossible to deduce the cause of a phenomenon in studies that are not based on random assignment. Matching methods are generally used in observational studies to reduce selection bias [20]. Propensity score matching (PSM) is used not only in observational studies but also in retrospective research where it is difficult to apply random assignment [21].
We investigated the effects of BMI on PONV, taking into account other risk factors for PONV. The validity of observational studies on the effects of BMI can be reduced by selection bias and confounders, so we performed propensity score matching.

2. Patients and Methods

2.1. Patients

The data were obtained from the Clinical Data Warehouse of Hallym University Medical Center, and the study was approved by the Clinical Research Ethics Committee of Chuncheon Sacred Heart Hospital, Hallym University (Institutional Review Board no. 2020-03-011). The patients were at least 18 years of age and had undergone surgery under general anesthesia at Hallym University Medical Center between January 2015 and December 2019. The exclusion criteria were as follows: patients who received repeat surgery within 24 h after anesthesia, patients who were unconscious after surgery, patients who underwent ventilator therapy after anesthesia, patients with nausea or vomiting before anesthesia, and patients with data missing from their medical records.

2.2. BMI, PONV, and Covariates

BMI is defined as weight (in kilograms) divided by the square of the height (in meters). In this study, patients with BMI <18.5, 18.5–25, 25.1–30, or >30 were considered underweight, normal weight, overweight, or obese, respectively. PONV was defined as the occurrence of nausea or vomiting within 24 h after anesthesia as recorded in medical records. This study did not consider nausea or vomiting events as separate outcomes because they have identical risk factors and predictors [17,22,23,24,25,26,27], postoperative nausea may be considered a symptom for potential vomiting [28], and the accompanying occurrence of nausea and vomiting is more than the individual occurrences of nausea and vomiting [6]. Covariates included age; sex; height; operation duration; American Society of Anesthesiologists physical status; use of N2O during anesthesia maintenance; patient-controlled analgesia after surgery; history of diabetes, gastroesophageal reflux disease, or smoking; use of antiemetics, opioids, proton-pump inhibitors, or antibiotics; use of a Levin tube during and after surgery; laparoscopic surgery; and transfusion during surgery.

2.3. Statistics

Continuous data are presented as means and standard deviations and categorical data as frequencies and percentages. For continuous data, t-tests were performed to compare between patients with and without PONV. Categorical data were analyzed by chi-squared test. First, the odds ratio (OR), with 95% confidence interval (CI), for occurrence of PONV within 24 h after surgery was calculated for each variable by logistic regression. The odds ratio (OR) is a measure of the association between an exposure and an outcome [29], and the OR in this study represented the likelihood of PONV given a particular exposure (underweight, overweight, obese) compared to the likelihood of PONV in the absence of this exposure. Next, the adjusted OR for PONV according to BMI category was determined. Finally, the ORs adjusted for all variables and for those variables selected by backward elimination were calculated.
As patients cannot be randomized based on BMI category, confounding and selection bias were accounted for by developing propensity scores for the BMI categories. The rationale for, and method of, using propensity scores for the proposed causal exposure variables have been described elsewhere [30,31]. We performed three rounds of propensity score matching: normal BMI matched with underweight, normal BMI matched with overweight, and normal BMI matched with obese patients. Anaconda (Python version 3.7, https://www.anaconda.com; Anaconda Inc., Austin, TX, USA) and pymatch (version 0.3.4; https://github.com/benmiroglio/pymatch) were used for propensity score matching. The propensity scores were 0.26–0.87, 0.30–0.68, and 0.21–0.83 for matched normal and underweight, normal and overweight, and normal and obese patients, respectively. All matched records had scores within 0.0001 of each other, and all matching ratios were 1:1. We matched 4063 underweight patients with 4063 normal-BMI patients, 9872 overweight patients with 9872 normal-BMI patients, and 7678 obese patients with 7678 normal-BMI patients.
The ORs for PONV in underweight, overweight, and obese patients were compared with that of normal-BMI patients. In each analysis, covariates and propensity scores were used to calculate the adjusted OR. All p-values were two-sided, and a p-value < 0.05 was considered indicative of statistical significance. SPSS software (version 24.0; IBM Corp., Armonk, NY, USA) was used for the statistical analyses. The dataset used is provided in Supplementary File S1.

3. Results

Patient Characteristics

Between January 2015 and December 2019, a total of 113,881 patients underwent general anesthesia in Hallym University Medical Center. After excluding 10,320 patients, 103,561 were included in the study (Figure 1). PONV occurred within 24 h after surgery in 10,404 of these patients; their baseline characteristics are listed in Table 1. The adjusted and unadjusted ORs of all variables for developing PONV are listed in Table 2. The ORs for PONV were higher in overweight (unadjusted OR, 0.85 (95% CI, 0.81–0.89); fully adjusted OR, 0.91 (95% CI, 0.87–096)) and obese (unadjusted OR, 0.79 (95% CI, 0.73–0.86); fully adjusted OR, 0.77 (95% CI, 0.71–084)) patients compared with normal-BMI patients.
Between normal-BMI and underweight patients, there were significant differences in 10 variables before matching and no significant difference in any variable after matching (Table 3). Between normal-BMI and overweight patients, there were significant differences in 14 variables before matching and a significant difference in 1 variable (diabetes, p = 0.008) after matching (Table 4). Between normal-BMI and obese patients, there were significant differences in nine variables before matching and no significant difference in any variable after matching (Table 5).
Figure 2 shows the ORs for development of PONV in underweight, overweight, and obese patients. The unadjusted and adjusted ORs for PONV did not differ significantly between underweight and normal-BMI patients. The unadjusted (p = 0.046) and adjusted (p = 0.015–0.016) ORs for PONV were lower in overweight patients than in normal-BMI patients. Moreover, the unadjusted (p < 0.0001) and adjusted (p < 0.0001) ORs for PONV were lower in overweight patients than in normal-BMI patients.

4. Discussion

We estimated the effects of being underweight, overweight, and obese based on BMI on the incidence of PONV among 113,881 patients who underwent general anesthesia during a five-year period. The ORs for PONV were lower for overweight and obese patients compared with normal-BMI patients. However, there was no difference in the ORs for PONV between underweight patients and normal-BMI patients. After propensity score matching, the results were essentially unchanged: overweight and obese patients exhibited lower ORs for PONV compared with normal-BMI patients.
Most anesthesiologists consider that an increase in BMI increases the incidence of PONV [11]. The reason may be explained as follows. Longer anesthesia time is associated with longer reduction time of the anesthetic in obese patients [32]. The action time of the anesthetic is increased when a hydrophilic anesthetic is administered based on total body weight [33]. Obese patients have high incidence rates of diabetes [34] and gastroesophageal reflux disease [35] as well as elevated abdominal pressure [36]. Bellville et al. reported that obese patients have a significantly higher incidence of nausea and vomiting compared with those who are thin, because they have a large fat reservoir to saturate [37]; others have confirmed this positive correlation [8,38,39,40,41]. However, the rate of recovery from anesthesia also depends on the time at which the anesthetic is administered [42]. Obesity is assumed to delay recovery, especially from prolonged anesthesia, but it is unclear how changes associated with obesity (such as fat distribution and increased mass) affect the pharmacokinetics of inhaled anesthetics during anesthesia. Obesity reportedly does not affect awakening time after anesthetic administration [43]. Obesity is associated with an increased adipose tissue mass, which accounts for 20–40% of the excess weight in obese individuals. Non-fat mass includes well-dispersed tissues, such as organ and muscle mass [44,45], in which anesthetics areabsorbed and diffuse quickly. Fat adjacent to well-perfused tissues rapidly absorbs anesthetics, but transfer of anesthetics between these tissues, such as subcutaneous fat or skeletal muscle fat, increases over 3 h [43]. N2O has a low fat/blood partition coefficient and is removed from the body rapidly [42].
Although a relatively high BMI has been reported to be associated with the development of PONV, our findings showed that an increased BMI reduced the incidence of PONV. However, the mechanism underlying this inverse association is unknown. Drug elimination is generally more rapid in obese patients than in non-obese patients [46]. The clearance of some volatile anesthetics, prednisolone, and some benzodiazepines is sometimes faster in obese patients [47]. Opioids are widely used as adjuvants for anesthesia and are risk factors for PONV [42,48]. However, opioids administered during surgery have little direct effect on PONV, irrespective of the opioid in question [49]. Most opioids are biotransformed primarily in the liver, via metabolism by the cytochrome p (CYP) system, conjugated in the liver, or both [42,50]. Obesity causes anatomical, physiological, and metabolic changes that can affect the pharmacokinetics of a drug (including its absorption, distribution, metabolism, and excretion) [51,52,53,54,55]. However, there is no correlation between CYP activity and BMI [50]. The pharmacokinetics of propofol, which is frequently used for anesthesia induction, are not affected by obesity [42]; moreover, propofol has antiemetic activity [56].
Kranke et al. reported that a relatively high BMI was not a risk factor for PONV [15]. In contrast, in this study, higher BMI was associated with a decreased incidence of PONV. A systematic review with meta-analysis is considered the best means of providing definitive answers to research questions. However, such analysis has flaws, such as the location and design of the studies analyzed, heterogeneity, loss of data, improper subgroup analysis, conflict with new experimental data, and publication overlap [57].
No mechanism for the reduced incidence of PONV in patients with higher-than-normal BMI has yet been reported, but histamine, a neurotransmitter that stimulates various pathways and receptors that mediate nausea and vomiting [58], may play a role. Leptin is an adipocyte-derived hormone that suppresses appetite, increases energy expenditure and activation of the histaminergic system in the hypothalamus, and controls body weight [59]. The amount of body fat is directly correlated with circulating leptin levels, and serum leptin level is elevated in obese individuals and drops during weight loss or fasting. The amount of reduction during the fasting period is significantly reduced compared to individuals of normal weight [60]. The decrease in activity of the histamine activation system may be greater in subjects with higher-than-normal BMI during perioperative fasting. Dopamine receptors, especially D2 and D3, have been shown to play important roles in inducing nausea and vomiting. This mechanism blocks adenylate cyclase, reducing the amount of cAMP in neurons in the solitary nucleus and area postrema [58,61]. Because dopamine level and global activation of dopaminergic systems are increased by stress [62], PONV can be increase after severe stress such as surgery. However, obese patients havefewer dopamine receptors than those with normal BMI [63], so patients with obesity may have less effect of dopamine for PONV than normal-BMI or underweight patients. Anticholinergics are one of the antiemetic agents. They block muscarinic receptors in the cerebral cortex and pons, causing an antiemetic effect [61]. In reversal of muscle relaxation, anticholinergics areadministered concurrently with cholinesterase inhibitors to reduce the side effects of cholinesterase inhibitors. In obese patients, more anticholinergic drugs are given to reverse muscle relaxation, which may be associated with a lower incidence of PONV in obese patients.
Studies of the effect of type of surgery on the incidence of PONV have yielded conflicting results [64]. A systemic review of PONV suggested that laparoscopic surgery is associated with increased risk of PONV [21]. In this study, we included laparoscopic surgery as a covariate for the incidence of PONV. Strabismus surgery [27,65,66], adenotonsillectomy [67], and inguinal scrotal and penile procedures [68] have been reported as risk factors for PONV. However, we did not analyze the surgeries separately because these previous studies were mostly performed in pediatric patients and thus the results cannot be directly compared to our adult cohort.
Our results support and extend previous findings in several important respects. First, we demonstrated that a relatively high BMI is associated with a reduction in the incidence of PONV, as reported by others [12,13,14]. Second, because we focused on BMI, we were able to account for the effect of BMI category (underweight, normal BMI, overweight, and obese) on the incidence of PONV. Most PONV studies did not focus on BMI [1,3,5,6,8,11,12,13,14]. However, this study also had several limitations. First, classification of BMI cannot be randomized. Although the use of observational studies to assess effectiveness is controversial [69], rigorous observational studies may not yield misleading or biased results [70,71]. Moreover, to prevent selection bias and confounding, we performed propensity score matching with tighter adjustments than are typically used in a general multivariate analysis [30]. Nevertheless, observational studies can only partially control the element that is actually measured, and it is difficult to control elements that cannot be measured [72]. Second, although we used BMI to classify patients as underweight, overweight, and obese, BMI does not differentiate between lean body mass and fat mass [73]. In addition, BMI does not reflect the distribution of adipose tissue, which affects the absorption and distribution of a drug [43,73]. However, BMI is a convenient rule of thumb for classifying certain categories of body mass as health problems, for example, in population-based studies [74]. Third, severe obesity also represents a major problem in anesthesia and surgery. However, this study did not analyze obese patients separately as they were too few in our data (n = 253) and propensity matching was insufficient for rigorous analysis. Further research is required to clarify the relationship between severe obesity and PONV.

5. Conclusions

Multivariate analysis with PSM showed that being overweight or obese was associated with a reduced incidence of PONV compared with that of having a normal BMI but being underweight did not. Our findings indicate that a higher-than-normal BMI reduces the risk of PONV. Further prospective population-based studies are needed to determine the mechanism underlying the association between higher-than-normal BMI and reduced risk of PONV.

Supplementary Materials

The following are available online at https://www.mdpi.com/2077-0383/9/6/1612/s1, Supplementary File S1 Data used for statistical analysis.

Author Contributions

J.H.K. and M.H. contributed equally to this work as the first authors. Y.S.K. and J.J.L. contributed equally to this work as the corresponding authors. Conceptualization, Y.S.K. and J.J.L.; methodology, M.H.; provision of software, J.H.K.; validation, J.H.K. and J.J.L.; formal analysis, Y.S.K.; investigation, H.S.L. and Y.J.K.; resources, H.S.L.; data curation, Y.J.K.; writing—original draft preparation, J.H.K and M.H.; writing—reviewing, and editing, Y.S.K.; data visualization, M.H.; project supervision, M.H.; project administration, J.J.L.; funding acquisition, J.J.L. All authors have read and agreed to the submitted version of the manuscript.

Funding

This research was supported by the Bio and Medical Technology Development Program of the National Research Foundation (NRF), funded by the South Korean government (MSIT) (NRF-2017M3A9E8049714 and 2017M3A9E8033205). This research was also supported by the Hallym University Reseach Fund (HURF).

Conflicts of Interest

The authors declare no conflicts of interest.

References

  1. Eberhart, L.H.; Hogel, J.; Seeling, W.; Staack, A.M.; Geldner, G.; Georgieff, M. Evaluation of three risk scores to predict postoperative nausea and vomiting. Acta Anaesthesiol. Scand. 2000, 44, 480–488. [Google Scholar] [CrossRef] [PubMed]
  2. Gan, T.J. Postoperative nausea and vomiting—Can it be eliminated? JAMA 2002, 287, 1233–1236. [Google Scholar] [CrossRef] [PubMed]
  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. [Google Scholar] [CrossRef]
  4. Tramer, M.R. Treatment of postoperative nausea and vomiting. BMJ 2003, 327, 762–763. [Google Scholar] [CrossRef]
  5. Pierre, S.; Whelan, R. Nausea and vomiting after surgery. Contin. Educ. Anaesth. Crit. Care Pain 2013, 13, 28–32. [Google Scholar] [CrossRef] [Green Version]
  6. Apfel, C.C.; Kranke, P.; Katz, M.H.; Goepfert, C.; Papenfuss, T.; Rauch, S.; Heineck, R.; Greim, C.A.; Roewer, N. Volatile anaesthetics may be the main cause of early but not delayed postoperative vomiting: A randomized controlled trial of factorial design. Br. J. Anaesth. 2002, 88, 659–668. [Google Scholar] [CrossRef] [Green Version]
  7. Scuderi, P.E.; Conlay, L.A. Postoperative nausea and vomiting and outcome. Int. Anesthesiol. Clin. 2003, 41, 165–174. [Google Scholar] [CrossRef]
  8. Watcha, M.F.; White, P.F. Postoperative nausea and vomiting. Its etiology, treatment, and prevention. Anesthesiology 1992, 77, 162–184. [Google Scholar] [CrossRef]
  9. World Health Organization. Physical status: The use and interpretation of anthropometry. Report of a WHO Expert Committee. World Health Organ. Tech. Rep. Ser. 1995, 854, 1–452. [Google Scholar]
  10. Kwon, Y.S.; Choi, J.W.; Lee, H.S.; Kim, J.H.; Kim, Y.; Lee, J.J. Effect of a Preoperative Proton Pump Inhibitor and Gastroesophageal Reflux Disease on Postoperative Nausea and Vomiting. J. Clin. Med. 2020, 9, 825. [Google Scholar] [CrossRef] [Green Version]
  11. Eberhart, L.; Morin, A.; Felbinger, T.; Falkner, Y.; Georgieff, M.; Seeling, W. Results of a survey of anesthetists on postoperative nausea and vomiting. Anasthesiol. Intensivmed. Notf. Schmerzther. AINS 1998, 33, 545–551. [Google Scholar] [CrossRef]
  12. Apipan, B.; Rummasak, D.; Wongsirichat, N. Postoperative nausea and vomiting after general anesthesia for oral and maxillofacial surgery. J. Dent. Anesth. Pain Med. 2016, 16, 273–281. [Google Scholar] [CrossRef] [PubMed] [Green Version]
  13. Silva, A.C.; O’Ryan, F.; Poor, D.B. Postoperative nausea and vomiting (PONV) after orthognathic surgery: A retrospective study and literature review. J. Oral Maxillofac. Surg. 2006, 64, 1385–1397. [Google Scholar] [CrossRef]
  14. Nitahara, K.; Sugi, Y.; Shono, S.; Hamada, T.; Higa, K. Risk factors for nausea and vomiting following vitrectomyin adults. Eur. J. Anaesthesiol. 2007, 24, 166–170. [Google Scholar] [CrossRef]
  15. Kranke, P.; Apfel, C.; Papenfuss, T.; Rauch, S.; Löbmann, U.; Rübsam, B.; Greim, C.A.; Roewer, N. An increased body mass index is no risk factor for postoperative nausea and vomiting: A systematic review and results of original data Note. Acta Anaesthesiol. Scand. 2001, 45, 160–166. [Google Scholar] [CrossRef]
  16. Cohen, M.M.; Duncan, P.G.; DeBoer, D.P.; Tweed, W.A. The postoperative interview: Assessing risk factors for nausea and vomiting. Anesth. Analg. 1994, 78, 7–16. [Google Scholar] [CrossRef]
  17. Koivuranta, M.; Laara, E.; Snare, L.; Alahuhta, S. A survey of postoperative nausea and vomiting. Anaesthesia 1997, 52, 443–449. [Google Scholar] [CrossRef] [PubMed]
  18. Fabling, J.M.; Gan, T.J.; Guy, J.; Borel, C.O.; el-Moalem, H.E.; Warner, D.S. Postoperative nausea and vomiting. A retrospective analysis in patients undergoing elective craniotomy. J. Neurosurg. Anesthesiol. 1997, 9, 308–312. [Google Scholar] [CrossRef] [PubMed]
  19. Junger, A.; Hartmann, B.; Benson, M.; Schindler, E.; Dietrich, G.; Jost, A.; Beye-Basse, A.; Hempelmannn, G. The use of an anesthesia information management system for prediction of antiemetic rescue treatment at the postanesthesia care unit. Anesth. Analg. 2001, 92, 1203–1209. [Google Scholar] [CrossRef] [PubMed]
  20. Luellen, J.K.; Shadish, W.R.; Clark, M. Propensity scores: An introduction and experimental test. Eval. Rev. 2005, 29, 530–558. [Google Scholar] [CrossRef] [Green Version]
  21. Day, A.G. Why the Propensity for Propensity Scores? Crit. Care Med. 2015, 43, 2024–2026. [Google Scholar] [CrossRef] [PubMed]
  22. Sinclair, D.R.; Chung, F.; Mezei, G. Can postoperative nausea and vomiting be predicted? Anesthesiology 1999, 91, 109–118. [Google Scholar] [CrossRef] [PubMed]
  23. Palazzo, M.; Evans, R. Logistic regression analysis of fixed patient factors for postoperative sickness: A model for risk assessment. Br. J. Anaesth. 1993, 70, 135–140. [Google Scholar] [CrossRef]
  24. Van den Bosch, J.E.; Moons, K.G.; Bonsel, G.J.; Kalkman, C.J. Does measurement of preoperative anxiety have added value for predicting postoperative nausea and vomiting? Anesth. Analg. 2005, 100, 1525–1532. [Google Scholar] [CrossRef] [PubMed]
  25. Apfel, C.C.; Greim, C.A.; Haubitz, I.; Goepfert, C.; Usadel, J.; Sefrin, P.; Roewer, N. A risk score to predict the probability of postoperative vomiting in adults. Acta Anaesthesiol. Scand. 1998, 42, 495–501. [Google Scholar] [CrossRef]
  26. Apfel Christian, C.; Läärä, E.; Koivuranta, M.; Greim, C.-A.; Roewer, N. A Simplified Risk Score for Predicting Postoperative Nausea and Vomiting: Conclusions from Cross-validations between Two Centers. Anesthesiol. J. Am. Soc. Anesthesiol. 1999, 91, 693–700. [Google Scholar]
  27. Eberhart, L.H.; Geldner, G.; Kranke, P.; Morin, A.M.; Schauffelen, A.; Treiber, H.; Wulf, H. The development and validation of a risk score to predict the probability of postoperative vomiting in pediatric patients. Anesth. Analg. 2004, 99, 1630–1637. [Google Scholar] [CrossRef]
  28. Gan, T.J. Risk Factors for Postoperative Nausea and Vomiting. Anesth. Analg. 2006, 102, 1884–1898. [Google Scholar] [CrossRef] [PubMed]
  29. Szumilas, M. Explaining odds ratios. J. Can. Acad. Child Adolesc. Psychiatry 2010, 19, 227–229. [Google Scholar]
  30. Joffe, M.M.; Rosenbaum, P.R. Invited commentary: Propensity scores. Am. J. Epidemiol. 1999, 150, 327–333. [Google Scholar] [CrossRef]
  31. Brookhart, M.A.; Schneeweiss, S.; Rothman, K.J.; Glynn, R.J.; Avorn, J.; Stürmer, T. Variable selection for propensity score models. Am. J. Epidemiol. 2006, 163, 1149–1156. [Google Scholar] [CrossRef] [PubMed] [Green Version]
  32. Weber, J.; Schmidt, J.; Wirth, S.; Schumann, S.; Philip, J.H.; Eberhart, L.H.J. Context-sensitive decrement times for inhaled anesthetics in obese patients explored with Gas Man(R). J. Clin. Monit. Comput. 2020, 1–12. [Google Scholar] [CrossRef] [PubMed] [Green Version]
  33. Lee, H. Anesthetic management of the bariatric surgery. J. Korean Med. Assoc. /TaehanUisaHyophoe Chi 2012, 55, 10. [Google Scholar] [CrossRef] [Green Version]
  34. Al-Goblan, A.S.; Al-Alfi, M.A.; Khan, M.Z. Mechanism linking diabetes mellitus and obesity. Diabetes Metab. Syndr. Obes. 2014, 7, 587–591. [Google Scholar] [CrossRef] [Green Version]
  35. El-Serag, H.B.; Graham, D.Y.; Satia, J.A.; Rabeneck, L. Obesity is an independent risk factor for GERD symptoms and erosive esophagitis. Am. J. Gastroenterol. 2005, 100, 1243–1250. [Google Scholar] [CrossRef]
  36. Lambert, D.M.; Marceau, S.; Forse, R.A. Intra-abdominal pressure in the morbidly obese. Obes. Surg. 2005, 15, 1225–1232. [Google Scholar] [CrossRef]
  37. Bellville, J.W.; Bross, I.; Howland, W.S. Postoperative nausea and vomiting. IV. Factors related to postoperative nausea and vomiting. Anesthesiology 1960, 21, 186–193. [Google Scholar] [CrossRef]
  38. McKie, B. Postoperative nausea and vomiting: A review of their incidence, causes and effects. Aust. N. Z. J. Surg. 1970, 39, 311–314. [Google Scholar] [CrossRef]
  39. Palazzo, M.; Strunin, L. Anaesthesiaand emesis. I: Etiology. Can. Anaesth. Soc. J. 1984, 31, 178–187. [Google Scholar] [CrossRef] [Green Version]
  40. Lerman, J. Surgical and patient factors involved in postoperative nausea and vomiting. Br. J. Anaesth. 1992, 69, 24S. [Google Scholar] [CrossRef]
  41. Muir, J.J.; Warner, M.A.; Offord, K.P.; Buck, C.F.; Harper, J.V.; Kunkel, S.E. Role of nitrous oxide and other factors in postoperative nausea and vomiting: A randomized and blinded prospective study. Anesthesiology 1987, 66, 513–518. [Google Scholar] [CrossRef] [PubMed]
  42. Butterworth, J.F.; Mackey, D.C.; Wasnick, J.D. Morgan and Mikhail’s Clinical Anesthesiology; McGraw-Hill Education: New York, NY, USA, 2018. [Google Scholar]
  43. Lemmens, H.J.M.; Saidman, L.J.; Eger, E.I.I.; Laster, M.J. Obesity Modestly Affects Inhaled Anesthetic Kinetics in Humans. Anesth. Analg. 2008, 107, 1864–1870. [Google Scholar] [CrossRef] [PubMed]
  44. Collis, T.; Devereux, R.B.; Roman, M.J.; de Simone, G.; Yeh, J.-L.; Howard, B.V.; Fabsitz, R.R.; Welty, T.K. Relations of stroke volume and cardiac output to body composition: The strong heart study. Circulation 2001, 103, 820–825. [Google Scholar] [CrossRef] [PubMed] [Green Version]
  45. Gallagher, D.; Belmonte, D.; Deurenberg, P.; Wang, Z.; Krasnow, N.; Pi-Sunyer, F.X.; Heymsfield, S.B. Organ-tissue mass measurement allows modeling of REE and metabolically active tissue mass. Am. J. Physiol. Endocrinol. Metab. 1998, 275, E249–E258. [Google Scholar] [CrossRef]
  46. Hanley, M.J.; Abernethy, D.R.; Greenblatt, D.J. Effect of obesity on the pharmacokinetics of drugs in humans. Clin. Pharmacokinet. 2010, 49, 71–87. [Google Scholar] [CrossRef] [PubMed]
  47. Blouin, R.A.; Warren, G.W. Pharmacokinetic considerations in obesity. J. Pharm. Sci. 1999, 88, 1–7. [Google Scholar] [CrossRef] [PubMed]
  48. Miller, R.D.; Eriksson, L.I.; Fleisher, L.A.; Wiener-Kronish, J.P.; Cohen, N.H.; Young, W.L. Miller’s Anesthesia E-Book; Philadelphia Elsevier Health Sciences: Amsterdam, The Netherlands, 2014. [Google Scholar]
  49. Gan, T.J.; Diemunsch, P.; Habib, A.S.; Kovac, A.; Kranke, P.; Meyer, T.A.; Watcha, M.; Chung, F.; Angus, S.; Apfel, C.C.; et al. Consensus Guidelines for the Management of Postoperative Nausea and Vomiting. Anesth. Analg. 2014, 118, 85–113. [Google Scholar] [CrossRef] [Green Version]
  50. Rodríguez-Morató, J.; Goday, A.; Langohr, K.; Pujadas, M.; Civit, E.; Pérez-Mañá, C.; Papaseit, E.; Ramon, J.M.; Benaiges, D.; Castañer, O.; et al. Short- and medium-term impact of bariatric surgery on the activities of CYP2D6, CYP3A4, CYP2C9, and CYP1A2 in morbid obesity. Sci. Rep. 2019, 9, 20405. [Google Scholar] [CrossRef]
  51. Jain, R.; Chung, S.; Jain, L.; Khurana, M.; Lau, S.; Lee, J.; Vaidyanathan, J.; Zadezensky, I.; Choe, S.; Sahajwalla, C. Implications of obesity for drug therapy: Limitations and challenges. Clin. Pharmacol. Ther. 2011, 90, 77–89. [Google Scholar] [CrossRef]
  52. Abernethy, D.R.; Greenblatt, D.J. Drug disposition in obese humans. Clin. Pharmacokinet. 1986, 11, 199–213. [Google Scholar] [CrossRef]
  53. Adams, J.; Murphy, P. Obesity in anaesthesia and intensive care. Br. J. Anaesth. 2000, 85, 91–108. [Google Scholar] [CrossRef] [Green Version]
  54. Cheymol, G. Clinical pharmacokinetics of drugs in obesity. Clin. Pharmacokinet. 1993, 25, 103–114. [Google Scholar] [CrossRef]
  55. Cheymol, G. Effects of obesity on pharmacokinetics. Clin. Pharmacokinet. 2000, 39, 215–231. [Google Scholar] [CrossRef] [PubMed]
  56. Kim, E.-G.; Park, H.J.; Kang, H.; Choi, J.; Lee, H.J. Antiemetic effect of propofol administered at the end of surgery in laparoscopic assisted vaginal hysterectomy. Korean J. Anesthesiol. 2014, 66, 210–215. [Google Scholar] [CrossRef] [PubMed]
  57. Gopalakrishnan, S.; Ganeshkumar, P. Systematic Reviews and Meta-analysis: Understanding the Best Evidence in Primary Healthcare. J. Family Med. Prim. Care 2013, 2, 9–14. [Google Scholar] [CrossRef] [PubMed]
  58. Shaikh, S.I.; Nagarekha, D.; Hegade, G.; Marutheesh, M. Postoperative nausea and vomiting: A simple yet complex problem. Anesth. Essays Res. 2016, 10, 388–396. [Google Scholar] [CrossRef] [Green Version]
  59. Jorgensen, E.A.; Knigge, U.; Warberg, J.; Kjaer, A. Histamine and the regulation of body weight. Neuroendocrinology 2007, 86, 210–214. [Google Scholar] [CrossRef] [PubMed]
  60. Boden, G.; Chen, X.; Mozzoli, M.; Ryan, I. Effect of fasting on serum leptin in normal human subjects. J. Clin. Endocrinol. Metab. 1996, 81, 3419–3423. [Google Scholar] [CrossRef] [Green Version]
  61. Moon, Y.E. Postoperative nausea and vomiting. Korean J. Anesthesiol. 2014, 67, 164–170. [Google Scholar] [CrossRef]
  62. Abercrombie, E.D.; Keefe, K.A.; DiFrischia, D.S.; Zigmond, M.J. Differential effect of stress on in vivo dopamine release in striatum, nucleus accumbens, and medial frontal cortex. J. Neurochem. 1989, 52, 1655–1658. [Google Scholar] [CrossRef]
  63. Volkow, N.D.; Wang, G.J.; Fowler, J.S.; Telang, F. Overlapping neuronal circuits in addiction and obesity: Evidence of systems pathology. Philos. Trans. R. Soc. Lond. Ser. B Biol. Sci. 2008, 363, 3191–3200. [Google Scholar] [CrossRef] [PubMed] [Green Version]
  64. Feinleib, J.; Kwan, L.H.; Yamani, A.; Davidson, A. Postoperative Nausea and Vomiting. UpToDate. 2018. Available online: https://www.uptodate.com/contents/postoperative-nausea-and-vomiting (accessed on 26 March 2020).
  65. Kranke, P.; Eberhart, L.H.; Toker, H.; Roewer, N.; Wulf, H.; Kiefer, P. A prospective evaluation of the POVOC score for the prediction of postoperative vomiting in children. Anesth. Analg. 2007, 105, 1592–1597. [Google Scholar] [CrossRef] [PubMed]
  66. Tramer, M.; Moore, A.; McQuay, H. Prevention of vomiting after paediatric strabismus surgery: A systematic review using the numbers-needed-to-treat method. Br. J. Anaesth. 1995, 75, 556–561. [Google Scholar] [CrossRef] [PubMed] [Green Version]
  67. Ferrari, L.R.; Donlon, J.V. Metoclopramide reduces the incidence of vomiting after tonsillectomy in children. Anesth. Analg. 1992, 75, 351–354. [Google Scholar] [CrossRef]
  68. Villeret, I.; Laffon, M.; Duchalais, A.; Blond, M.H.; Lecuyer, A.I.; Mercier, C. Incidence of postoperative nausea and vomiting in paediatric ambulatory surgery. Paediatr. Anaesth. 2002, 12, 712–717. [Google Scholar] [CrossRef]
  69. Pocock, S.J.; Elbourne, D.R. Randomized trials or observational tribulations? N. Engl. J. Med. 2000, 342, 1907–1909. [Google Scholar] [CrossRef] [Green Version]
  70. Concato, J.; Shah, N.; Horwitz, R.I. Randomized, controlled trials, observational studies, and the hierarchy of research designs. N. Engl. J. Med. 2000, 342, 1887–1892. [Google Scholar] [CrossRef] [Green Version]
  71. Benson, K.; Hartz, A.J. A comparison of observational studies and randomized, controlled trials. N. Engl. J. Med. 2000, 342, 1878–1886. [Google Scholar] [CrossRef]
  72. Gum, P.A.; Thamilarasan, M.; Watanabe, J.; Blackstone, E.H.; Lauer, M.S. Aspirin use and all-cause mortality among patients being evaluated for known or suspected coronary artery disease: A propensity analysis. JAMA 2001, 286, 1187–1194. [Google Scholar] [CrossRef] [Green Version]
  73. Hainer, V.; Aldhoon-Hainerová, I. Obesity paradox does exist. Diabetes Care 2013, 36, S276–S281. [Google Scholar] [CrossRef] [Green Version]
  74. Nuttall, F.Q. Body Mass Index: Obesity, BMI, and Health: A Critical Review. Nutr. Today 2015, 50, 117–128. [Google Scholar] [CrossRef] [PubMed] [Green Version]
Jcm 09 01612 g001 550
Figure 1. Flow chart.
Figure 1. Flow chart.
Jcm 09 01612 g001
Jcm 09 01612 g002 550
Figure 2. ORs for development of PONV in underweight, overweight, and obese patients. UA, unadjusted; FA, fully adjusted; FS, all covariates + propensity score adjusted; BE, backward elimination, CI, confidence interval; OR, odds ratio. Covariates for overweight BE: age, female, operation duration, American Society of Anesthesiologists physical status, use of N2O, patient-controlled analgesia, smoking, use of antiemetics, neostigmine, proton-pump inhibitors, or antibiotics, laparoscopic surgery, and transfusion. Covariates for obese BE: age, female, operation duration, use of N2O, patient-controlled analgesia, smoking, use of antiemetics, neostigmine, or proton-pump inhibitors, gastroesophageal reflux disease, and Levin tube.
Figure 2. ORs for development of PONV in underweight, overweight, and obese patients. UA, unadjusted; FA, fully adjusted; FS, all covariates + propensity score adjusted; BE, backward elimination, CI, confidence interval; OR, odds ratio. Covariates for overweight BE: age, female, operation duration, American Society of Anesthesiologists physical status, use of N2O, patient-controlled analgesia, smoking, use of antiemetics, neostigmine, proton-pump inhibitors, or antibiotics, laparoscopic surgery, and transfusion. Covariates for obese BE: age, female, operation duration, use of N2O, patient-controlled analgesia, smoking, use of antiemetics, neostigmine, or proton-pump inhibitors, gastroesophageal reflux disease, and Levin tube.
Jcm 09 01612 g002
Table
Table 1. Baseline characteristics of the subjects.
Table 1. Baseline characteristics of the subjects.
PONV (+)
n = 10,404		PONV (−)
n = 93,157		p
Age (years, mean ± SD) 50.7 ± 16.550.6 ± 17.10.538
Female (n, (%)) 7561 (72.7)45,470 (48.8)<0.0001
Height (cm, mean ± SD) 160.5 ± 9.1163.6 ± 9.4<0.0001
BMI (n, (%))<19.9469 (4.5)3595 (3.9)<0.0001
20–24.96250 (60.1)52,573 (56.4)
25–29.93023 (29.1)29,972 (32.2)
≤30662 (6.4)7017 (7.5)
Operation time (h, mean ± SD) 2.5 ± 1.52.1 ± 1.5<0.0001
ASA PS ≥ 3 (n, (%)) 1540 (14.8)14,162 (15.2)0.280
N2O (n, (%)) 1474 (14.2)16,357 (17.6)<0.0001
PCA (n, (%)) 7261 (69.8)40,869 (43.9)<0.0001
DM (n, (%)) 1184 (11.4)12,274 (13.2)<0.0001
Smoking (n, (%)) 899 (8.6)18,118 (19.4)<0.0001
Opioids (n, (%)) 9465 (91.0)81,974 (88.0)<0.0001
Antiemetics (n, (%)) 7563 (72.7)47,421 (50.9)<0.0001
Neostigmine (n, (%)) 3292 (31.6)23,380 (25.1)<0.0001
PPI (n, (%)) 709 (6.8)6599 (7.1)0.309
GERD (n, (%)) 171 (1.6)1653 (1.8)0.336
Antibiotics (n, (%)) 9150 (87.9)81,224 (87.2)0.028
Levin tube (n, (%)) 227 (2.2)1743 (1.9)0.028
Laparoscopic surgery (n, (%)) 3189 (30.7)21,657 (23.2)<0.0001
Transfusion (n, (%)) 455 (4.4)3425 (3.7)<0.0001
PONV, postoperative nausea and vomiting; SD, standard deviation; ASAPS, American Society of Anesthesiologists physical status; PCA, patient-controlled analgesia; DM, diabetes; GERD, gastroesophageal reflux disease; PPI, proton-pump inhibitor; BMI, body mass index.
Table
Table 2. Unadjusted and fully adjusted odds ratios (ORs) of each variable for postoperative nausea and vomiting.
Table 2. Unadjusted and fully adjusted odds ratios (ORs) of each variable for postoperative nausea and vomiting.
UnadjustedFully Adjusted
OR (95% CI)pOR (95% CI)p
Age1.00 (1.00–1.00)0.5490.99 (0.99–1.00)<0.0001
Female2.79 (2.67–2.92)<0.00012.21 (2.06–2.36)<0.0001
Height0.97 (0.96–0.97)<0.00011.00 (0.99–1.00) 0.039
Operation time1.14 (1.12–1.15)<0.00011.06 (1.04–1.07)<0.0001
ASA PS 3–5 vs. 1–20.97 (0.92–1.03)0.2800.88 (0.83–0.95)<0.0001
N2O0.78 (0.73–0.82)<0.00010.81 (0.76–0.87)<0.0001
PCA2.96 (2.83–3.09)<0.00012.21 (2.05–2.39)<0.0001
Diabetes0.85 (0.79–0.90)<0.00010.93 (0.87–1.00)0.049
Smoking0.39 (0.37–0.42)<0.00010.61 (0.56–0.65)<0.0001
Opioids1.38 (1.28–1.48)<0.00011.10 (1.01–1.20)0.025
Antiemetics2.57 (2.46–2.69)<0.00011.47 (1.36–1.60)<0.0001
Neostigmine1.38 (1.32–1.44)<0.00011.40 (1.33–1.47)<0.0001
Proton-pump inhibitor0.96 (0.89–1.04)0.3100.84 (0.77–0. 92)<0.0001
GERD0.93 (0.79–1.08)0.3361.14 (0.97–1.34)0.115
Antibiotics1.07 (1.01–1.14)0.0280.88 (0.83–0.95)0.001
Levin tube1.17 (1.02–1.35)0.0280.80 (0.70–0.93)0.003
Laparoscopic surgery1.46 (1.40–1.53)<0.00011.17 (1.12–1.23)<0.0001
Transfusion1.20 (1.08–1.32)<0.00010.85 (0.77–0.94)0.002
Underweight vs. normal BMI1.10 (0.99–1.21)0.0681.05 (0.94–1.16)0.406
Overweight vs. normal BMI0.85 (0.81–0.89)<0.00010.91 (0.87–0.96)<0.0001
Obese vs. normal BMI0.79 (0.73–0.86)<0.00010.77 (0.71–0.84)<0.0001
PONV, postoperative nausea and vomiting; OR, odds ratio; CI, confidence interval; ASAPS, American Society of Anesthesiologists physical status; PCA, patient-controlled analgesia; GERD, gastroesophageal reflux disease; PPI, proton-pump inhibitor; BMI, body mass index.
Table
Table 3. Baseline characteristics of normal-BMI and underweight subjects, and comparison before and after propensity score matching.
Table 3. Baseline characteristics of normal-BMI and underweight subjects, and comparison before and after propensity score matching.
Before PSMAfter PSM
Normal (n = 58,823)UW
(n = 4064)		DpNormal
(n = 4064)		UW
(n = 4064)		Dp
Age50.3 (17.4)49.8 (21.9)0.020.14750.1 (18.4)49.8 (21.9)0.010.598
Height163.1 (9.0)162.5 (8.8)0.07<0.0001162.3 (8.8)162.5 (8.8)0.010.535
Female31,555 (53.6)2498 (61.5)0.18<0.00012501 (61.5)2498 (61.5)0.030.945
Operation time2.1 (1.5)2.1 (1.4)0.010.6302.1(1.4)2.1 (1.4)0.040.108
ASA PS ≥ 38735 (14.8)953 (23.4)0.31<0.0001983 (24.2)953 (23.4)0.020.435
N2O10,127 (17.2)699 (17.2)<0.010.797749 (18.4)699 (17.2)0.050.147
PCA27,337 (46.5)2002 (49.3)0.060.0011942 (48.2)2002 (49.3)0.020.340
Diabetes6567 (11.2)417 (10.3)0.050.076423 (10.4)417 (10.3)0.010.827
Smoking10,500(17.9)781 (19.2)0.050.028796 (19.6)781 (19.2)0.030.293
Opioids51,867 (88.2)3521 (86.6)0.080.0033480 (85.6)3521 (86.6)0.050.188
Antiemetics31,178 (53.0)2288 (56.3)0.07<0.00012272 (55.9)2288 (56.3)0.010.721
Neostigmine15,374 (26.1)1059 (26.1)<0.010.9131023 (25.2)1059 (26.1)0.030.360
PPI4268 (7.3)406 (10.0)0.19<0.0001442 (10.9)406 (10.0)0.050.191
GERD975 (1.7)63 (1.6)0.040.60465 (1.6)63 (1.6)0.020.859
Antibiotics51,372 (87.3)3533 (86.9)0.020.4603527 (86.8)3533 (86.9)0.010.844
Levin tube1184 (2.0)112 (2.8)0.180.00199 (2.4)112 (2.8)0.070.365
Laparoscopic surgery14,692 (25.0)990 (24.4)0.020.380986 (24.3)990 (24.4)<0.010.918
Transfusion2380 (4.0)327 (8.0)0.40<0.0001291 (7.2)327 (8.0)0.070.132
BMI, body mass index; PSM, propensity score matching; UW, underweight; D, standard mean difference; ASA PS, American Society of Anesthesiologists physical status; PCA, patient-controlled analgesia; PPI, proton-pump inhibitor; GERD, gastroesophageal reflux disease.Type of Surgery other than laparoscopic surgery before propensity score matching: Normal (brain surgery, 479; eye surgery, 1372; pharynx and tonsil surgery, 1361; ear surgery, 1030) vs. UW (brain surgery, 48; eye surgery, 96; pharynx and tonsil surgery, 76; ear surgery, 44).Type of Surgery other than laparoscopic surgery after propensity score matching: Normal (brain surgery, 42; eye surgery, 78; pharynx and tonsil surgery, 108; ear surgery, 50) vs. UW (brain surgery, 48; eye surgery, 96; pharynx and tonsil surgery, 76; ear surgery, 44).
Table
Table 4. Baseline characteristics of normal-BMI and overweight subjects, and comparison before and after propensity score matching.
Table 4. Baseline characteristics of normal-BMI and overweight subjects, and comparison before and after propensity score matching.
Before PSMAfter PSM
Normal
(n = 58,823)		OW
(n = 32,995)		DpNormal
(n = 9872)		OW (n = 9872)Dp
Age50.3 (17.4)52.1 (15.7)0.11<0.000151.0 (17.1)50.6 (15.5)0.020.159
Height163.1 (9.0)163.6 (9.8)0.05<0.0001163.5 (9.6)163.4 (10.1)0.010.512
Female31,555 (53.6)14,862 (45.0)0.19<0.00014806 (48.7)4939 (50.0)0.030.058
Operation time2.1 (1.5)2.2 (1.5)0.04<0.00012.1 (1.4)2.1 (1.4)0.010.554
ASA PS ≥ 38735 (14.8)4847 (14.7)0.010.5141419 (14.4)1370 (13.9)0.020.317
N2O10,127 (17.2)5739 (17.4)0.010.7971801 (18.2)1728 (17.5)0.030.175
PCA27,337 (46.5)15,281 (46.3)<0.010.0014512 (45.7)4491 (45.5)<0.010.764
Diabetes6567 (11.2)5049 (15.3)0.20<0.0001889 (9.0)998 (10.1)0.070.008
Smoking10,500 (17.9)6243 (18.9)0.04<0.00011965 (19.9)1865 (18.9)0.040.072
Opioids51,867 (88.2)29,277 (88.7)0.030.0128776 (88.9)8772 (88.9)<0.010.928
Antiemetics31,178 (53.0)17,474 (53.0)<0.010.89917,525 (53.1)17,474 (53.0)0.020.332
Neostigmine15,374 (26.1)8411 (25.5)0.020.0332693 (25.2)2585 (25.5)0.040.082
PPI4268 (7.3)2215 (6.7)0.050.002667 (6.8)182 (6.9)0.010.672
GERD975 (1.7)655 (2.0)0.10<0.0001165 (1.9)149 (2.0)0.060.363
Antibiotics51,372 (87.3)28,781 (86.9)0.010.6478647 (87.6)8632 (86.9)0.010.747
Levin tube1184 (2.0)579 (1.8)0.080.006175 (1.8)146 (1.5)0.100.103
Laparoscopic surgery14,692 (25.0)7446 (22.6)0.07<0.00012180 (22.1)2277 (23.1)0.030.099
Transfusion2380 (4.0)915 (2.8)0.22<0.0001232 (2.4)184 (1.9)0.130.230
BMI, body mass index; PSM, propensity score matching; OW, overweight; D, standard mean difference; ASA PS, American society of Anesthesiologists physical status; PCA, patient-controlled analgesia; GERD, gastroesophageal reflux disease.Type of Surgery other than laparoscopic surgery before propensity score matching: Normal (brain surgery, 479; eye surgery, 1372; pharynx and tonsil surgery, 1361; ear surgery, 1030) vs. OW (brain surgery, 258; eye surgery, 830; pharynx and tonsil surgery, 817; ear surgery, 657).Type of Surgery other than laparoscopic surgery after propensity score matching: Normal (brain surgery, 70; eye surgery, 237; pharynx and tonsil surgery, 225; ear surgery, 159) vs. OW (brain surgery, 75; eye surgery, 235; pharynx and tonsil surgery, 292; ear surgery, 196).
Table
Table 5. Baseline characteristics of normal-BMI and obese subjects, and comparison before and after propensity score matching.
Table 5. Baseline characteristics of normal-BMI and obese subjects, and comparison before and after propensity score matching.
Before PSMAfter PSM
Normal
(n = 58,823)		Obese
(n = 7679)		DpNormal
(n = 7679)		Obese (n = 7679)Dp
Age50.3 (17.4)46.4 (16.1)0.020.14746.5 (16.8)46.4 (16.1)0.010.670
Height163.1 (9.0)163.7 (10.4)0.06<0.0001163.5 (9.0)163.7 (10.4)0.010.598
Female31,555 (53.6)4119 (53.6)0.020.9944114 (53.6)4119 (53.6)<0.010.936
Operation time2.1 (1.5)2.2 (1.5)0.04<0.00012.1 (1.4)2.2 (1.5)<0.010.988
ASA PS ≥ 38735 (14.8)1167 (15.2)0.310.4211188 (15.5)1167 (15.2)0.010.638
N2O10,127 (17.2)1266 (16.5)0.030.1111301 (16.9)1266 (16.5)0.020.449
PCA27,337 (46.5)3510 (45.7)0.020.2073562 (46.4)3510 (45.7)0.020.400
Diabetes6567 (11.2)1425 (18.6)0.33<0.00011422 (18.5)1425 (18.6)<0.010.950
Smoking10,500 (17.9)1493 (19.4)0.060.0011485 (19.3)1493 (19.4)<0.010.870
Opioids51,867 (88.2)6774 (88.2)<0.010.9196775 (85.6)6774 (88.2)<0.010.980
Antiemetics31,178 (53.0)4044 (52.7)0.010.5754110 (53.5)4044 (52.7)0.020.286
Neostigmine15,374 (26.1)1828 (23.8)0.07<0.00011784 (25.2)1828 (23.8)0.020.403
PPI4268 (7.3)419 (5.5)0.17<0.0001442 (10.9)419 (5.5)<0.010.943
GERD975 (1.7)131 (1.7)0.020.755144 (1.9)131 (1.7)0.050.429
Antibiotics51,372 (87.3)6688 (87.1)0.010.5556659 (86.7)6688 (87.1)0.020.488
Levin tube1184 (2.0)95 (1.2)0.27<0.000197 (1.3)95 (1.2)0.010.885
Laparoscopic surgery14,692 (25.0)1718 (22.4)0.08<0.00011709 (22.3)1718 (22.4)<0.010.862
Transfusion2380 (4.0)258 (3.4)0.110.004253 (3.3)258 (3.4)0.010.822
BMI, body mass index; PSM, propensity score matching; D, standard mean difference; ASA PS, American Society of Anesthesiologists physical status; PCA, patient-controlled analgesia; GERD, gastroesophageal reflux disease.Type of Surgery other than laparoscopic surgery before propensity score matching: Normal (brain surgery, 479; eye surgery, 1372; pharynx and tonsil surgery, 1361; ear surgery, 1030) vs. Obese (brain surgery, 56; eye surgery, 170; pharynx and tonsil surgery, 283; ear surgery, 107).Type of Surgery other than laparoscopic surgery after propensity score matching: Normal (brain surgery, 82; eye surgery, 190; pharynx and tonsil surgery, 221; ear surgery, 132) vs. Obese (brain surgery, 56; eye surgery, 170; pharynx and tonsil surgery, 283; ear surgery, 107).

Share and Cite

MDPI and ACS Style

Kim, J.H.; Hong, M.; Kim, Y.J.; Lee, H.S.; Kwon, Y.S.; Lee, J.J. Effect of Body Mass Index on Postoperative Nausea and Vomiting: Propensity Analysis. J. Clin. Med. 2020, 9, 1612. https://doi.org/10.3390/jcm9061612

AMA Style

Kim JH, Hong M, Kim YJ, Lee HS, Kwon YS, Lee JJ. Effect of Body Mass Index on Postoperative Nausea and Vomiting: Propensity Analysis. Journal of Clinical Medicine. 2020; 9(6):1612. https://doi.org/10.3390/jcm9061612

Chicago/Turabian Style

Kim, Jong Ho, Mingi Hong, Young Joon Kim, Ho Seok Lee, Young Suk Kwon, and Jae Jun Lee. 2020. "Effect of Body Mass Index on Postoperative Nausea and Vomiting: Propensity Analysis" Journal of Clinical Medicine 9, no. 6: 1612. https://doi.org/10.3390/jcm9061612

APA Style

Kim, J. H., Hong, M., Kim, Y. J., Lee, H. S., Kwon, Y. S., & Lee, J. J. (2020). Effect of Body Mass Index on Postoperative Nausea and Vomiting: Propensity Analysis. Journal of Clinical Medicine, 9(6), 1612. https://doi.org/10.3390/jcm9061612

Note that from the first issue of 2016, this journal uses article numbers instead of page numbers. See further details here.

Article Metrics

Back to TopTop