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Changes in blood catecholamines during induction of general anesthesia in patients with post-induction hypotension undergoing laparoscopic cholecystectomy: A single-center prospective cohort study

  • Yi Yao ,

    Contributed equally to this work with: Yi Yao, Xia Kong

    Roles Data curation, Formal analysis, Investigation, Writing – original draft

    Affiliation Department of Anesthesiology, The Affiliated Hospital of Southwest Medical University, Luzhou, Sichuan Province, China

  • Xia Kong ,

    Contributed equally to this work with: Yi Yao, Xia Kong

    Roles Data curation, Formal analysis, Investigation, Writing – original draft

    Affiliation Department of Anesthesiology, The Affiliated Hospital of Southwest Medical University, Luzhou, Sichuan Province, China

  • Xuhui Chen,

    Roles Data curation, Formal analysis, Investigation, Writing – original draft

    Affiliation Department of Anesthesiology, The Affiliated Hospital of Southwest Medical University, Luzhou, Sichuan Province, China

  • Yingying Zhang,

    Roles Conceptualization, Formal analysis, Writing – review & editing

    Affiliation Department of Anesthesiology, The Affiliated Hospital of Southwest Medical University, Luzhou, Sichuan Province, China

  • Xueru Liu,

    Roles Supervision, Validation, Writing – review & editing

    Affiliation Department of Anesthesiology, The Affiliated Hospital of Southwest Medical University, Luzhou, Sichuan Province, China

  • Xiaobin Wang

    Roles Conceptualization, Funding acquisition, Writing – review & editing

    wangxiaobin67@163.com

    Affiliations Department of Anesthesiology, The Affiliated Hospital of Southwest Medical University, Luzhou, Sichuan Province, China, Department of Anesthesiology, Anesthesiology and Critical Care Medicine Key Laboratory of Luzhou, Southwest Medical University, Luzhou, Sichuan Province, China

Abstract

Background

Post-induction hypotension (PIH) often occurs during general anesthesia induction. This study aimed to investigate blood catecholamine levels during induction of general anesthesia in patients with PIH undergoing laparoscopic cholecystectomy.

Methods

This prospective study included 557 adult patients who underwent laparoscopic cholecystectomy under general anesthesia. PIH was defined as a greater than 20% decrease in systolic blood pressure from the pre-induction value, a systolic arterial pressure of less than 90 mmHg, or both. Plasma concentrations of epinephrine and norepinephrine during the induction of general anesthesia were determined using enzyme-linked immunosorbent assay. Multivariate logistic regression analysis evaluated the association between the clinical factors and PIH.

Results

Of the 557 patients, 390 had PIH, and the remaining 167 were allocated to the non-PIH group. Changes in blood adrenaline, noradrenaline levels, or both were more pronounced in the PIH than in the non-PIH group (p<0.05). Age, body mass index, a history of hypertension, preoperative systolic blood pressure, and propofol or sufentanil dose were independent predictors of PIH.

Conclusion

The changes of blood catecholamines in patients with more stable hemodynamics during the induction of general anesthesia are smaller than that in patients with post-induction hypotension.

Trial registration

ChiCTR2200055549, 12/01/2022.

Background

Laparoscopic cholecystectomy is a common procedure, with post-induction hypotension (PIH) occurring in approximately 50% of patients [1]. PIH is a common complication of anesthesia that is associated with postoperative acute renal injury [24], myocardial injury [5], ischemic stroke, and even death [69].

PIH is defined as hypotension occurring within 20 min of induction of general anesthesia [6, 10, 11]. The mechanism of PIH is likely multifactorial and remains unclear. Specific factors have been associated with PIH, including aging, emergency surgery, baseline hypovolaemia, and the use of propofol induction [1215]. Furthermore, previous studies have reported an association between catecholamine use and PIH incidence [16]. However, changes in catecholamine levels during PIH remain unclear. Accordingly, this study aimed to analyze the changes in blood catecholamine levels related to PIH to elucidate the mechanisms of action, aiding anesthesiologists in implementing preemptive appropriate measures based on the changes in catecholamine levels in clinical practice to reduce the occurrence of PIH and improve the prognosis of patients.

Materials and methods

The Ethics Committee of the Affiliated Hospital of Southwest Medical University approved the methods and procedures for this prospective cohort study (approval number: KY2021293, S1 and S3 Files). The trial was registered at the Chinese Clinical Trial Registration Center (ChiCTR2200055549, 12/01/2022) and was conducted between February 28, 2022, and November 31, 2022. Participants provided consent for the use of their anonymized medical data for research (S2 File), this study was conducted according to the principles expressed in the Declaration of Helsinki.

Study design

Eligible patients who underwent elective laparoscopic cholecystectomy under general anesthesia were ≥18 years of age and had an American Society of Anesthesiologists (ASA) score of I–III. Exclusion criteria were as follows: conversion to open surgery; severe preoperative comorbidities, including a New York Heart Association class ≥IV, moderate-to-severe impairment of pulmonary ventilation, Child C grade of liver function, and stage III renal insufficiency; history of peripheral arterial disease or atherosclerosis; opioid abuse or addiction to alcohol and other drugs; cardiac rhythm other than sinus and cardiomyopathy; as well as poor compliance and loss to follow-up (S4S6 Files).

Anesthesia and surgical protocols

All patients underwent standard preoperative fasting and were routinely monitored in the operating room. Intravenous anesthesia, comprising sufentanil (0.2–0.4 μg kg−1), propofol (1.5–2.5 mg kg−1), and CIS atracurium (0.1–0.3 mg kg−1) sequentially, was administrated. Subsequently, endotracheal intubation and mechanical ventilation were performed, and inhalation anesthesia with sevoflurane was maintained.

During induction, PIH was defined as a greater than 20% decrease in systolic blood pressure (SBP) from the pre-induction value, a systolic arterial pressure of less than 90 mmHg, or both. Appropriate treatment was provided by the anesthesiologist, which included fluid rehydration and intravenous injection of metaraminol bitartrate (0.5 mg) or methoxyamine (1 mg). Hypertension, defined as SBP >160 mmHg, was properly managed by the anesthesiologist.

Indications for placing and removing drainage tubes were based on previous studies [17]. If a patient had an abdominal drainage tube, it was removed 24–48 h after surgery in the absence of bile or bleeding. The main technical route used for surgery is shown in Fig 1.

thumbnail
Fig 1. Flow chart of patient inclusion PIH: Post-induction hypotension.

https://doi.org/10.1371/journal.pone.0305980.g001

Main indicators

The main indicators for evaluation were the incidence of PIH and blood catecholamine (adrenaline and norepinephrine) levels during anesthesia induction. The criterion for PIH was at least one episode of a greater than 20% decrease in SBP from the pre-induction value or systolic arterial pressure of less than 90 mmHg within 20 min after induction. The occurrence rate over the period of observation was calculated. To ensure blood perfusion in important organs, measures such as volume supplementation and vasopressor drug use were implemented immediately after PIH onset. Therefore, the duration of PIH was not included in the observation period. Radial artery blood (>5 mL) was collected from all patients at three time points: before anesthesia induction (T0), immediately after anesthesia induction (T1), and 3–5 min after tracheal intubation (T2). Heart rate (HR), SBP, and diastolic blood pressure (DBP) were recorded. Blood was collected and stored as previously described [18]. Plasma concentrations of epinephrine and norepinephrine were determined using enzyme-linked immunosorbent assay.

Based on the results of this experiment, we set a ratio for the hypotension and non-hypotension groups and the sample size using the software PASS 2011. The corresponding quantity was randomly selected from all samples to detect adrenaline and norepinephrine concentrations using radioimmunoassay.

Secondary indicators

The secondary indicators encompassed risk factors for PIH, which included pre-anesthesia data (age, sex, body mass index [BMI], ASA grade, chronic diseases, history of hypertension, creatinine level, eGFR [estimated Glomerular Filtration Rate], and baseline blood pressure) and induction period data (dose of propofol, sufentanil, or CIS atracurium and initial carbon dioxide pressure (PETCO2)]. The median dose of the induction drug was calculated, and the number of patients receiving a dose greater or less than the median dose was counted. The initial PETCO2 value was calculated based on the electronic anesthesia system records. Additionally, postoperative data, such as sleep quality, sedation classification, time to first exhaustion or defecation, nausea and vomiting, shoulder and back pain, headache, urinary retention, and time to discharge, were recorded. The Ramsay score was used to grade sedation. Sleep status was evaluated using the Athens Insomnia Scale (AIS), with a score ≥4 indicating insomnia. Data were collected by two researchers through a review of electronic medical charts and interviews with patients, family members, and surgeons. Both researchers completed standardized training during the interview process. The data were audited regularly to ensure reliability and quality.

Statistical analysis

Descriptive statistics were used to summarize the variables, with counts and percentages (%) used for categorical data and mean ± standard deviation or median and quartile range for continuous data, as appropriate for data distribution. Patients were classified into PIH and non-PIH groups. Between-group differences in continuous variables were evaluated using an independent t-test for normally distributed data and the Mann–Whitney U-test for variables with a non-normal distribution. The chi-squared test was used to compare categorical variables. Variables with a between-group difference of p≤0.1 were included in a multivariate logistic regression model to identify independent risk factors for PIH. Adrenaline and noradrenaline levels were compared using two-way repeated-measures analysis of variance, considering the interaction between time and group. All tests were two-sided, and the significance level was set at p<0.05. All statistical analyses were performed using R 4.0.5.

Results

Characteristics of the study sample and perioperative data

Of the 687 patients eligible for the study, 91 and 39 patients in the PIH and non-PIH groups, respectively, were excluded for the following reasons: conversion to laparotomy, missing anesthesia records, and loss to follow-up. Accordingly, 557 patients were included in the final analysis(S1 Table): 390 and 167 in the PIH and non-PIH groups, respectively (70% vs. 30%). The perioperative data for the PIH and non-PIH groups are shown in Table 1. Significant between-group differences were identified for the following factors: age, BMI, creatinine level, history of hypertension, preoperative SBP, DBP, HR, post-induction SBP, and dosage of propofol or sufentanil. Additionally, between-group differences were noted in the following postoperative factors: time of first defecation, headache, and urinary retention.

As shown in Table 2, the following factors were independently associated with PIH: age [odds ratio (OR), 1.04; 95% confidence interval (CI), 1.01–1.05; p<0.001]; BMI (OR, 0.87; 95%CI, 0.80–0.93; p<0.001); history of hypertension(OR, 3.07; 95%CI, 1.60–6.24; p = 0.001); preoperative SBP (OR, 1.04; 95% CI, 1.02–1.05; p<0.001); propofol dose >2 mg/kg (OR, 2.47; 95%CI, 1.47–4.24; p = 0.001); and sufentanil dose > 0.3 ug/kg (OR, 2.37; 95%CI; 1.53–3.68; p<0.001).

Catecholamine levels and PIH

Based on the results of this study, the incidence of hypotension was 70%. We set a ratio of 7:3 for the hypotension and non-hypotension groups, assuming that α = 0.05, β = 0.20, requiring at least 50 plasma samples from patients with PIH and 22 plasma samples from patients without PIH. Assuming a loss-to-follow-up rate of 10%, 80 study participants were required. Therefore, based on double-blind random sampling, plasma samples from 56 and 24 patients in the induced hypotension and non-induced hypotension groups, respectively, were selected for the detection of adrenaline and norepinephrine concentrations using radioimmunoassays(S2 Table).

As shown in Table 3, the two-way repeated-measures analysis of variance between the PIH and non-PIH groups showed that there were statistical differences at different time points; the level of adrenaline in the PIH group was significantly higher than that in the non-PIH group at T2 (p<0.05), and norepinephrine levels in the PIH group were significantly higher than those in the non-PIH group at T1 and T2 (p<0.05). Further comparison of the differences in values showed that the increase in norepinephrine at T1 and T2 and the increase in epinephrine at T2 were greater in PIH group. Compared with T0 before anesthesia induction, the levels of epinephrine and norepinephrine were significantly increased in both groups at T2 (p<0.05), and the levels of norepinephrine were significantly increased in both groups at T1 (p<0.05).

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Table 3. Comparison of adrenaline (pg/mL) and noradrenaline (ng/mL) levels.

https://doi.org/10.1371/journal.pone.0305980.t003

Discussion

This study observed more pronounced changes in adrenaline, noradrenaline levels, or both in the PIH group than in the non-PIH group during induction of general anesthesia. One possible explanation is that the lower blood pressure in the PIH group may have activated the renin-angiotensin and vasopressin systems, increasing the secretion of norepinephrine and epinephrine in the PIH group [19]. Injurious stimuli such as tracheal intubation and surgical incision trigger stress reactions mediated via the sympathetic-adrenal medullary axis, releasing catecholamines. Accordingly, blood levels of catecholamine hormones are frequently used as reliable indicators of stress during surgery [20]. Our finding of higher plasma norepinephrine and epinephrine levels at T2 in the PIH and non-PIH groups compared to the baseline value (T0) may reflect the noxious stimulation generated during tracheal intubation. Plasma norepinephrine levels in both groups at T1 were higher than those at baseline (T0), potentially attributed to the notable decrease in the patient’s blood pressure during anesthesia induction, activating the stress system and increasing the compensatory effect of norepinephrine [21].

This study identified age, BMI, a history of hypertension, preoperative SBP, and propofol and sufentanil doses as independent predictors of PIH in patients who underwent laparoscopic cholecystectomy under general anesthesia. Older patients had a higher risk for PIH [2224]. The negative correlation between BMI and PIH likely reflects a reduction in autonomic nervous activity and retention of salt and water in patients with a low BMI [25, 26]. Hypertension as a risk factor for PIH has been previously reported [27]. To explore the influence of the induction drug dose on the risk of PIH, we compared the incidence of PIH among subgroups of patients who received doses greater or less than the median dose. The median dosages are as follows: propofol, 2 mg/kg; sufentanil, 0.3 μg/kg; and CIS atracurium, 0.2 mg/kg [13]. Higher doses of propofol or sufentanil are risk factors for PIH, consistent with the dose-dependent relationship previously described for these drugs and intraoperative hypotension [10]. The decrease in blood pressure caused by the above factors primarily stems from reduced sympathetic activity [28, 29], directly affecting the vascular smooth muscle, which leads to arterial vessel dilation and venous relaxation [3032]. The study revealed a positive association between higher preoperative SBP and PIH. Elevated preoperative SBP could be linked to the “white coat” effect and increased sympathetic excitability before surgery [33]; however, the specific reasons need further exploration.

Additionally, prolonged exhaustion, defecation, and eating were mainly related to older age, drainage tube placement, and refusal to eat owing to severe digestive tract reactions. Notably, these postoperative factors extend the length of the hospital stay. Moreover, a higher incidence of postoperative headache was observed in the PIH group than in the non-PIH group, which may be related to the negative effect of hypotension on cerebral blood flow, contributing to the potential mechanism of PIH-related headache [34].

The limitations of this study should be acknowledged. First, these independent risk factors for PIH need further confirmation in multicenter studies with larger sample sizes. Second, because of the short hospital stay of the patients who underwent laparoscopic cholecystectomy, follow-up was difficult, resulting in insufficient long-term follow-up results.

In summary, during the induction of general anesthesia, more obvious changes in adrenaline, noradrenaline levels, or both were observed in the PIH group than in the non-PIH group. Age, BMI, history of hypertension, preoperative SBP, and propofol or sufentanil dose were independent predictors of PIH in patients who underwent laparoscopic cholecystectomy under general anesthesia. Our findings highlights the importance of preoperative risk stratification and tailored management approaches for at-risk patients.

Supporting information

S1 File. The approval of clinical trial ethics committee.

https://doi.org/10.1371/journal.pone.0305980.s001

(PDF)

S2 File. Translation-informed consent form.

https://doi.org/10.1371/journal.pone.0305980.s002

(PDF)

S3 File. Translation-the approval of clinical trial ethics committee.

https://doi.org/10.1371/journal.pone.0305980.s003

(PDF)

S4 File. Research plan for induced hypotension project.

https://doi.org/10.1371/journal.pone.0305980.s004

(PDF)

S5 File. Human participants research checklist.

https://doi.org/10.1371/journal.pone.0305980.s005

(PDF)

Acknowledgments

We thank editage editage for its linguistic assistance during the preparation of this manuscript (S7 File).

References

  1. 1. Lee J, Woo J, Kang AR, Jeong Y-S, Jung W, Lee M, et al. Comparative analysis on machine learning and deep learning to predict post-induction hypotension. Sensors. 2020;20:4575. pmid:32824073
  2. 2. Maheshwari K, Turan A, Mao G, Yang D, Niazi AK, Agarwal D, et al. The association of hypotension during non‐cardiac surgery, before and after skin incision, with postoperative acute kidney injury: a retrospective cohort analysis. Anaesthesia. 2018;73:1223–8. pmid:30144029
  3. 3. Vaara ST, Bellomo R. Postoperative renal dysfunction after noncardiac surgery: Current Opinion in Critical Care. 2017;23:440–6.
  4. 4. Mathis MR, Naik BI, Freundlich RE, Shanks AM, Heung M, Kim M, et al. Preoperative risk and the association between hypotension and postoperative acute kidney injury. Anesthesiology. 2020;132:461–75. pmid:31794513
  5. 5. Salmasi V, Mascha EJ. Relationship between Intraoperative Hypotension, Defined by either reduction from baseline or absolute thresholds, and acute kidney and myocardial injury after noncardiac surgery: a retrospective cohort analysis. PERIOPERATIVE MEDICINE. 2017;126:47–65. pmid:27792044
  6. 6. Südfeld S, Brechnitz S, Wagner JY, Reese PC, Pinnschmidt HO, Reuter DA, et al. Post-induction hypotension and early intraoperative hypotension associated with general anaesthesia. British Journal of Anaesthesia. 2017;119:57–64. pmid:28974066
  7. 7. Sessler DI, Bloomstone JA, Aronson S, Berry C, Gan TJ, Kellum JA, et al. Perioperative quality initiative consensus statement on intraoperative blood pressure, risk and outcomes for elective surgery. British Journal of Anaesthesia. 2019;122:563–74. pmid:30916004
  8. 8. Althoff FC, Agnihotri A, Grabitz SD, Santer P, Nabel S, Tran T, et al. Outcomes after endoscopic retrograde cholangiopancreatography with general anesthesia versus sedation. British Journal of Anaesthesia. 2021;126:191–200.
  9. 9. Smischney NJ, Shaw AD, Stapelfeldt WH, Boero IJ, Chen Q, Stevens M, et al. Postoperative hypotension in patients discharged to the intensive care unit after non-cardiac surgery is associated with adverse clinical outcomes. Crit Care. 2020;24:682. pmid:33287872
  10. 10. Tarao K, Daimon M, Son K, Nakanishi K, Nakao T, Suwazono Y, et al. Risk factors including preoperative echocardiographic parameters for post-induction hypotension in general anesthesia. Journal of Cardiology. 2021;78:230–6. pmid:33838982
  11. 11. Wani TM, Hakim M, Ramesh A, Rehman S, Majid Y, Miller R, et al. Risk factors for post-induction hypotension in children presenting for surgery. Pediatr Surg Int. 2018;34:1333–8. pmid:30350110
  12. 12. Engel D, Beilstein CM, Löffel LM, Wuethrich PY. The impact of fluid optimisation before induction of anesthesia on hypotension after induction. Anaesthesia. 2020;75:1402–1402.
  13. 13. Reich DL, Hossain S, Krol M, Baez B, Patel P, Bernstein A, et al. Predictors of hypotension after induction of general anesthesia: anesthesia & analgesia. 2005;101:622–8.
  14. 14. Okamura K. Pre-anesthetic ultrasonographic assessment of the internal jugular vein for prediction of hypotension during the induction of general anesthesia. Journal of Anesthesia. 2019;33:612–9. pmid:31451896
  15. 15. Lankadeva YR, May CN, Bellomo R, Evans RG. Role of perioperative hypotension in postoperative acute kidney injury: a narrative review. British Journal of Anaesthesia. 2022;128:931–48. pmid:35465952
  16. 16. Macnab MSP, Manninen PH, Lam AM, Gelb AW. The stress response to induced hypotension for cerebral aneurysm surgery: a comparison of two hypotensive techniques. Can J Anaesth. 1988;35:111–5. pmid:3281763
  17. 17. Picchio M, De Cesare A, Di Filippo A, Spaziani M, Spaziani E. Prophylactic drainage after laparoscopic cholecystectomy for acute cholecystitis: a systematic review and meta-analysis. Updates Surg. 2019;71:247–54. pmid:30945148
  18. 18. Tu W, Yuan H, Zhang S, Lu F, Yin L, Chen C, et al. Influence of anesthetic induction of propofol combined with esketamine on perioperative stress and inflammatory responses and postoperative cognition of elderly surgical patients. Am J Transl Res. 2021;13:1701–9. pmid:33841692
  19. 19. Schulte E, Ziegler D, Philippi-Höhne C, Kaczmarczyk G, Boemke W. Angiotensin-converting enzyme inhibition and blood pressure response during total intravenous anesthesia for minor surgery. Acta Anaesthesiologica Scandinavica. 2011;55:435–43.
  20. 20. Fukusaki M, Maekawa T, Kobayashi I, Hara T, Sumikawa K. Catecholamine and renin-angiotensin response during controlled hypotension induced by prostaglandin E1 combined with hemodilution during isoflurane anesthesia. Journal of Clinical Anesthesia. 1997;9:321–7. pmid:9195357
  21. 21. Helander EM, Webb MP, Menard B, Prabhakar A, Helmstetter J, Cornett EM, et al. Metabolic and the surgical stress response considerations to improve postoperative recovery. Curr Pain Headache Rep. 2019;23:33. pmid:30976992
  22. 22. Zivaljevic V. Risk factors for intraoperative hypotension during thyroid surgery. Med Sci Monit. 2013;19:236–41. pmid:23548975
  23. 23. Nakasuji M, Nakasuji K. Causes of arterial hypotension during anesthetic induction with propofol investigated with perfusion index and clearsight in young and elderly patients. Minerva Anestesiol. 2021;87:640–7.
  24. 24. Chen B. A systematic review of risk factors for postinduction hypotension in surgical patients undergoing general anesthesia. R An. 2021;25:7044–50. pmid:34859868
  25. 25. Coimbra S, Brandão Proença J, Santos-Silva A, Neuparth MJ. Adiponectin, leptin, and chemerin in elderly patients with type 2 diabetes mellitus: a close linkage with obesity and length of the disease. BioMed Research International. 2014;2014:1–8. pmid:25105135
  26. 26. Nakamura T, Suzuki M, Ueda M, Hirayama M, Katsuno M. Lower body mass index is associated with orthostatic hypotension in Parkinson’s disease. Journal of the Neurological Sciences. 2017;372:14–8. pmid:28017201
  27. 27. Hojo T, Kimura Y, Shibuya M, Fujisawa T. Predictors of hypotension during anesthesia induction in patients with hypertension on medication: a retrospective observational study. BMC Anesthesiol. 2022;22:343. pmid:36368916
  28. 28. Alizadeh R, Fard ZA. Renal effects of general anesthesia from old to recent studies. Journal Cellular Physiology. 2019;234:16944–52. pmid:30843210
  29. 29. Araújo AM, Machado HS, Falcão AC, Soares-da-Silva P. Reliability of body-weight scalars on the assessment of propofol induction dose in obese patients. Acta Anaesthesiol Scand. 2018;62:464–73. pmid:29159892
  30. 30. Jang CH, Cho YB, Lee JS, Kim GH, Jung W-K, Pak SC. The effect of propofol infusion with topical epinephrine on cochlear blood flow and hearing: an experimental study. International Journal of Pediatric Otorhinolaryngology. 2016;91:23–6. pmid:27863636
  31. 31. Darvall J, Vijayakumar R, Leslie K. Prewarming neurosurgical patients to minimize hypotension on induction of anesthesia: a randomized trial. Can J Anesth/J Can Anesth. 2016;63:577–83. pmid:26858092
  32. 32. Saugel B, Bebert E-J, Briesenick L, Hoppe P, Greiwe G, Yang D, et al. Mechanisms contributing to hypotension after anesthetic induction with sufentanil, propofol, and rocuronium: a prospective observational study. J Clin Monit Comput. 2022;36:341–7. pmid:33523352
  33. 33. Koutsaki M, Thomopoulos C, Achimastos A, Kallistratos M, Batistaki C, Chatziagelaki E, et al. Perioperative SBP changes during orthopedic surgery in the elderly: clinical implications. Journal of Hypertension. 2019;37:1705–13. pmid:30950973
  34. 34. Matsota PK, Christodoulopoulou TC, Batistaki CZ, Arvaniti CC, Voumvourakis KI, Kostopanagiotou GG. Factors associated with the presence of postoperative headache in elective surgery patients: a prospective single center cohort study. J Anesth. 2017;31:225–36. pmid:27864621