Abstract
Background
The aim of this study was to evaluate the influence of combined general/epidural anesthesia (GEA) on hemodynamics, respiratory function and stress hormone levels in patients with ovarian neoplasm undergoing laparoscopy.
Material/Methods
A total of 177 patients with ovarian neoplasm (screened by inclusion/exclusion criteria) receiving laparoscopy were divided into groups G (general anesthesia alone), L1.0 (GEA with 1.0% lidocaine), and L1.5 (GEA with 1.5% lidocaine). Hemodynamics, respiratory parameters and stress hormone levels in the 3 groups were recorded and analyzed.
Results
Hemodynamic indexes and PaO2/PaCO2 in group L1.0 showed no differences at each time point (all P>0.05). At the end of anesthesia tracheal intubation (T1), 10 min after pneumoperitoneum (T2) and the end of anesthesia tracheal extubation (T3), there were significant differences in hemodynamic indexes, respiratory parameters, epinephrine (E), and noradrenalin (NE) of group G/L1.5, compared with before anesthesia induction (T0) (all P<0.05). Compared with group G, there were big differences in dosage of anesthetics (sufentanil, vecuronium, and propofol) and pharmaceutic adjuvants (ephedrine, atropine, and nitroglycerin), postoperative recovery time, extubation time, and incidence of agitation in group L1.0/L1.5 (all P<0.05).
Conclusions
GEA can improve the quality and efficiency in laparoscopy for ovarian neoplasm, with the advantages of reduced anesthetics dosage, satisfactory postoperative analgesia, maintained hemodynamic stability, excellent uterine relaxation, and reduced time of anesthesia induction, surgery, recovery, and extubation. In addition, compared with group L1.5, group L1.0 was more secure and worthy of clinical promotion in laparoscopy.
MeSH Keywords: Hemodynamics; Laparoscopy; Ovarian Neoplasms; Anesthesia, Caudal; Anesthesia, General
Background
Ovarian neoplasms with an overall cure rate of nearly 30% are common; 80% of the tumors arise from the epithelium [1,2]. The majority of ovarian neoplasms are benign, but 25% of them are malignant [3]. Ovarian cancer, one of the leading causes of death around the world, is the sixth most common cancer and one of the deadliest gynecological malignancies [4]. Annually more than 21,000 new cases were diagnosed and 14,500 died from ovarian cancer worldwide [5]. More than 75% of ovarian cancers recrudesced within 12 to 24 months [6]. Patients with ovarian cancer may experience symptoms such as loss of sensory perception, nausea, severe fatigue, abdominal discomfort, vomiting, pain, and change in body image not only during chemotherapy but also after treatment [7]. Currently, laparoscopy, as a positive minimally invasive surgery, is an efficient way to manage benign ovarian neoplasms; it can reduce postoperative pain, urinary tract infections, total cost, and time admitted to hospital and is an alternative to open surgery [8,9]. Studies showed that certain anesthetic techniques (regional anesthesia, general anesthesia, or combined general/epidural anesthesia [GEA]) or certain anesthetic agents could affect the recurrence/metastasis of cancers [10–13].
GEA is a frequently applied anesthetic technique in thoracic or abdominal surgery. It has several advantages including early recovery from postoperative analgesia, prevention of deep vein thrombosis, reducing risk of cardiac dysrhythmia, and other cardiovascular and ischemic events. Thus, GEA was commonly used in certain centers all around the world [14]. A study showed that GEA influenced cerebral hemodynamics, adverse cerebrovascular response, and intracranial pressure in patients undergoing laparoscopy [15]. GEA was proved able to improve the postoperative prognosis of breast cancer and prostate cancer [10]. As for larynx or hypopharynx and gastroesophageal cancer, GEA was proved able to significantly reduce cancer recurrence and prolong cancer-free survival [13]. The relation between GEA and clinical outcomes of patients with ovarian neoplasm undergoing laparoscopy was not reported. Thus, this study aims to investigate the association between GEA and the hemodynamics, respiratory function, and stress hormone levels in patients with ovarian neoplasm undergoing laparoscopy.
Material and Methods
Study subjects
A total of 243 patients (age, 46–63 years; mean age, 54.46±3.44 years; height, 1.57–1.79 m; weight, 45–61 kg; the American Society of Anesthesiologists [16] physical status I and II) were admitted at Linyi People’s Hospital from January 2012 to January 2015, receiving laparoscopy of ovarian neoplasm. Screened by inclusion/exclusion criteria, 177 cases were finally selected for the study and, according to the random number table, divided into 3 groups (each 59 cases), including the general anesthesia − alone group (group G), combined epidural (where 1.0% lidocaine was used)/general anesthesia group (group L1.0) and combined epidural (where 1.5% lidocaine was used)/general anesthesia group (group L1.5). Inclusion criteria: (1) no solid components of the accessory cyst (except for teratoma) were found on ultrasonic examination; (2) the inner diameter of the accessory cyst was >7 cm in ultrasonography examination; (3) there was no thick separation or nipple in the cyst wall; (4) there was no ascites; (5) all the patients received ultrasound examination 8 to 12 weeks later and only those with no functional tumors of the ovary were included; (6) no severe heart or lung diseases, hypertension, diabetes, severe anemia, or endocrine diseases were found in preoperative examination. Exclusion criteria: (1) patients with severe liver or renal failure; (2) patients with contraindications for laparoscopic gynecologic surgery or with no reaction to anesthesia. All the subjects (or their family members) in our study agreed to receive laparoscopy of ovarian neoplasm and signed informed consent. The study was approved by the Committee of Ethics of Linyi People’s Hospital.
Preoperative administration
All the patients were intramuscularly injected with 0.5 mg atropine 15 min before the surgery; simultaneously their heart rate (HR), blood pressure (BP), pulse oxygen saturation (SPO2), and end-tidal carbon dioxide pressure (PETCO2) were monitored.
Anesthesia induction
For groups L1.0 and L1.5, according to the extent of the surgery, puncture points were selected at T1–2 and catheter position near the head end with the depth of 4 to 5 cm. After an injection of 2% lidocaine (3 mL), which controlled the level of anesthesia T1–8, the patients were closely monitored for events, such as local anesthetic poisoning, incorrect catheter insertion into the subarachnoid space, or wide block. Induction of general anesthesia was performed 5 min after the level of anesthesia stabilized if none of those events occurred. General anesthesia was induced by vecuronium (0.l mg/kg), sufentanil (0.5 μg/kg), and propofol (1.5–2.0 mg/kg) through a catheter into the right jugular vein. In order to keep the muscles relaxed, the patients were given a single injection of sufentanil (0.3 μg/kg) and vecuronium (0 05 mg/kg) independently during the surgery. To maintain the patients’ sedation, propofol (3.6–6.6 mg/kg/h) was pumped during anesthesia, and the dose was adjusted in time according to the patients’ BP and HR changes.
Anesthesia maintenance
At the beginning of the surgery, 1.0% and 1.5% lidocaine (each 5 mL) were respectively given to the group L1.0 and L1.5 with the injection speed at 0.25 mL/s, and additional micropump infusions (corresponding concentration) were given during the surgery at the rate of 4–6 mL/h. The administration of general anesthesia medications was stopped after the laparoscopy and after the elimination of pneumoperitoneum. Tracheal extubation was performed once the patients regained consciousness, the rest of the surgery being performed under the effect of epidural anesthetics. The procedures of venipuncture and inducing and maintaining anesthesia were the same for groups G, L1.0, and L1.5; the same anesthesia machine was used for all 3 groups.
Ventilation in anesthesia
Mechanical ventilation by anesthesia machine was applied for all 3 groups, with fraction of inspired oxygen (FIO2)=1.0, tidal volume (VT)=6–8 mL/kg, respiratory rate=12 bpm, respiratory ratio=1:2, and PETCO2=35–45 mm Hg. One hour after the surgery, the infusion speed was accordingly adjusted to the patient’s blood loss volume, generally maintained at 4 mL/kg/h. Timely blood transfusions should be given to patients observed to have <100 g/L hemoglobin. During anesthesia, compared with the basic arterial pressure, if the patient’s mean arterial pressure (MAP) decreased >20%, and HR was <50 bpm, the patient was given an intravenous injection of atropine 0.3 mg and ephedrine 5 mg per time; and if the MAP rose more than 30%, the patient was given an intravenous injection of nitroglycerin 200 μg per time. All the data were recorded for statistical analysis, including the operation time, duration of anesthesia, dosage of anesthesia drugs and pharmaceutic adjuvants, blood loss volume, and infusion volume.
Parameters monitoring
Noninvasive multifunctional monitoring instrument was used to detect the HR, systolic blood pressure (SBP), diastolic blood pressure (DBP), and SPO2 at 4 time points: before anesthesia induction (T0), at the end of anesthesia tracheal intubation (T1), 10 min after pneumoperitoneum (T2), and at the end of anesthesia tracheal extubation (T3).
Arterial blood gas analysis was performed at the 4 time points, recording the data results of the pH value (pH), base excess (BE), pressure of arterial carbon dioxide (PaCO2), pressure of arterial oxygen (PaO2), central venous pressure (CVP), and MAP.
The surgery time, duration of anesthesia, blood loss volume, and infusion volume were recorded, as were the dosage of sufentanil, propofol, and vecuronium for anesthesia and the dosage of the pharmaceutic adjuvants, including ephedrine, atropine, and nitroglycerin. The recovery time and the anesthesia tracheal extubation time were recorded. The incidence of agitation was calculated.
The uterine relaxation degree was compared and decided as (1) excellent if the uterus and ligaments are excellent in relaxation and the cervix can be smoothly pulled out from the vagina; (2) fine if the uterus and ligaments are in general relaxation and the cervix can be forced out from the vagina; (3) bad if the uterus and ligaments are tight and the cervix cannot be pulled out from the vagina. The excellent and fine rate = (the number of excellent cases + the number of fine cases)/the number of total cases ×100% [17].
At each of the 4 time points, 4 mL venous blood was collected from the patient’s forearm (nontransfusion side), followed by an immediate centrifugation for 5 min (3000 rpm). The isolated plasma was then preserved at −4°C. The concentration determination of epinephrine (E) and norepinephrine (NE) was performed using ion-pair high-performance liquid chromatography (HPLC), specifically, the plasma E kit (Beijing North Institute of Biotechnology, Beijing, China) and NE detection kit (Beijing North Institute of Biotechnology, Beijing, China), respectively. The levels of the E and NE were detected at the 4 time points.
Statistics
All the data were analyzed using SPSS software version 20.0 (SPSS Inc, Chicago, IL, USA). Measurement data were expressed as mean plus or minus standard deviation (χ̄ ±s). Multigroup comparisons were performed by single factor variance and comparisons between groups were validated by unpaired t test. Comparison of enumeration data was validated using chi-square test. Statistical power was analyzed using Power and Program. P<0.05 was considered as statistically significant.
Results
Random grouping scheme
Among the 243 patients with ovarian neoplasm, a total of 66 cases were excluded, including cases with hypertension (n=18), coronary heart disease (n=5), rheumatoid heart disease (n=6), gastric ulcer (n=5), cirrhosis (n=6), emphysema (n=4), diabetes (n=13), hyperthyroidism (n=4), and allergic constitution (n=5). The remaining 177 cases were finally enrolled and divided according to the random number table into group G, L1.0, or L1.5 (each 59 cases; Figure 1). Specifically, the random numbers in the third row and fifth column were taken for all the patients, skipping ones that were greater than 177 or occurred again, until all the numbers from 1 to 177 were randomly taken. The patients with numbers 1 to 59 were assigned to group G, 60 to 118 to group L1.0, and 119 to 177 to group L1.5.
Figure 1.
Grouping scheme for the patients with ovarian neoplasm.
Baseline characteristics
The ovarian cysts’ diameters ranged from 2.6 to 10.4 cm, with an average diameter of 6.05±1.76 cm, and all the cysts were unilateral; group G included 31 people with right-sided cysts and 28 people with left-sided cysts; group L1.0 and L1.5 contained 30 individuals with right-sided cysts and 29 individuals with left-sided cysts, respectively. None of the patients had severe anemia, heart disease, hypertension, or other complications, although these are not contraindications for laparoscopy. There were no differences in age, body features, or history of cesarean delivery among the 3 groups (P>0.05), suggesting a comparability (Table 1).
Table 1.
Comparison of baseline characteristics among group G, L1.0 and L1.5.
| Group G (n=59) | Group L1.0 (n=59) | Group L1.5 (n=59) | ||
|---|---|---|---|---|
| Age (year) | 55.12±5.25 | 54.14±3.74 | 54.58±1.18 | |
| Height (m) | 1.68±0.19 | 1.67±0.18 | 1.68±0.17 | |
| Weight (kg) | 52.86±4.32 | 53.14±3.17 | 53.72±4.21 | |
| HR (beats/min) | 76.1±8.9 | 77.2±7.1 | 77.5±2.8 | |
| BP (mmHg) | SBP | 124.8±6.7 | 125.2±7.6 | 125.6±8.4 |
| DBP | 76.4±5.7 | 76.9±4.6 | 74.8±6.9 | |
| Cyst (cm) | Diameter | 6.1±1.7 | 6.1±2.2 | 6.0±1.3 |
| Left (n) | 28 | 29 | 29 | |
| Right (n) | 31 | 30 | 30 | |
| ASA score (n) | Grade I | 26 | 32 | 31 |
| Grade II | 33 | 27 | 28 |
HR – heart rate; BP – blood pressure; SBP – systolic blood pressure; DBP – diastolic blood pressure; ASA – American society of anesthesiologists.
Hemodynamic changes
Compared with T0, there were no apparent differences in hemodynamic indexes (HR, DBP, and SpO2) in group L1.0 at T1–3 (all P>0.05); SBP in group L1.0 at T2/3 was higher (all P<0.05), and hemodynamic indexes (HR, SBP, DBP, and SpO2) of groups G and L1.5 evidently increased (all P<0.05, power >0.8). Compared with group L1.0, HR of groups G and L1.5 were different at T1–3 (all P<0.05, power >0.8), DPB of the 2 groups were different at T3 (both P<0.05, power >0.8), and SpO2 of the 2 groups were different at T2 (both P<0.05, power >0.8). HR in group L1. 5 was higher than that in group G at each time point during surgery (all P<0.05, power >0.8). Compared with the SBP at T1, SBP of the 3 groups significantly increased at T2/3 (all P<0.05, power >0.8), and compared with DBP at T1, DBP of groups G and L1.5 greatly increased at T3 (all P<0.05, power >0.8; Table 2).
Table 2.
Comparison of hemodynamic parameters among group G, L1.0 and L1.5 (χ̄±s).
| Groups | n | Before anesthesia induction (T0) | End of tracheal intubation (T1) | 10 min after pneumoperitoneum (T2) | End of tracheal extubation (T3) |
|---|---|---|---|---|---|
| HR (beats/min) | |||||
| G | 59 | 77.3±7.5 | 80.7±6.7#*$ | 82.1±7.1#*$ | 79.9±4.9*$ |
| L1.0 | 59 | 76.5±7.2 | 77.8±5.5 | 78.5±4.9 | 76.8±5.6 |
| L1.5 | 59 | 76.3±1.9 | 84.8±2.4#*!$ | 85.2±5.7#*!$ | 83.8±6.6#*!$ |
| DBP | |||||
| G | 59 | 76.2±8.1 | 80.0±3.8#$ | 85.4±6.0#*@$ | 87.2±6.8#*@$ |
| L1.0 | 59 | 76.9±8.5 | 79.2±4.8 | 80.6±6.4 | 78.3±7.4 |
| L1.5 | 59 | 74.1±6.5 | 79.6±5.4#$ | 82.2±7.5#!$ | 84.7±7.2#*@$ |
| SBP | |||||
| G | 59 | 125.6±7.6 | 129.9±8.9#$ | 138.2±7.9#@$ | 134.9±7.9#@$ |
| L1.0 | 59 | 125.0±9.5 | 128.9±9.8 | 140.5±9.1#@$ | 136.2±9.4#@$ |
| L1.5 | 59 | 125.4±8.9 | 129.6±8.7#$ | 137.9±8.4#@$ | 131.3±8.7#@$ |
| SpO2 | |||||
| G | 59 | 102.7±2.8 | 100.98±3.2#$ | 100.4±2.6#*$ | 101.9±3.9 |
| L1.0 | 59 | 103.2±3.3 | 101.7±1.8 | 101.9±1.5 | 102.5±2.7@$ |
| L1.5 | 59 | 103.5±2.2 | 101.4±1.9#$ | 100.7±3.7#*$ | 104.2±2.8#$ |
Compared with T0, P<0.05;
compared with group L 1.0 at the same time point, P<0.05;
compared with group G at the same time point, P<0.05;
compared with T1, P<0.05;
power >0.8.
HR – heart rate; DBP – diastolic blood pressure; SBP – systolic blood pressure; SpO2 – pulse oxygen saturation.
Changes in respiratory function
Compared with T0, PaCO2 of groups G and L1.5 showed an increasing tendency at T1–3 (P<0.05). Compared with T0, BE of the 3 groups increased at T2/3 (P<0.05), MAP of the 3 groups increased at T1–3 (P<0.05, power >0.8), and CVP of the 3 groups showed an upward trend at T1–3 (all P<0.05). There were no differences in pH in the 3 groups at each time point (P>0.05). MAP of group L1.0 and L1.5 were higher than that in group G during surgery (at T1–3) (P<0.05, power >0.8) (Table 3).
Table 3.
Comparison of respiratory function indexes among group G, L1.0 and L1.5.
| Groups | n | Before anesthesia induction (T0) | End of tracheal intubation (T1) | 10 min after pneumoperitoneum (T2) | End of tracheal extubation (T3) |
|---|---|---|---|---|---|
| PH | |||||
| G | 59 | 7.37±0.28 | 7.34±0.42 | 7.31±0.34 | 7.22±0.27 |
| L1.0 | 59 | 7.38±0.31 | 7.36±0.23 | 7.24±0.46 | 7.21±0.34a |
| L1.5 | 59 | 7.35±0.24 | 7.34±0.18 | 7.21±0.043 | 7.20±0.54a |
| BE | |||||
| G | 59 | −1.8±2.1 | −2.2±2.1 | −3.0±1.7a | −2.8±2.0a |
| L1.0 | 59 | −1.6±1.4 | −2.3±1.7 | −2.9±1.2a | −2.3±2.2a |
| L1.5 | 59 | −1.9±0.9 | −2.5±1.0 | −3.3±1.1a | −2.7±2.3a |
| PaO2 | |||||
| G | 59 | 154.1±6.6 | 148.3±12.3a | 146.1±7.8a$ | 144.7±8.2a$ |
| L1.0 | 59 | 153.2±14.9 | 149.7±16.3 | 149.7±10.4bc$ | 147.4±12.4bc$ |
| L1.5 | 59 | 156.7±8.2 | 153.9±12.1a | 145.2±8.5a$ | 140.6±12.6a$ |
| PaCO2 | |||||
| G | 59 | 38.9±10.3 | 43.3±6.3a | 46.1±7.9a | 47.3±6.9a |
| L1.0 | 59 | 41.3±9.2 | 42.7±7.3 | 44.2±6.9 | 41.6±10.9c |
| L1.5 | 59 | 40.2±9.0 | 45.3±9.9a | 46.2±10.6a | 48.5±11.1a |
| CVP (cmH2O) | |||||
| G | 59 | 6.1±1.7 | 7.1±1.1a | 7.6±1.47a | 9.3±1.9a |
| L1.0 | 59 | 6.4±1.7 | 7.4±1.5a | 8.3±2.1ac | 9.7±2.4ac |
| L1.5 | 59 | 6.3±1.5 | 7.1±1.2a | 7.5±1.5a | 8.8±1.3a |
| MAP (mmHg) | |||||
| G | 59 | 79.4±10.0 | 85.7±8.60a$ | 85.8±10.4a | 83.2±11.2a$ |
| L1.0 | 59 | 81.3±10.2 | 108.2±10.7ab$ | 106.1±13.7ab$ | 96.6±9.8ab$ |
| L1.5 | 59 | 82.4±9.6 | 110.7±7.6ab$ | 108.9±11.3ab$ | 97.4±11.6ab$ |
Compared with T0, P<0.05;
compared with group G at the same time point, P<0.05;
compared with group L1.5, P<0.05;
power >0.8;
BE – base excess; PaO2 – partial pressure of oxygen; PaCO2 – partial pressure of carbon dioxide; CVP – central venous pressure; MAP – mean artery pressure.
There were no differences in PaO2 and PaCO2 of group L1.0 at each time point (all P>0.05). Compared with group L1.5, there was no significant difference in CVP of group L1.0 at T1 (P>0.05), but CVP of group L1.0 were higher at T2/3 (both P<0.05, power >0.8). MAP of group L1.0 and L1.5 were higher than that of group G at each time point (P<0.05, power >0.8). There were no obvious differences in pH, PaCO2, and BE of the 3 groups at each time point before and after anesthesia (all P>0.05). Comparisons among 3 groups revealed no difference in each index (all P>0.05; Table 3).
Changes in plasma epinephrine and norepinephrine
Epinephrine in the 3 groups had no statistical significance at T0/1 (P>0.05) but was different at T2/3 (P<0.05). Compared with T0, E of the 3 groups tended to increase at T1–3 (P<0.05). There were no differences in NE of the 3 groups at T0/1 (P>0.05), but there were differences at T2/3 (all P<0.05). Compared with T0, NE of the 3 groups showed an upward trend at T1–3 (all P<0.05; Figure 2).
Figure 2.
Comparison of the changes of epinephrine (A) and norepinephrine (B) in the serum of patients in groups G, L1.0, and L1.5. * Compared with T0 (before anesthesia induction), P<0.05; # Compared with group G at the same time point, P<0.05; @ Compared with group L1.0, P<0.05.
Comparison of anesthetic drug dosage
The dosage of anesthetic agents and drugs used at maintenance period in GEA groups (L1.0 and L1.5) were lower than that in group G (P<0.05, power >0.8). There were significant differences in dosages of the 3 drugs between groups L1.0 and L1.5 (Table 4).
Table 4.
Comparison of drug dosage among group G, L 1.0 and L1.5 during anesthesia process.
| Group G | Group L1.0 | Group L1.5 | |
|---|---|---|---|
| Sufentanil (ng) | 45.3±3.2 | 25.8±2.8&! | 27.4±3.5&$! |
| Propofol (mg) | 260.8±25.6 | 195.4±13.3&! | 186.2±18.1&$! |
| Vecuronium (mg) | 10.2±1.6 | 7.9±1.2&! | 7.2±1.6&$! |
Compared with group G, P<0.05;
comparing group L1.5 and group L1.0, P<0.05;
power >0.8.
Intraoperative laparoscopy and postanesthesia recovery
There were no exceptions during laparoscopy. There were no differences in anesthesia time, surgery time, blood loss volume, or transfusion volume among the 3 groups (all P>0.05). The dosage of ephedrine and atropine in group L1.0 and L1.5 were larger than that in group G but the dosage of nitroglycerin was lower than that in group G; the degree of uterine relaxation of patients was higher in group L1.0 and L1.5 than that in group G (P<0.05). Compared with group L1.5, there were no differences in the dosage of ephedrine, nitroglycerin, or atropine in group L1.0 (all P>0.05), but the degree of uterine relaxation of patients in group L1.0 was higher than that in group L1.5 (P<0.05; Table 5). Compared with group G, the recovery and tracheal extubation time were shorter and the incidence of agitation was lower in groups L1.0 and L1.5 (P<0.05). There were no differences in recovery and tracheal extubation time or the incidence of agitation between groups L1.0 and L1.5 (P>0.05; Table 6).
Table 5.
Comparison of intra-operative findings among group G, L1.0 and L1.5.
| Group G | Group L1.0 | Group L1.5 | |
|---|---|---|---|
| Surgery time (min) | 70.7±19.5 | 67.3±13.6 | 68.5±10.3 |
| Anesthesia time (min) | 84.8±20.7 | 83.6±18.4 | 85.4±11.4 |
| Blood loss volume (ml) | 73.6±21.8 | 72.5±19.1 | 73.7±26.6 |
| Transfusion volume (ml) | 870.8±102.6 | 845.5±115.0 | 860.3±98.8 |
| Ephedrine (mg) | 5.6±1.4 | 22.7±3.4#$ | 22.5±3.9#$ |
| Atropine (mg) | 0.3±0.03 | 0.7±0.04#$ | 0.6±0.04#$ |
| Nitroglycerin (μg) | 1.3±0.3 | 0.8±0.4#$ | 0.9±0.3#$ |
Compared with group G, P<0.05;
power >0.8.
Table 6.
Comparison of postanesthesia recovery among group G, L1.0 and L1.5.
| Groups | Extubation time (min) | Recovery time (min) | Agitation | Uterine relaxation | |||
|---|---|---|---|---|---|---|---|
| n | Incidence (%) | Excellent | Fine | Bad | |||
| G | 18.4±2.7 | 15.7±5.1 | 12 | 20.3 | 18 (30.5%) | 27 (45.8%) | 14 (23.7%) |
| L1.0 | 16.9±2.1#$ | 12.3±1.5#$ | 0# | 0# | 41 (69.5%)*# | 15 (25.4%)*# | 3 (5.1%)*# |
| L1.5 | 17.3±2.5# | 13.9±1.9#$ | 3# | 5.1# | 29 (49.2%)* | 18 (30.5%)* | 12 (20.3%)* |
Compared with group G, P<0.05;
compared with group L1.5, P<0.05;
power >0.8.
Discussion
General anesthesia has a promotion in reducing lung volume and forming atelectasis, associated with deteriorating gas exchange and respiratory mechanics [18]. In general anesthesia, mechanical ventilation is mandatory [19]. According to Gajic et al., mechanical ventilation potentially aggravates or even causes lung injury [20]. Epidural anesthesia has become a routine component of abdominal surgery, especially preferable in patients depending on active expiration, where a slow onset of sympathetic block and minimized muscle weakness are demanded [21,22]. In our study, the patients were given a neuraxial blockade by the epidural anesthesia covering T1–2/T2–3 level. According to Clemente et al., segmental blocks can impair the activity of respiratory muscles in the rib cage, and a block level above T4 may lead to significant cardiac depression [23]. van Zundert et al. have shown that under regional anesthesia, the respiratory mechanism and the main inspiratory muscle are not affected, and no significant changes were found in ventilatory parameters or CO2 levels [24]. Under epidural anesthesia, intermittent positive pressure ventilation is a must to minimize the possibility of arrhythmias [25]. Mechanical ventilation was applied for the subjects in our study. Decreased MAP is a common adverse effect of epidural anesthesia, although easily controlled using ephedrine administration [22]. In our study, we interestingly found in group L1.0 that PaO2 and PaCO2 showed no significant difference in the 4 time points, which showed a respiratory stability, although CVP, HR, DBP, and MAP parameters showed statistical significance.
It was reported that general anesthesia has a potential to cause hemodynamic instability and local anesthesia contributes to more stable hemodynamics [26]. The most interesting finding in our study was that the hemodynamics parameters (including HR, DBP, and SpO2) in group L1.0 were detected to have no statistical significance in the 4 time points in the surgery, whereas those in group G and L1.5 showed significant differences in T1–3 compared with T0. Therefore, we may reasonably arrive at a conclusion that GEA, especially epidural anesthesia with a concentration of 1.0% lidocaine, can benefit hemodynamic stability. According to Roofthooft et al., low-dose intrathecal bupivacaine in spinal anesthesia guaranteed maternal hemodynamic stability for cesarean delivery and simultaneously provided adequate anesthesia [27].
In our study, we found the concentration of plasma E and NE increased significantly at T1–3 compared with T0 in all the 3 groups and meanwhile the group L1.0 showed significantly higher level of E and NE than the group L1.5 did. According to Shono et al. epidural anesthesia could incompletely suppress the stress response in upper abdominal surgery and larger concentration of lidocaine inhibited the stress hormonal response better, which may be attributed to the differences in extent/intensity of the block [28].
Accumulated evidence suggests that epidural anesthesia with different epidural anesthetics may contribute to less-demanding requirements for general anesthesia [29,30]. Consistent with the previous studies, our study also found an obvious reduction of the dosage of anesthesia drugs in the surgery. We administered 5 mL lidocaine epidurally with a maintenance pump rate of 4 to 6 mL/h. Our statistic data demonstrated that of the 3 anesthesia drugs (sufentanil, propofol, and vecuronium), all except propofol were reduced significantly in patients who received epidural lidocaine before anesthesia compared with those in the general anesthesia group. We also found advantages of GEA in our study, including reduction of recovery and tracheal extubation time, excellent uterine relaxation, and a low incidence of agitation. Marret et al. demonstrated that continuous intravenous administration of lidocaine during abdominal surgery could reduce the length of hospitalization and postoperative pain [31]. One of the most important problems of laparoscopic cholecystectomy under regional anesthesia is inadequate relaxation of abdominal musculature [22]. In our study, especially in group L1.0, 69.5% were found in excellent uterine relaxation state, significantly compared with groups G and L1.5. Therefore, GEA has the potential to be popularized in clinical laparoscopy of ovarian neoplasm.
Conclusions
We have for the first time monitored the changes of metabolic cycling, respiration, and stress hormone level of patients with ovarian neoplasm undergoing laparoscopy with the application of GEA, and explored the safety of its application in patients undergoing ovariectomy, by studying the effects of GEA with different concentrations of lidocaine on the respiratory system, to afford a better understanding of clinical anesthesia. We found in this study that GEA could effectively maintain the stability of hemodynamics, reduce the dosage of anesthetics, and shorten postanesthesia recovery time, and that GEA with a low concentration (1.0%) of lidocaine might be more worthwhile for clinical application because of its not-significant effect on intrapulmonary shunt and arterial oxygenation in patients. In this study, however, we set only 2 concentrations of lidocaine in a relatively small sample size; further studies will be made in the future based on a multiple gradient in concentration and larger sample size.
Footnotes
Competing interests: The authors have declared that no competing interests exist.
Source of support: Departmental sources
References
- 1.Deng Y, Zhang J, Wang Z, et al. Antibiotic monensin synergizes with EGFR inhibitors and oxaliplatin to suppress the proliferation of human ovarian cancer cells. Sci Rep. 2015;5:17523. doi: 10.1038/srep17523. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 2.Gubbels JA, Felder M, Horibata S, et al. MUC16 provides immune protection by inhibiting synapse formation between NK and ovarian tumor cells. Mol Cancer. 2010;9:11. doi: 10.1186/1476-4598-9-11. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 3.Sallinen H, Heikura T, Laidinen S, et al. Preoperative angiopoietin-2 serum levels: A marker of malignant potential in ovarian neoplasms and poor prognosis in epithelial ovarian cancer. Int J Gynecol Cancer. 2010;20:1498–505. doi: 10.1111/IGC.0b013e3181f936e3. [DOI] [PubMed] [Google Scholar]
- 4.Cont NT, Ferrero A, Peccatori FA, et al. Medical treatment of early stage and rare histological variants of epithelial ovarian cancer. Ecancermedicalscience. 2015;9:584. doi: 10.3332/ecancer.2015.584. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 5.Parson EN, Lentz S, Russell G, et al. Outcomes after cytoreductive surgery and hyperthermic intraperitoneal chemotherapy for peritoneal surface dissemination from ovarian neoplasms. Am J Surg. 2011;202:481–86. doi: 10.1016/j.amjsurg.2011.02.004. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 6.Yeung TL, Leung CS, Wong KK, et al. TGF-beta modulates ovarian cancer invasion by upregulating CAF-derived versican in the tumor microenvironment. Cancer Res. 2013;73:5016–28. doi: 10.1158/0008-5472.CAN-13-0023. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 7.Hwang KH, Cho OH, Yoo YS. Symptom clusters of ovarian cancer patients undergoing chemotherapy, and their emotional status and quality of life. Eur J Oncol Nurs. 2016;21:215–22. doi: 10.1016/j.ejon.2015.10.007. [DOI] [PubMed] [Google Scholar]
- 8.Lee YY, Kim TJ, Choi CH, et al. Factors influencing the choice of laparoscopy or laparotomy in pregnant women with presumptive benign ovarian tumors. Int J Gynaecol Obstet. 2010;108:12–15. doi: 10.1016/j.ijgo.2009.07.040. [DOI] [PubMed] [Google Scholar]
- 9.van der Pas MH, Haglind E, Cuesta MA, et al. Laparoscopic versus open surgery for rectal cancer (COLOR II): short-term outcomes of a randomised, phase 3 trial. Lancet Oncol. 2013;14:210–18. doi: 10.1016/S1470-2045(13)70016-0. [DOI] [PubMed] [Google Scholar]
- 10.Pei L, Tan G, Wang L, et al. Comparison of combined general-epidural anesthesia with general anesthesia effects on survival and cancer recurrence: A meta-analysis of retrospective and prospective studies. PLoS One. 2014;9:e114667. doi: 10.1371/journal.pone.0114667. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 11.Forget P, Collet V, Lavand’homme P, De Kock M. Does analgesia and condition influence immunity after surgery? Effects of fentanyl, ketamine and clonidine on natural killer activity at different ages. Eur J Anaesthesiol. 2010;27:233–40. doi: 10.1097/EJA.0b013e32832d540e. [DOI] [PubMed] [Google Scholar]
- 12.Wuethrich PY, Hsu Schmitz SF, Kessler TM, et al. Potential influence of the anesthetic technique used during open radical prostatectomy on prostate cancer-related outcome: A retrospective study. Anesthesiology. 2010;113:570–76. doi: 10.1097/ALN.0b013e3181e4f6ec. [DOI] [PubMed] [Google Scholar]
- 13.Merquiol F, Montelimard AS, Nourissat A, et al. Cervical epidural anesthesia is associated with increased cancer-free survival in laryngeal and hypopharyngeal cancer surgery: A retrospective propensity-matched analysis. Reg Anesth Pain Med. 2013;38:398–402. doi: 10.1097/AAP.0b013e31829cc3fb. [DOI] [PubMed] [Google Scholar]
- 14.Shariat Moharari R, Samadi A, Imani F, et al. The effect of epidural bupivacaine on BIS levels in the awake phase and on the maintenance doses of propofol and fentanyl during general anesthesia. Anesth Pain Med. 2013;2:149–53. doi: 10.5812/aapm.5461. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 15.Kim SJ, Kwon JY, Cho AR, et al. The effects of sevoflurane and propofol anesthesia on cerebral oxygenation in gynecological laparoscopic surgery. Korean J Anesthesiol. 2011;61:225–32. doi: 10.4097/kjae.2011.61.3.225. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 16.Magi E. ASA classification and perioperative variables as predictors of postoperative outcome. Br J Anaesth. 1997;78:228. doi: 10.1093/bja/78.2.228. [DOI] [PubMed] [Google Scholar]
- 17.Zhang DN, Chen JP. Anesthesia effect analysis of epidural/general anesthesia in gynecological laparoscopic surgery. Chinese Modern Doctor. 2014;52:67–69. [Google Scholar]
- 18.Reinius H, Jonsson L, Gustafsson S, et al. Prevention of atelectasis in morbidly obese patients during general anesthesia and paralysis: A computerized tomography study. Anesthesiology. 2009;111:979–87. doi: 10.1097/ALN.0b013e3181b87edb. [DOI] [PubMed] [Google Scholar]
- 19.Severgnini P, Selmo G, Lanza C, et al. Protective mechanical ventilation during general anesthesia for open abdominal surgery improves postoperative pulmonary function. Anesthesiology. 2013;118:1307–21. doi: 10.1097/ALN.0b013e31829102de. [DOI] [PubMed] [Google Scholar]
- 20.Gajic O, Frutos-Vivar F, Esteban A, et al. Ventilator settings as a risk factor for acute respiratory distress syndrome in mechanically ventilated patients. Intensive Care Med. 2005;31:922–26. doi: 10.1007/s00134-005-2625-1. [DOI] [PubMed] [Google Scholar]
- 21.Zabolotskikh I, Trembach N. Safety and efficacy of combined epidural/general anesthesia during major abdominal surgery in patients with increased intracranial pressure: A cohort study. BMC Anesthesiol. 2015;15:76. doi: 10.1186/s12871-015-0056-2. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 22.Lee JH, Huh J, Kim DK, et al. Laparoscopic cholecystectomy under epidural anesthesia: A clinical feasibility study. Korean J Anesthesiol. 2010;59:383–88. doi: 10.4097/kjae.2010.59.6.383. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 23.Clemente A, Carli F. The physiological effects of thoracic epidural anesthesia and analgesia on the cardiovascular, respiratory and gastrointestinal systems. Minerva Anestesiol. 2008;74:549–63. [PubMed] [Google Scholar]
- 24.van Zundert AA, Stultiens G, Jakimowicz JJ, et al. Segmental spinal anaesthesia for cholecystectomy in a patient with severe lung disease. Br J Anaesth. 2006;96:464–66. doi: 10.1093/bja/ael036. [DOI] [PubMed] [Google Scholar]
- 25.Lal P, Philips P, Saxena KN, et al. Laparoscopic total extraperitoneal (TEP) inguinal hernia repair under epidural anesthesia: a detailed evaluation. Surg Endosc. 2007;21:595–601. doi: 10.1007/s00464-006-9050-6. [DOI] [PubMed] [Google Scholar]
- 26.Bettex DA, Lachat M, Pfammatter T, et al. To compare general, epidural and local anaesthesia for endovascular aneurysm repair (EVAR) Eur J Vasc Endovasc Surg. 2001;21:179–84. doi: 10.1053/ejvs.2000.1295. [DOI] [PubMed] [Google Scholar]
- 27.Roofthooft E, Van de Velde M. Low-dose spinal anaesthesia for Caesarean section to prevent spinal-induced hypotension. Curr Opin Anaesthesiol. 2008;21:259–62. doi: 10.1097/ACO.0b013e3282ff5e41. [DOI] [PubMed] [Google Scholar]
- 28.Shono A, Sakura S, Saito Y, et al. Comparison of 1% and 2% lidocaine epidural anaesthesia combined with sevoflurane general anaesthesia utilizing a constant bispectral index. Br J Anaesth. 2003;91:825–29. doi: 10.1093/bja/aeg266. [DOI] [PubMed] [Google Scholar]
- 29.Sinha PK, Unnikrishnan KP. Reduction in requirement of propofol during combined epidural (bupivacaine) and general anesthesia guided by bispectral index. Anesth Analg. 2005;101:613. doi: 10.1213/01.ANE.0000159017.97601.F1. author reply 613–14. [DOI] [PubMed] [Google Scholar]
- 30.Lu CH, Borel CO, Wu CT, et al. Combined general-epidural anesthesia decreases the desflurane requirement for equivalent A-line ARX index in colorectal surgery. Acta Anaesthesiol Scand. 2005;49:1063–67. doi: 10.1111/j.1399-6576.2005.00726.x. [DOI] [PubMed] [Google Scholar]
- 31.Marret E, Rolin M, Beaussier M, Bonnet F. Meta-analysis of intravenous lidocaine and postoperative recovery after abdominal surgery. Br J Surg. 2008;95:1331–38. doi: 10.1002/bjs.6375. [DOI] [PubMed] [Google Scholar]