Effect of dexmedetomidine on perioperative blood glucose regulation in type 2 diabetic patients undergoing laparoscopic colorectal cancer radical resection: a randomised double-blinded controlled trial

Abstract

Background

The stability of blood glucose levels in diabetic patients is more susceptible to fluctuations than in nondiabetic individuals. The effect of dexmedetomidine on glucose fluctuations in diabetic patients remains unclear. This study aimed to investigate the effect of intraoperative dexmedetomidine on glucose homeostasis in patients with type 2 diabetes undergoing laparoscopic colorectal cancer radical resection.

Methods

80 participants with T2DM preparing for laparoscopic colorectal cancer radical resection were randomly divided into four groups: control group (group C), dexmedetomidine 1 μg ⋅ kg⁻¹ + 0.25 μg ⋅ kg⁻¹ ⋅ h⁻¹ (group D1), 1 μg ⋅ kg⁻¹ + 0.5 μg ⋅ kg⁻¹ ⋅ h⁻¹ (group D2), and 1 μg ⋅ kg⁻¹ + 0.75 μg ⋅ kg⁻¹ ⋅ h⁻¹ (group D3). Levels of blood glucose were measured before the intravenous infusion of dexmedetomidine (T1), 15 min after the intubation(T2), 1 h after the beginning of the surgery (T3), at the end of the surgery (T4), and 30 min after the extubation in PACU (T5).

Results

Compared with the baseline levels, the levels of blood glucose from T2 to T5 in group C increased gradually but were not significantly different at each time point (p > 0.05), and there was a statistically significant rise in blood glucose in group D1 at T3, T4, and T5 and in groups D2 and D3 at T2, T3, and T4 (p < 0.05). Compared with group C, blood glucose in groups D2 and D3 was significantly higher at T3, andT4 (p < 0.05). Compared with group C, the rangeability from T1 to T3 and T1 to T4 was significantly higher in groups D2 and D3 (p < 0.05).

Conclusion

Dexmedetomidine loading dose 1 μg/kg and a Maintenance dose 0.25 μg/kg/h can be used in type 2 diabetic patients for better glucose regulation without increasing the incidence of perioperative hyperglycemia, adverse effects, and extending extubation time.

Trial registration

ChiCTR2100042050. Registered on January 13, 2021, with ChiCTR. https://www.chictr.org.cn/showproj.html?proj=120133.

Background

Hyperglycaemia, defined as blood glucose levels exceeding > 10 mmol/L, is prevalent during the perioperative period, particularly in patients experiencing surgical stress, insulin resistance, impaired glucose use, and iatrogenic influences [1]. The prevalence of hyperglycaemia increased from 3% in patients without diabetes to 15.3% in patients with diabetes [2]. This incidence May increase to 49% after major noncardiac surgeries [3]. Previous research has established a correlation between hyperglycaemia and adverse outcomes, including increased risk of infection and delayed wound healing [3–6].

Dexmedetomidine, a highly selective α−2 adrenergic agonist, is extensively used for clinical anaesthesia because of its sympatholytic, sedative, and analgesic properties. Numerous studies have demonstrated that dexmedetomidine can reduce blood glucose levels through sympatholytic effects [7–9]. However, its effect on α−2A receptors in pancreatic islets, which inhibit insulin secretion, suggests the potential for increased blood glucose levels [10–12]. A recent dose–response analysis by Zhou et al. showed that glucose levels might be influenced by dexmedetomidine dosage [13]. Higher doses may significantly increase glucose levels, whereas lower doses may have a minimal effect. Similar findings have been observed in paediatric surgical patients and healthy volunteers [14, 15].

Epidemiological data indicate an increasing trend in the number of patients with diabetes, with approximately 90% diagnosed with type 2 diabetes. These patients are more susceptible to blood glucose instability because of insulin resistance and declined insulin secretion. However, the effect of dexmedetomidine on glucose fluctuations in patients with diabetes remains unclear. This study aimed to examine the effect of intraoperative dexmedetomidine on glucose homeostasis in patients with type 2 diabetes who underwent radical colorectal cancer resection.

Material and methods

Study setting

The study was conducted at the First Affiliated Hospital of Chongqing Medical University.

Type of study

The study was a randomised controlled trial conducted between February 2021 and March 2022.

Ethical consideration

This study was approved by the ethics committee of the associated hospital (approval number: 2020–406, approval date: 06/08/2020). Verbal and written voluntary informed consent was obtained from all participants before starting the study.

Randomisation and participants

Patients were randomly divided into four groups preoperatively using the random number table method. The randomisation procedure was conducted by an individual outside of the project implementation. This study included 80 patients with type 2 diabetes who underwent radical laparoscopic colorectal cancer resection under general anaesthesia. The inclusion criteria were ASA physical status II or III, aged 20–80 years, haemoglobin A1c (HbA1c) levels between 6.5 and 9%, BMI from 18.5 to 28, and early-stage colorectal cancer defined by cTNM staging. Patients were excluded if they reported type 1 diabetes, sick sinus syndrome, bradycardia, arrhythmia, abnormal liver or kidney function, long-term use of glucocorticoid hormones, conditions that contraindicated the use of dexmedetomidine, or refused to participate. Patients who used glucocorticoids perioperatively, intraoperative blood transfusions, or liquids containing glucose were excluded.

Sample size

The necessary sample size was calculated using PASS 15.0. Based on the pharmacokinetics of dexmedetomidine, we calculated the sample size based on blood glucose concentration at 1 h postoperatively. Based on a pilot study, which included eight surgical patients in each of the four groups, blood glucose concentrations in patients receiving dexmedetomidine infusion were expected to increase by an average of 1 mmol/L, with a standard deviation of 2 mmol/L. Consequently, we determined that each group must enroll a minimum of 17 patients to obtain a power of 90% (β = 0.1) at a significance level of 0.05 (α = 0.05, two-tailed). Considering study withdrawals or protocol violations, 20 participants were recruited from each group.

The patients included in the study and their reasons for leaving are specified in Fig. 1. A total of 80 patients were assessed for eligibility. Three patients were excluded because they did not meet the inclusion criteria (n = 3) or refused to participate (n = 1). Therefore, 76 patients were included in this study. After excluding patients owing to protocol violations and difficulties with follow-up, 71 patients completed the study (C = 18, D1 = 17, D2 = 18, D3 = 18).

Fig. 1.

The consort flow chart

Intervention protocol

All surgical procedures were performed by the same team. Preoperative short-term insulin was used to control blood glucose levels in all patients. None of the patients was premedicated preoperatively. Upon arrival in the operating room, the patients were monitored using noninvasive blood pressure measurements, pulse oxygen saturation, and electrocardiography. After the modified Allen test, left radial artery catheterisation was performed under local anaesthesia to monitor the invasive arterial blood pressure and collect blood samples. All patients underwent NarcoTrend (MT MonitorTechnik GmbH & Co., KG, Germany) to monitor the depth of anaesthesia. Before general anaesthesia induction, patients in groups D1, D2, and D3 were infused with dexmedetomidine intravenously (4 μg/mL with normal saline) at 1 μg/kg for 15 min, followed by continuous infusion of dexmedetomidine 0.25, 0.5, and 0.75 μg/kg/h until the end of the surgery. In group C, NS was infused at 60 mL/h for 15 min and Maintained at 5 mL/h until the end of the surgery. An anaesthetic nurse who was not involved in data collection prepared the dexmedetomidine and normal saline solutions. For all groups, a special infusion pump covered with an opaque sheet was prepared to blind the anaesthetist to the experimental treatment. Perioperative management and data collection were performed by an anaesthetist blinded to the experimental treatments.

For all patients, general anaesthesia was induced with propofol (1.0–1.5 mg/kg), midazolam (0.05 mg/kg), sufentanil (0.4–0.5 μg/kg), and vecuronium (0.1 mg/kg). After oral tracheal cannula administration, patients received mechanical ventilation with an inhaled oxygen concentration of 50%, tidal volume of 6–8 mL/kg, respiratory rate of 12–14 times/min, and inspiration/expiration ratio of 1:1.5. Respiratory parameters were continuously adjusted to Maintain an end-expiratory carbon dioxide partial pressure between 35 and 45 mmHg. Anaesthetic depth was maintained with intravenous propofol and remifentanil, along with inhaled sevoflurane (0.6 MAC). The remifentanil and propofol doses were modified simultaneously and gradually to maintain NarcoTrend monitoring within stages D0 and D2 (index; 40–60) perioperatively for all patients. Vecuronium was injected intermittently during general anaesthesia to Maintain muscle relaxation based on muscle relaxant monitoring. The rate of fluid infusion is 8–10 mL/kg/h. All participants may have bradycardia, hypertension or hypotension, arrhythmia, hyperglycaemia, or hypoglycaemia. If blood glucose concentration was > 12 mmol/L, insulin was used to correct hyperglycaemia [16]. If bradycardia was severe (HR < 50 bpm), atropine was administered. IAP fluctuations were maintained within ± 30% of the baseline values, and ephedrine was used if necessary. Sevoflurane inhalation and rocuronium injection for the last time were stopped approximately 30 min before the end of surgery, whereas propofol and remifentanil were increased and discontinued at the end of surgery. All patients were transferred to the post-anesthesia care unit (PACU) and extubated if they met the inclusion criteria. The patient-controlled intravenous analgesia (PCIA) scheme was initiated by administering 800-mg tramadol and 100-mg flurbiprofen axetil.

Outcomes

The primary outcomes were blood glucose concentrations measured before dexmedetomidine infusion (T1), 15 min after intubation (T2), 1 h postoperatively (T3), at the end of surgery (T4), and 30 min after extubation in the PACU (T5). Secondary outcomes were age, sex, BMI, ASA status, fasting C-peptide, and cortisol at 6:00 a.m. on the day and following day of operation, operative time, blood loss, and type of surgery. The quantification of insulin resistance and calculation of surgical stress were performed by the modified homeostasis model assessment through fasting C-peptide (HOMA_IRCP) [17] and surgical stress score (SSS) model [18].

Recruitment

Participants were recruited by selecting a surgical application List. Eligible patients were screened based on inclusion and exclusion criteria. The recruitment was between 14 January 2021 and 30 March 2022. The trial ended after recruiting all participants.

Statistical analysis

Statistical analyses were performed using SPSS (version 25.0; SPSS Inc., USA). Data with a normal distribution were expressed as mean ± standard deviation, and nonnormal distribution was expressed as median (interquartile range). QQ plots were generated to test for normality, and Levene’s test was used to assess the homogeneity of variance. For data of normal distribution, one-way ANOVA was used to compare homogeneous data. LSD method was used to analyse the post hoc comparisons between groups; otherwise, Welch and Dunnett T3 tests were used for comparison between groups. If the experimental data did not conform to the normal distribution, the Kruskal–Wallis test was used for multigroup analysis, and the Bonferroni method was used for post hoc comparisons between groups. Data from the repeated measurements (blood glucose levels) were compared using repeated measures analysis ANOVA. Count data were compared using the chi-square (χ²) test. Statistical significance was set at p < 0.05. An experienced physician who was blinded to the experimental conditions independently analysed the data.

Results

Eighty patients were assessed for eligibility. Three patients were excluded because they did not meet the inclusion criteria (n = 3) or refused to participate (n = 1). Therefore, this study included 76 patients. After excluding patients because of protocol violations and difficulties with follow-up, 71 patients completed the study (C = 18, D1 = 17, D2 = 18, D3 = 18). Demographic characteristics, such as age, sex, and BMI, were uniform in all groups. There were no statistically significant differences in operative time, type of surgery, tumour stage, blood loss, urine volume, preoperative fasting C-peptide level, SSS, HbA1c, or HOMA_IRCP among all groups (p > 0.05) (Table 1).

Table 1.

Patients’ demographic data and operative characteristics

Factors	Group C (n = 18)	Group D1 (n = 17)	Group D2 (n = 18)	Group D3 (n = 18)	p-value
Age (year)	69 ± 8	61 ± 9	65 ± 9	65 ± 8	0.08
Gender (male/female)	10/8	9/8	11/7	9/9	0.75
ASA grade (II/III)	3/15	4/13	7/11	7/11	0.38
BMI (kg/m2)	24.01 ± 3.54	24.64 ± 2.33	24.53 ± 2.04	23.18 ± 2.25	0.34
Duration of surgery (min)	208 ± 71	215 ± 69	213 ± 69	173 ± 56	0.20
Blood loss (mL)	64 ± 43	94 ± 75	76 ± 69	64 ± 34	0.37
Urine volume (mL)	356 ± 197	591 ± 470	442 ± 336	462 ± 209	0.23
Type of surgeries
Colectomy	10	11	7	6	0.22
Proctocolectomy	8	6	11	12	0.21
Fasting C-peptide (ng/mL)	2.19 ± 1.41	2.55 ± 1.17	2.89 ± 1.75	2.32 ± 1.49	0.50
Tumour staging (I/IIA)	12/6	12/5	13/5	11/7	0.90
SSS	0.16 ± 0.05	0.17 ± 0.05	0.16 ± 0.05	0.14 ± 0.04	0.23
HbA1c	7.09 ± 1.05	7.1 ± 0.79	7.34 ± 0.79	7.3 ± 0.55	0.71
HOMA_IRCP	3.26 ± 1.89	3.88 ± 1.65	4.91 ± 3.39	3.73 ± 2.44	0.24

Data are expressed as mean ± SD

Surgical Stress Score (SSS) = −0.342 + 0.0139*(blood loss/weight) + 0.0392*(operative time/60) + 0.352

Modified Homeostasis Model Assessment through fasting C-peptide (HOMA_IRCP) = 1.5 + fasting blood glucose × fasting C-peptide/2800 

There was no difference in plasma glucose levels between all groups at baseline. Compared with the baseline levels, the blood glucose levels from T2–T5 in group C increased gradually but were not significantly different at each time point (p > 0.05). Compared with the baseline level, there was a statistically significant increase in blood glucose in group D1 from T3 to T5 and groups D2 and D3 from T2 to T4 (p < 0.05). Compared with group C, no significant differences in blood glucose levels were observed in group D1 at any time point (p > 0.05); however, blood glucose levels in group D2 and D3 were significantly higher at T3 and T4 (p < 0.05). There were no significant differences between group D1, D2, and D3 (p > 0.05) (Table 2). Compared with group C, the range from T1–T3 to T1–T4 was significantly higher in groups D2 and D3 (p < 0.05), and no significant differences in the range from T1–T2, T1–T3, T1–T4, and T1–T5 were observed in groups D1(p > 0.05) (Table 3).

Table 2.

Comparison of blood glucose levels (mmol/L) at five continuous times ($\overline{\text{X}}$ ± S)

	Group C (n = 18)	Group D1 (n = 17)	Group D2 (n = 18)	Group D3 (n = 18)	F	p-value
T1	6.47 ± 1.6	6.4 ± 1.5	6.7 ± 1.4	6.5 ± 1.7	0.17	0.92
T2	6.76 ± 1.7	6.7 ± 1.4	7.7 ± 1.7	7.1 ± 1.9	1.42	0.25
T3	7.18 ± 1.4	7.7 ± 1.6a	8.7 ± 2.0a, b	8.6 ± 2.1a, b	2.85	0.04
T4	7.32 ± 0.9	8.5 ± 2.1a	9.4 ± 2.2a, b	9.1 ± 1.9a, b	4.28	0.01
T5	7.66 ± 1.3	8.1 ± 2.0a	8.3 ± 2.0 a	8.0 ± 1.9 a	0.36	0.78
F	1.784	4.692	4.932	5.654
p2	0.150	0.002	0.001	< 0.001

Data are expressed as mean ± SD

The results of repeated measurement ANOVA: Mauchly ball test: p = 0.001 < 0.05, according to multivariate test: time and time* group p = 0.001/0.006 < 0.05, respectively

^ap < 0.05 compared with T1; ^bp < 0.05 compared with group C

T1: before dexmedetomidine intravenous infusion; T2: 15 min after intubation; T3: 1 h after surgery beginning; T4: at the end of surgery; T5: 30 min after extubation in PACU 

Table 3.

Comparison of blood glucose levels’ fluctuation (mmol/L) ($\overline{\text{X}}$ ± S)

Factors	Group C n = 18	Group D1 (n = 17)	Group D2 (n = 18)	Group D3 (n = 18)	F	p-value
DGlu(T2–T1)	0.3 ± 0.8	0.4 ± 0.8	1.0 ± 1.1	0.6 ± 0.7	2.75	0.05
DGlu(T3–T1)	0.7 ± 1.2	1.4 ± 0.8	1.9 ± 1.6a	2.1 ± 0.9a	5.13	0.03
DGlu(T4–T1)	0.9 ± 1.5	2.2 ± 1.7	2.6 ± 1.8a	2.6 ± 1.1a	5.42	0.02
DGlu(T5–T1)	1.2 ± 2.1	1.8 ± 1.6	1.5 ± 2.2	1.5 ± 1.5	0.28	0.84

Data are expressed as mean ± SD

^ap < 0.05 compared with group C

There was no significant difference in the C-peptide and cortisol levels at 6:00 a.m. on postoperative day 1 in all groups (p > 0.05) (Table 4).

Table 4.

Comparison of preoperative and postoperative C-peptide and Cor

Factors	Group C (n = 18)	Group D1 (n = 17)	Group D2 (n = 18)	Group D3 (n = 18)	p(F)
C-peptide1	2.2 ± 1.4	2.6 ± 1.2	2.9 ± 1.8	2.3 ± 1.5	0.50 (0.79)
C-peptide2	2.8 ± 2.7	3.7 ± 2.7	4.2 ± 2.5	2.2 ± 1.2	0.06 (2.53)
P(t)	0.22 (−1.27)	0.10 (−1.73)	0.07 (−1.91)	0.46 (0.75)
Cor1	519.8 ± 88.2	500.7 ± 132.2	465.3 ± 153.2	558.4 ± 252.4	0.42 (0.96)
Cor2	377.4 ± 205.2	485.1 ± 267.8	481.9 ± 303.6	437.2 ± 185.7	0.52 (0.76)
P(t)	0.13 (1.61)	0.84 (−0.21)	0.84 (−0.20)	0.12 (1.62)

 Data are expressed as mean ± SD or Median(IQR)

 ^ap < 0.05 compared with group C

 C peptide1 and Cor1: the level at 6:00 a.m. on the day of operation. C peptide2 and Cor2: the level and 6:00 a.m on the next day of operation

Compared to group C, the required dose of propofol was significantly lower in groups D1, D2, and D3 (p < 0.05) (Fig. 2). Morphine equivalents gradually decreased with increasing DEX doses in each group. However, there were no significant differences between groups (p > 0.05) (Fig. 2). The extubation time was significantly longer in groups D2 and D3 than in groups C and D1 (p < 0.05), but Group C and Group D1 had no significant difference (Fig. 2). No significant differences were observed in the use of atropine and ephedrine between all groups (p > 0.05) (Table 5).

Fig. 2.

Comparison of the required dose for anaesthetics and extubation time. ^ap < 0.05 compared with group C. ^bp < 0.05 compared with group D1

Table 5.

The consumptions of vasoactive drugs [M, (IQR)]

Group	Atropine (mg)	Ephedrine (mg)
Group C (n = 18)	0 (0)	0 (0)
Group D1 (n = 17)	0 (0.25)	0 (0)
Group D2 (n = 18)	0 (0.50)	0 (1.50)
Group D3 (n = 18)	0 (0.50)	3 (6)
p	0.11	0.13

Data are expressed as mean ± SD or Median(IQR)

^ap < 0.05 compared with group C

Compared to group C, the incidence of severe bradycardia and hypotension on D3 increased significantly (p < 0.05). The incidence of hyperglycaemia was significantly higher in group D3 than in group C (p < 0.05) (Table 6). None of the patients in either group had blood glucose levels > 12 mmol/L, necessitating insulin administration to correct hyperglycaemia.

Table 6.

Comparison of the incidence of adverse effects, hyperglycaemia [n, (%)]

Factors	Group C (n = 18)	Group D1 (n = 17)	Group D2 (n = 18)	Group D3 (n = 18)	p-value
Bradycardia [n, (%)]	0	1 (5.9)	5 (27.8)	8 (44.4)a	0.01
Hypotension [n, (%)]	0	1 (5.9)	3 (16.7)	6 (33.3)a	0.01
Hyperglycaemia [n, (%)]	1 (5.6)	5 (29.4)	7 (38.9)	9 (50)a	0.03

Data are expressed as mean ± SD or number (%)

^ap < 0.05 compared with group C

Discussion

Perioperative blood homeostasis is influenced by various factors, including therapeutic interventions, stress-induced cortisol and catecholamines, and impaired insulin signalling, which typically manifests as hyperglycaemia. Numerous studies have established an association between perioperative hyperglycaemia and adverse clinical outcomes, such as delirium, infection, acute kidney injury, mortality, prolonged hospital stay, and delayed wound healing [3–6]. Real-world research data indicate that individuals with diabetes are more prone to hyperglycaemia than nondiabetic patients, particularly under the influence of their disease or surgery [19]. Therefore, blood glucose stability in patients with DM is crucial. However, there is no consensus regarding the criteria for perioperative glucose regulation. Some recommendations for perioperative glycaemic control emphasise long-term indicators, such as glycated haemoglobin A1c (A1c levels < 7% for young, nonpregnant patients and < 8% for older patients with multiple comorbidities) [20]. Others have suggested that Maintaining perioperative blood glucose levels from 4.4 to 10 mmol/L is beneficial for managing hyperglycaemia and preventing hypoglycaemia [21]. Hsieh et al. discovered that fluctuations in blood glucose levels within a specified period could lead to the overproduction of free radicals, inducing oxidative stress, especially in patients with type 2 diabetes [4].

Dexmedetomidine has been shown to decrease the incidence of hyperglycaemia in surgical patients [8, 9]. Potential mechanisms include direct or indirect antistress effects from inhibiting the stress response in the locus coeruleus, inhibiting pain signalling in the descending noradrenergic pathway of the spinal cord, and suppressing inflammatory responses via the cholinergic anti-inflammatory pathway [22–24]. However, animal studies have indicated that the activation of α−2A adrenoceptors in islet cells could inhibit insulin secretion, suggesting that dexmedetomidine may increase blood glucose levels [25, 26]. Further research in healthy human volunteers revealed that low-dose dexmedetomidine slightly decreased plasma insulin levels and increased plasma glucose levels [15]. Collectively, these findings suggest that dexmedetomidine influences glucose fluctuations by suppressing stress responses and inhibiting insulin secretion. Zhou et al. found that a lower dose of dexmedetomidine stabilised perioperative glucose levels, whereas a higher dose increased the risk of hyperglycaemia in nondiabetic patients undergoing major gastrointestinal surgery [13]. However, the effects of dexmedetomidine on perioperative glucose levels in patients with type 2 diabetes undergoing radical resection of malignant gastrointestinal tumours under general anaesthesia remain unclear.

Here, blood glucose levels in the experimental group increased significantly with dosage, but not in the control group. Compared to baseline, blood glucose levels increased significantly at T2 and T3 and peaked at T4 in groups D2 and D3, whereas in group D1 they increased significantly at T3 and T4. The delayed increase in blood glucose levels in group D1 may have been due to the dose-dependent inhibition of insulin secretion by dexmedetomidine [10]. However, a study by Li et al. involving 600 elderly nondiabetic patients undergoing noncardiac Major surgery with a loading dose of dexmedetomidine 0.6 µg/kg and Maintenance dose of 0.5 µg/kg/h reported no effect on intraoperative hyperglycaemia [27]. The discrepancy between our study results and those of Li et al. May be related to the presence of diabetes and different loading dosages. In this study, each experimental group received a loading dose of dexmedetomidine 1 µg/kg, accounting for approximately 50% of the total dose. Our study showed that dexmedetomidine use in patients with type 2 diabetes may lead to significant oscillations in blood glucose levels. The glucose level fluctuations (ΔGlu) between T1 and T4 in each experimental group were > 1.7 mmol/L, and in groups D2 and D3, even > 2.6 mmol/L. Studies have suggested that variability in blood glucose levels may affect wound healing and infection by reducing antioxidant factors [28]. However, there is no consensus on the threshold for initiating sugar-lowering treatments if glucose levels do not meet the hyperglycaemic criteria. Our research suggests that dexmedetomidine used in patients with type 2 diabetes may lead to an increase in glucose levels; however, the incidence of hyperglycaemia significantly increased only with higher doses of dexmedetomidine. Zhou et al. [13] reported similar findings for dexmedetomidine in nondiabetic patients.

However, compared with the work by Zhou et al., although the trend aligns with ours, the amplitude of the glucose fluctuations differs. In this study, the fluctuations in glucose levels with different doses of dexmedetomidine were greater than those observed in the study by Zhou et al. This may be partly due to the deteriorated insulin-secreting capacity of patients with diabetes. Contrastingly, Zhou et al. did not consider insulin resistance. Here, insulin resistance was quantified using a modified HOMA_IRCP. Additionally, we evaluated surgical stress using a surgical stress score while monitoring the depth of sedation using the NarcoTrend. Therefore, we believe that these variables can be effectively controlled. Interestingly, another study showed that a loading dose of 1 µg/kg and Maintenance dose of 0.25 µg/kg/h had no significant effect on insulin secretion inhibition in nondiabetic patients [29]. In patients with diabetes, the effects of dexmedetomidine on glucose-related hormones require further investigation.

In this study, dexmedetomidine at a loading dose of 1 µg/kg and Maintenance dose of 0.25 µg/kg/h could increase blood glucose but could not significantly differ from group C nor increase the incidence of hyperglycaemia in patients with type 2 diabetes undergoing colorectal cancer radical resection. Moreover, this dose decreased the required dose of propofol without increasing the incidence of adverse effects, such as bradycardia, hypotension, or prolonged extubation time.

Conclusions

Dexmedetomidine May increase perioperative glucose levels in patients with type 2 diabetes in a dose-independent Manner. During radical resection of colorectal cancer, a loading dose of 1 μg/kg and Maintenance dose 0.25 μg/kg/h of dexmedetomidine significantly decreased the required dose of propofol without increasing the incidence of perioperative hyperglycaemia, adverse effects, or extension of extubation time. This dose of dexmedetomidine can be used in patients with type 2 diabetes for better glucose regulation.

Limitations

This study has several Limitations that should be considered when interpreting the findings. First, the operative duration was restricted to 3–4 h for most cases, leaving the potential for further perioperative blood glucose elevation beyond this timeframe unexplored. Second, the absence of postoperative follow-up data regarding infection rates, wound healing progression, and immunosuppressive parameters precludes evaluation of dexmedetomidine’s impact on surgical outcomes in relation to glycaemic variability in type 2 diabetic patients. Third, due to funding constraints, we did not measure C-peptide and cortisol during the operation.

Abbreviations

T2DM

Type 2 diabetes

ASA

American Society of Anesthesiologists

Cor

Cortisol

Authors’ contributions

All authors made substantial contributions to the study and approved the final version of the manuscript. Study concept and design, DW and JLZ; acquisition and analyses of the data, LJQ; statistical analyses, DW and HKH; and drafting of the manuscript, JLZ, DW, and HKH. The author(s) read and approved the final manuscript.

Funding

None.

Data availability

Applicable.

Declarations

Ethics approval and consent to participate

This study was conducted in accordance with the Declaration of Helsinki and followed the guidelines of Consolidated Standards of Reporting Trials (CONSORT). Ethics approval was obtained from the ethics committee of the First Affiliated Hospital of Chongqing Medical University, Chongqing, China (approval number: 2020–406), approval date: 26 July 2021). Letters of informed consent signed by patients were obtained. The trial was registered at the Chinese Clinical Trial Registry (registration number: ChiCTR2100042050, registration date: 2021 January 13).

Consent for publication

Not applicable.

Competing interests

The authors declare no competing interests.