Intrathecal Nalbuphine and Dexmedetomidine as Adjuvants to Bupivacaine versus Plain Bupivacaine for Orthopedic Surgeries under Subarachnoid Block: A Comparative Study : Anesthesia Essays and Researches

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Intrathecal Nalbuphine and Dexmedetomidine as Adjuvants to Bupivacaine versus Plain Bupivacaine for Orthopedic Surgeries under Subarachnoid Block

A Comparative Study

Nagaraj, Bindu; Vinay, B. R.; Vani, N. V.; Dayananda, V. P.

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Anesthesia: Essays and Researches 16(3):p 381-385, Jul–Sep 2022. | DOI: 10.4103/aer.aer_127_22
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Subarachnoid block (SAB) is a safe, time-tested technique in anesthesia due to its rapid onset and effective sensory, and motor blockade. SAB with bupivacaine is a popular method. In orthopedic surgeries, the severity of pain is more with the involvement of periosteum. In SAB, adding adjuvants to local anesthetic is synergistic for producing quality anesthesia and prolonging the duration of analgesia.[123] Nalbuphine is a highly lipid-soluble opioid analgesic. It acts at the kappa receptor as an agonist and as an antagonist at the mu receptor to provide potent analgesia of visceral nociception.[4] Studies have shown that intrathecal nalbuphine with bupivacaine improved the quality of intraoperative and postoperative analgesia with minimal respiratory depression.[5] Dexmedetomidine is a highly selective α2-adrenergic receptor agonist. It inhibits the release of norepinephrine and the propagation of pain signals. It has a dose-dependent effect on the onset and regression of sensory and motor blocks.[678] Our study aimed to compare the efficacy of nalbuphine and dexmedetomidine as adjuvants to bupivacaine versus bupivacaine alone in lower limb orthopedic surgeries under SAB.


We conducted this prospective double-blind randomized control study after obtaining approval from the institutional ethics committee registration No.BMCRI/PS/254/2020-21, Dated 04/01/2021. The study period was 6 months. Keeping a 95% confidence interval, power at 80%, the standard deviation of 26.7, and a minimum difference of 25, 18 patients were required in each group. We included 20 patients in each group to compensate for dropouts. We selected 60 patients of the American Society of Anesthesiologists (ASA) physical status (PS) Classes I and II between 18 and 60 years of either sex, scheduled for elective lower limb orthopedic surgeries lasting for 90–120 min under SAB with informed written consent. Those patients refusing to participate in the study, with any absolute or relative contraindications for SAB, allergy to the study drug, polytrauma, and associated with other injuries, were excluded from the study. After routine preanesthetic evaluation, patients were allocated into one of three groups by computer-generated randomized numbers ( To ensure double blindness, the study drug solutions were prepared by a resident anesthesiologist, while SAB was instituted by another anesthesiologist. Both patients and observers who recorded and analyzed the data were blinded to the study drug received.

  • Group A received 2.7 mL of 0.5% hyperbaric bupivacaine with 1.5 mg nalbuphine
  • Group B received 2.7 mL of 0.5% hyperbaric bupivacaine with 10 μg dexmedetomidine
  • Group C received 2.7 mL of 0.5% hyperbaric bupivacaine with 0.5 mL of normal saline (intrathecal drug volume made to 3.2 mL with normal saline in all three groups).

All patients were kept fasting for 8 h. Tablet alprazolam 0.25 mg and tablet ranitidine 150 mg were given the night before the day of surgery. Before the commencement of anesthesia, patients were explained the methods of sensory and motor blockade assessment. All patients were explained regarding the visual analog score (VAS) scoring system. The VAS consisted of a 10-cm horizontal paper strip with two endpoints: 0 = no pain and 10 = worst possible pain. On arrival to the operating room, noninvasive blood pressure (BP), pulse oximetry, and three-lead electrocardiogram were connected. Intravenous (i.v.) access with 18G cannula was secured, and patients were preloaded with 10−1 of Ringer lactate. The baseline BP, heart rate (HR), and oxygen saturation (SpO2) were recorded. Under strict aseptic precautions, SAB was performed using 25G Quincke's spinal needle in L3– L4 space with the patient in the left lateral position. The study drug was injected over 10–15 s. The time at which injection was completed was considered 0 time of the study and all measurements were recorded from that point. Following intrathecal drug administration, patients were made to lie supine. They were supplemented with oxygen at a rate of 4 L.min−1 through a facemask. i.v. fluid and blood were administered according to the hemodynamic parameters and blood loss.

Sensory block was assessed by loss of pinprick sensation to 23 G sterile hypodermic needle for onset and dermatomal levels were tested every 2 min until the highest level was achieved and stabilized for consecutive tests. Time of onset of sensory and motor blockade (using modified Bromage scale), maximum height of sensory block, and time to reach maximum block were noted. The surgical anesthesia was considered to be achieved when the level of sensory block reached T10 thoracic dermatome level or above with attainment of complete motor block (Bromage 3).

Cases with failed SAB that needed general anesthesia were excluded from the study.

A proforma was used to collect the data, which included the patient's particulars, indication for surgery anesthetic details, and intraoperative monitoring. Hemodynamic variables were recorded every min for the first 5 min, at every 5 min interval for the next half an hour after the administration of SAB, and every 10 min thereafter up to 150 min after the block. In the postoperative period, patients were monitored hourly for the first 4 h. Hypotension was treated with i.v. fluids and i.v. mephentermine 6 mg, whereas bradycardia was treated with i.v. atropine 0.6 mg. Respiratory depression was defined as respiratory rate <8 breaths/min or SpO2 <94% on room air and treated with oxygen supplementation.

Postoperatively, quality of anesthesia was observed, complete motor regression and ambulation time were noted. VAS was assessed at every 30 min for 6 h and then at every 2 h till patients complained of pain (VAS >3). Hemodynamic variables and SpO2 were recorded. i.v. tramadol 50 mg was given for rescue analgesia when VAS was >4, and the time was noted.

Statistical analysis

Data were entered into a Microsoft Excel sheet and were analyzed using SPSS 22 version software (IBM SPSS Statistics, Somers NY, USA). Categorical data were represented in the form of frequencies and proportions. The Chi-square test was used as a test of significance for parametric data. Analysis of variance test was used as a test of significance for nonparametric data. P < 0.05 was considered statistically significant.


All the three groups studied were comparable with respect to age, gender, weight, and ASA-PS classes distribution.

The mean time of onset of sensory block in Group A was 2.10 min, in Group B was 1.85 min, and in Group C was 2.30 min. There was no statistical significance (P = 0.325) in the time taken for the onset of sensory block (T10) in all three groups. However, the dexmedetomidine group showed early onset of sensory block [Figure 1].

Figure 1:
Mean onset of sensory block at T10 (min)

Patients in Group A and Group C achieved a higher level (T6) of sensory block in 7.45 min. Those in Group B achieved the same level of block earlier in 6.65 min [Figure 2].

Figure 2:
Mean time to achieve highest sensory level block at T6 (min)

The duration of postoperative analgesia in Group A was 323 min, in Group B was 417 min, and in Group C was 146.5 min. This was statistically significant with P < 0.001 [Figure 3].

Figure 3:
Mean duration of postoperative analgesia (Min)

The time taken for regression of motor block to Bromage 6 in Group A was 328.50 min. The same in Group B was 419.5 min. In Group C, it took 156.5 min. This was statistically significant with P < 0.001 [Table 1].

Table 1:
Regression of motor block to Bromage 6 (min)


Spinal anesthesia has been commonly used for lower limb surgeries because of its simplicity, speed of onset, reliability, and minimal exposure to depressant drugs. The aim of good postoperative analgesia is to produce a long-lasting continuous effective analgesia with minimal side effects. Adding an intrathecal adjuvant to local anesthetics forms a reliable method to prolong the duration of anesthesia.[1910]

In our study, we compared the efficacy of dexmedetomidine and nalbuphine when used as adjuvants with bupivacaine versus bupivacaine alone for SAB.

A randomized controlled study by Hala et al.[11] concluded that intrathecal dexmedetomidine in doses of 10 and 15 μg significantly prolongs the anesthetic effects of spinal hyperbaric bupivacaine in a dose-dependent manner.

Mukherjee et al.[5] studied the duration of analgesia with different dosages of intrathecal nalbuphine (0.2, 0.4, and 0.8 mg) to find out the optimum dose of intrathecal nalbuphine, which could prolong the postoperative analgesia without increasing the side effects.

In view of the above-mentioned studies, we added 10 μg of dexmedetomidine and 1.5 mg of nalbuphine to 2.7 mL of 0.5% hyperbaric bupivacaine individually for SAB and compared with the control group receiving 0.5% hyperbaric bupivacaine alone.

The main objectives of our study were to compare these drugs for time for onset of blockade at T10, highest sensory blockade uptoT6, complete motor blockade when the patient is unable to move hip, knee, and ankle (Bromage 3), hemodynamic parameters intraoperatively, duration of postoperative analgesia, time for complete sensory and motor regression, and side effect.

At various doses of Dexmedetomidine, onset of sensory block was rapid with 10 μg dose, as shown in the study by Shukla D et al. (2011).[2] In a similar study conducted by Kathuria S et al. (2015)[3] in Punjab, the mean onset of sensory blockade was 9.75 ± 4.23 minutes in Dexmedetomidine group. In the studies by Al-Ghanem SM et al. (2009)[8] mean onset of sensory block in Dexmedetomidine group by using 10 μg was 4.7 ± 2 mins, mean Duration of analgesia was 338.9 ± 44.8 mins and mean duration of motor blockade was 302.9 ± 36.7 min.

Mohan et al.[12] compared 1.4 and 0.8 mg of nalbuphine as adjuvants added to 17.5 mg of 0.5% hyperbaric bupivacaine for SAB and observed that they provided faster onset of sensory and motor blockade of 1.56 and 1.48 min, respectively. The total duration of sensory and motor blocks was 194.66 and 228.83 min, respectively,[12] which was similar to our study. In our study, the onset of sensory blockade was 2.10 min that lasted up to 328.50 min with 1.5 mg of nalbuphine [Figures 2 and 3]. This suggested that nalbuphine as an adjuvant to bupivacaine provided better anesthesia and analgesia than bupivacaine alone.

Basunia et al.,[13] in their study, observed that 1.2 mg is the optimum intrathecal dose of nalbuphine as an adjuvant to 15 mg of 0.5% hyperbaric bupivacaine to prolong postoperative analgesia of 482.6 min in the lower abdominal and lower limb surgeries. It has also been documented that nalbuphine exhibits an analgesic ceiling effect at a 1.2 mg dosage, above which it will not increase analgesia efficacy. Our study also yielded similar results at 1.5 mg dosage intrathecally.

Das A et al. (2015)[14] compared 5 μg and 10 μg of Dexmedetomidine, intrathecally as an adjuvant to 15 mg Bupivacaine and concluded that dose dependent intrathecal Dexmedetomidine increases the sensory, motor block duration and time to first analgesic use and decreases analgesic consumption in a dose-dependent manner. Das A et al. (2015)[14] concluded that dose dependent intrathecal Dexmedetomidine increases the motor block duration.

Halder et al.[15] concluded that the addition of 10 μg in comparison to 5 μg dexmedetomidine to 0.5% hyperbaric bupivacaine more efficiently hastens the onset and prolongs the duration of sensory and motor blockade and reduces the requirement of rescue analgesia in postoperative period which provided postoperative analgesia for 241.80 min with 10 μg and 227.0 min with 5 μg of dexmedetomidine. We used 10 μg of intrathecal dexmedetomidine as an adjuvant to bupivacaine. This provided faster onset of sensory block (1.85 min), quality anesthesia, and excellent postoperative analgesia of 417 min.

Dubey R et al. (2014)[16] conducted a randomized study and concluded that Nalbuphine provides better quality of block as compared to Bupivacaine alone. It also prolongs postoperative analgesia when used as adjuvant to spinal bupivacaine in elderly patients (P < 0.001).

When we compared 1.5 mg nalbuphine (Group A), 10 μg dexmedetomidine (Group B) as adjuvants along with 2.7 mL of 0.5% hyperbaric bupivacaine, we observed faster onset of the sensory block that is 2.10 and 1.85 min, respectively, compared to control group (Group C) that was 2.30 min [Figure 1].

The duration of sensory block was 323 and 417 min, respectively. The duration of motor block was 328.5 and 419.5 min, respectively [Figures 2, 3 and Table 1]. This was much less in the control group with sensory block for 146.5 min and motor block for 156.5 min [Figures 2, 3 and [Table 1]. These observations were statistically significant with P < 0.001. This was comparable with the observations by Michael and Mehta[1] where they used 10 μg dexmedetomidine with 15 mg of 0.5% bupivacaine.

The results of our study were corresponding to the abovementioned studies[11415] reiterating the fact that dexmedetomidine is a better adjuvant to bupivacaine. It decreased the mean onset of sensory and motor block (1.85 min) and also prolonged the mean duration of sensory and motor block by 419.50 and 487.75 min, respectively. The mean time of two-segment regression was significantly longer with dexmedetomidine as compared to nalbuphine [Figures 2 and 3].

We also observed that the time for first rescue analgesia in nalbuphine and dexmedetomidine groups was 323 and 417 min, respectively. Thus, dexmedetomidine provided a longer duration of postoperative analgesia compared to nalbuphine and plain bupivacaine [Figure 3].

Bhalavat et al.,[17] in their study, observed that mean HR and mean arterial pressure (MAP) were lower with the use of dexmedetomidine than nalbuphine as adjuvants. However, there was no significant difference in HR and MAP between the two groups at all intervals of follow-up. Incidence of hypotension and bradycardia with dexmedetomidine was 6.67% and 3.3%, respectively, and incidence with nalbuphine was 3.3% and 3.3%, respectively. The findings in our study were almost similar to this study.

Similarly, in the study by Gupta et al.[18] in group dexmedetomidine, 6.6% had bradycardia and hypotension, respectively. Hence, the addition of dexmedetomidine as an adjuvant does not cause variation in vital parameters and is comparable with nalbuphine and safe to use as an alternative. In our study, we compared nalbuphine, dexmedetomidine, and normal saline as adjuvants to bupivacaine and achieved minimal side effects such as hypotension and bradycardia similar to this study. We observed that HR, MAP, and SpO2 between the three groups although showed statistically significant differences at few intervals, there was no bradycardia, tachycardia, hypertension, and hypoxia. In the nalbuphine group, 0.5% had hypotension, and in the dexmedetomidine group, 7.5% had hypotension. However, there was no significant difference in the incidence of hypotension between the three groups.


We conclude that adding 10 μg of dexmedetomidine to 0.5% hyperbaric bupivacaine as an adjuvant during SAB for lower limb orthopedic surgeries gives faster onset of the sensory block with quality anesthesia and excellent postoperative analgesia when compared to 1.5 mg of nalbuphine as an adjuvant to 0.5% hyperbaric bupivacaine and 0.5% hyperbaric bupivacaine alone, without significant side effects.

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Conflicts of interest

There are no conflicts of interest.


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Bupivacaine; dexmedetomidine; nalbuphine; orthopedic surgeries

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