After review and approval from institutional ethical committee and informed consent, 60 adult patients who were scheduled to undergo lower limb vascular surgery were included in the study. On the basis of pilot study data, present study was designed to be able to detect a 15% difference among study groups with regard to duration of sensory block and haemodynamic side effects. A power calculation based on these assumptions with an alpha of 0.05 and a beta of 0.8 resulted in the need for more than or equal to 20 patients in each treatment group. Patients with history of hypersensitivity to amide local anaesthetics, presence of a blood-clotting disorder, platelet count <100 000 mm³, blood dyscrasia, refusal of or inability to receive an epidural block, cutaneous infections or anatomical malformation at the puncture site, severe respiratory, renal, hepatic disease, A-V or intraventricular conduction abnormalities, seizure disorders and patients with weight more than 110 kg or height less than 150 cm were excluded from the study.

Patients who were included in the study (n=60) were randomly divided into three groups using computer generated table of random numbers, group (n=20), group L (n=20) and group LD (n=20). All patients were premedicated with Diazepam 5 mg on the night before and on the morning of surgery. On arrival in the operating room, peripheral venous access was established with a wide bore cannula, inj Midazolam 1 mg iv was administered, preloaded with 10ml/kg of normal saline, Lidocaine 1% (3 mL) was used to infiltrate the skin and subcutaneous tissues at the L1-L2 or L2-3 interspace. The epidural space was identified in the lateral decubitus position by using an 18-gauge Tuohy needle and a loss of resistance technique, epidural catheter was inserted 3-4 mm into the epidural space and patient turned supine. 15 microgram of epinephrine was added to 3 mL study drug, after negative aspiration, it was administered as a “test dose”. When there was no evidence of intravascular or subarachnoid injection (heart rate > 100 bpm, systolic blood pressure >90 mm Hg, or presence of sensory block) after 2 min, an additional 12 ml of the study drug was administered as slow injection at 1ml/min rate. Heart rate, Invasive blood pressure, Spo₂ and respiration were monitored throughout the study period. Hypotension, defined as more than 30% fall in systolic blood pressure as compared to the baseline, or SBP<90 mm of Hg was treated with a bolus of fluids, if not responding to the bolus, inj Ephidrine 6 mg incremental bolus was administered. Bradycardia defined as more than 30% fall in heart rate as compared to the baseline or<40 bpm was treated with inj atropine 0.6 mg IV.

Adequate block to initiate surgery was defined as a sensory block bilaterally to dermatome T10. Sensory block was assessed bilaterally in the mid-clavicular line by using the blunt end of a 27-gauge dental needle.

Time taken to achieve this level of anaesthesia was noted. Block height, time to reach peak block, time to two-segment regression and total duration of sensory block was noted.

The onset, degree, and duration of motor block were measured in both legs by using a modified Bromage scale and scored as:

Motor block was measured every 30 min postsurgery until the patient returned to a score of zero in both legs.

Haemodynamic parameters were monitored throughout study period, sedation level achieved, patients assessment of quality of anaesthesia, time to request of first dose of analgesia, any adverse effects associated were monitored and appropriately treated.

Age, height, weight and block characteristics were analysed by analysis of variance (ANOVA) and Kruskal Wallis test. Serial data were analysed with repeated-measures analysis of variance. Chi-square test and Fisher-exact test was used for non-parametric data. Data was analysed using SPSS version 18.P less than 0.05 was considered significant.

Sixty patients were enrolled in the study. Adequate level of block was achieved in all the study patients with 15 ml of the study drug. Baseline characteristics.

There was no difference among the groups in terms of age, sex, weight, height. Duration of surgery was comparable among the groups [Table/Fig-1].

Time to onset of sensory block to T-10 was comparable among the groups with average time to onset being 12 min [Table/Fig-2]. Maximum sensory level achieved was around T-4 to T-8 and was comparable among the groups. Time to maximum sensory block was also comparable among the groups [Table/Fig-2].

Maximum motor block was more in Bromage 1 in the Levobupivacaine and LD group compared to Bupivacaine which had more intense block with more patients achieving Bromage score of 2 and 3 though the findings have not reached statistical significance. (p=0.523, [Table/Fig-2]).

Patients in Levobupivacaine with Dexmedetomedine group had significantly better sedation levels achieved compared to the other two groups. Also, none of the patients had desaturation or respiratory depression requiring intervention in any of the groups. This indicates the active sedation inducing property of Dexmedetomidine. Patient’s assessment of quality of anaesthesia was also better in LD group compared to the B and L groups accounting for sedative, anxiolytic and analgesic action of Dexmedetomedine [5,6] [Table/Fig-2].

There was significant increase in the duration for two segment regression, regression to S1and motor block regression to Bromage 0 in LD group compared to other two groups which have comparable findings among themselves [Table/Fig-3].

Time to first request of analgesia was also significantly prolonged in LD group compared to other two groups [Table/Fig-3].

Baseline heart rates were comparable among the groups. From 15 min heart rate reduced significantly in LD group compared to the other two groups. None of the patients in groups B and L groups required atropine in contrast to 5 patients in LD group who required atropine, however all patients who required atropine responded to single dose of atropine and remained haemodynamically stable throughout the study period [Table/Fig-4].

Baseline systolic blood pressures were comparable among the groups [Table/Fig-5]. From 20 min post drug administration, mean systolic blood pressure decreased in LD group when compared to B and L groups and in LD group, though there was a initial fall in the blood pressure below the baseline, patients remained haemodynamically stable throughout the study period [Table/Fig-5].

Baseline diastolic blood pressure was comparable among the groups, and there was no significant difference in DBP among the groups throughout the study period [Table/Fig-6].

None of the patients in any group had any significant side effects throughout the study period. Two patients in LD group complained of dryness of mouth. Number of patients requiring Vasopressor did not differ among the groups of patients [Table/Fig-7].

This study demonstrates that epidural levobupivacaine is a suitable anaesthetic for use in vascular surgery. Levobupivacaine provided adequate sensory block for surgery in all patients. Levobupivacaine and Bupivacaine showed equivalent efficacy for the time taken to reach sensory block adequate for surgery. Sensory block to T10 was achieved within 15 minutes of administering the epidural injection in all groups and the maximum spread of sensory block was observed within 30 minutes.

Levobupivacaine is the second local anaesthetic to be studied clinically as a pure single isomer. Ropivacaine was the first single enantiomer local anaesthetic to be approved. However, studies suggest that Ropivacaine is less potent than Bupivacaine when administered by epidural injection [8].

Cardiovascular toxicity by local anaesthetics results in either direct myocardial depression, or arrhythmogenicity. Studies have shown that Levobupivacaine has a reduced potential to cause cardiotoxic effects. In a study which involved 14 volunteers (the intentional intravascular administration at10 mg/minutes until mild CNS symptoms developed) Levobupivacaine produced significantly less effects on myocardial function than racemic Bupivacaine. Changes in stroke index, acceleration index, and ejection fraction were less marked with Levobupivacaine. Mild CNS symptoms developed at a larger dose level of Levobupivacaine (56.1 mg) than with racemic Bupivacaine (47.9 mg). Evidence suggests that Levobupivacaine may provide a greater safety margin than Bupivacaine from direct depression of myocardial contractility in humans, same findings have also been observed in animal studies [3,4].

In the present study, onset, duration of sensory block were comparable between B and L groups which have a similar tolerability profile with comparable rates of adverse events. Our findings are in agreement with study by Dan J Kopacz et al., who studied the effects of epidural Levobupivacaine 0.75% with Racemic Bupivacaine for Lower Abdominal Surgery. They did not notice any difference in the onset, duration and tolerability profile among the two groups [9]. In the present study we noticed less intense motor blockade in L and LD groups compared to Bupivacaine group, which is in agreement with study by Dan J Kopacz et al.. Pasquale De Negri et al., studied the effect of Epidural Bupivacaine, Levobupivacaine, and Ropivacaine on postoperative analgesia and motor blockade and found that Bupivacaine had significantly higher motor block compared to the other groups. Study by B Locatelli et al., also showed higher motor blockade in Bupivacaine group compared to Levobupivacaine [10,11]

There has been a constant search for adjuvants for local anaesthetics to improve quality of regional anaesthesia. Alpha2 adrenoceptor agonists are now being used with great interest in anaesthesia practice for their sympatholytic, sedative, analgesic, and anaesthetic-sparing effects. Clonidine has been used extensively for this purpose. Dexmedetomidine is a more selective alpha 2 agonist with a greater selectivity for the apha2 receptors than the alpha1 receptor. It was introduced in clinical practice in the United States in 1999 and approved by the FDA only as a short-term (<24 hours) sedative Dexmedetomidine is shorter acting drug than clonidine and has a reversal drug, Atipamezole, for its sedative effect [5,6].

At the spinal cord level, stimulation of alpha receptors at the substantiagelatinosa of the dorsal horn leads to inhibition of the ring of nociceptive neurons and inhibition of the release of substance P. Alpha 2-adrenoceptors located at the nerve endings have a role in the analgesic mechanisms by preventing Norepinephrine release. The spinal mechanism is the principal mechanism for the analgesic action of Dexmedetomidine. There are studies which show evidence for both a supra spinal and peripheral sites of action [5,6].

Bajwa et al., studied the effect of Clonindine and Dexmedetomidine on patients undergoing surgery under epidural anaesthesia. They noticed an increase in time to two segment regression, sensory and motor block duration and also increase in time to first request of analgesia and better sedation in the Dexmedetomidine group, in the present study we have similar findings. They noticed decrease in HR and SBP in Dexmedetomidine group of patients which is similar in the present study. Patients in Dexmedetomedine group responded to treatment with atropine and Ephedrine and remained haemodynamically stable throughout the study period [12].

Sandip Sinha et al., studied the effect of Dexmedetomidine on paravertebral block using ropivacaine and noticed significant increase in duration of sensory, motor block and also sedation levels, they also noticed bradycardia and hypotension in the Dexemeditomidine group which responded to treatment. Our findings are similar to their study, though blood pressure decreased from baseline in Dexmedetomidne patients, they remained haemodynamically stable throughout the study period [13].

XZ Zeng et al., studied the effect of adding 0.5mics/kg of dexmedetomidine to 0.75% levobupivacaine epidurally in patients undergoing nephrectomy, they noticed that duration of sensory and motor blockade was prolonged in Dexmedetomidine group compared to placebo. Sedation levels, muscle relaxation was significantly better in dexmedetomidine group compared to placebo, our findings are similar to Zeng et al., as we noticed increase duration of sensory blockde, better sedation levels in demedetomidine group [14].

Studies have used dose of 0.5-2mics/kg of Dexmedetomidine, in the present study we have used a lower dose i.e. 0.5 mics/kg as majority of our study population was elderly with associated co-morbidities and a pilot study with 1mics/kg was associated with excessive hypotension. None of the patients in our study had any other significant side effects like, nausea vomiting, rhythm abnormalities or respiratory depression [12–14].

Limitations of our study are that we did not use blinding techniques, we did not measure the plasma concentration of local anaesthetics during the study period. We did not record the PR interval, QT and corrected QT interval in ECG or mechanical parameters like stroke index, acceleration index, ejection fraction during the study period which might have demonstrated differences among the drugs.

Above study shows that Levobupivacaine is a safe alternative to Bupivacaine for patients undergoing lower limb vascular surgery, with epidural block characteristics similar to Bupivacaine. Addition of Dexmedetomidine prolongs the duration of anaesthesia and provides excellent sedation and postoperative analgesia and hence, is a good adjuvant to regional anaesthesia in patients undergoing vascular surgery.