|Year : 2014 | Volume
| Issue : 4 | Page : 530-533
The effect of adding ketamine to bupivacaine in spinal anesthesia in day-case surgery
Manal M Kamal, Dalia El-Fawy
Department of Anesthesiology, Intensive Care and Pain Management, Faculty of Medicine, Ain Shams University, Cairo, Egypt
|Date of Submission||13-May-2014|
|Date of Acceptance||12-Jul-2014|
|Date of Web Publication||28-Nov-2014|
Department of Anesthesiology, Intensive Care and Pain Management, Faculty of Medicine, Ain Shams University, Cairo
Source of Support: None, Conflict of Interest: None
In this paper, we evaluate the effect of adding ketamine to spinal anesthesia in day-case surgery with regard to the time of onset of block, the duration of the block, hemodynamic variables, postoperative time to full motor power, time to walking, and side effects.
Materials and methods
Sixty patients scheduled for day-case surgeries under spinal anesthesia were studied in a prospective double-blinded randomized manner. Patients were allocated to receive either 3 ml hyperbaric bupivacaine (0.5%) (group I) or 2 ml hyperbaric bupivacaine (0.5%) combined with ml ketamine (25 mg) + ml normal saline (group II).
The onset time and the duration of the block were shorter in group II than in group I. The postoperative time to walking, the time to full motor power recovery, and the duration of spinal analgesia were shorter in group II. There were no significant differences in hemodynamic variables or side effects.
Ketamine added to hyperbaric bupivacaine in spinal anesthesia provides a shorter time of onset of block, a shorter duration of the block, and a shorter time to full motor power and to walking postoperatively in day-case surgery.
Keywords: bupivacaine, day-case surgery, ketamine, spinal anesthesia
|How to cite this article:|
Kamal MM, El-Fawy D. The effect of adding ketamine to bupivacaine in spinal anesthesia in day-case surgery. Ain-Shams J Anaesthesiol 2014;7:530-3
|How to cite this URL:|
Kamal MM, El-Fawy D. The effect of adding ketamine to bupivacaine in spinal anesthesia in day-case surgery. Ain-Shams J Anaesthesiol [serial online] 2014 [cited 2021 May 6];7:530-3. Available from: http://www.asja.eg.net/text.asp?2014/7/4/530/145697
| Introduction|| |
Spinal anesthesia provides satisfactory anesthesia for many day-case surgeries (orthopedic, gynecological, and urological procedures).
Reducing the dose of bupivacaine used in spinal anesthesia helps to achieve rapid anesthetic recovery, but may result in anesthetic failure . Intrathecal adjuncts such as opioids , vasoconstrictors , α-2 agonists , and neostigmine  are often added to enhance spinal anesthesia.
Ketamine is an anesthetic agent with potent analgesic properties used as an adjunct in spinal anesthesia. It has a local anesthetic effect and a noncompetitive antagonistic effect on N-methyl d-aspartate receptors .
However, the frequency of psychomimetic disturbances, inadequate analgesia, and a short duration of action have limited its use as the sole anesthetic agent in spinal anesthesia .
In this study, the effect of adding ketamine to bupivacaine in spinal anesthesia in day-case surgery was evaluated.
| Materials and methods|| |
This prospective randomized double-blind study was carried out during the period from April 2010 to April 2012 in Ain Shams University Hospital, Cairo, Egypt. After obtaining approval from our ethical committee and patient consent, 60 patients with ASA physical status I or II who were to undergo day-case surgery (orthopedic, urological, gynecological, or lower abdominal surgery) were enrolled. Patients with deformities of the vertebral column, neurological diseases, mental disease or bleeding tendency, and any surgery lasting more than 60 min were excluded.
No premedication was given. Ringer's solution (500 ml) was given before giving spinal anesthesia. Patients were randomly allocated using computer-generated random numbers into one of two groups in a double-blinded manner: group I received 3 ml hyperbaric bupivacaine (0.5%) and group II received 2 ml hyperbaric bupivacaine (0.5%) combined with ml ketamine (25 mg) + ½ ml normal saline. The patients and the anesthetist were not aware of the group division or the drug preparation. Lumbar puncture was performed using an aseptic technique with the patient in the sitting position with a 25-G spinal needle at the L2-L3 interspace using a midline technique. Hemodynamic changes (heart rate, oxygen saturation, and noninvasive blood pressure) were monitored by a blinded observer every 2 min for 15 min and then every 15 min until the end of the procedure. If the systolic blood pressure decreased more than 20% from baseline, it was treated by ephedrine given intravenously. Sensory and motor block were assessed by a blind observer. Sensory block was assessed by cold sensation and motor block was assessed by the modified Bromage score (0, no motor loss; 1, inability to flex the hip; 2, inability to flex the knee; 3, inability to flex the ankle). Patients were assessed every 3 min until the maximum spread of the blockade. The onset time of sensory block was measured from the time of epidural injection till bilateral sensation was lost. The onset time of motor block was measured from the time of epidural injection till the modified Bromage score was 3. The duration of sensory block was measured from the time of epidural injection until bilateral sensation was recovered. The duration of motor block was measured from the time of epidural injection till the modified Bromage score was 0. The duration of spinal analgesia was measured from the time of spinal administration to the first time at which the patient complained of pain in the postoperative period.
Side effects such as sedation, nystagmus, headache, dizziness, nausea, vomiting, hallucinations, and psychomimetic effects were assessed by a blind observer every 15 min until recovery. Sedation was assessed by the sedation score (1, awake; 2, drowsy but responsive to verbal stimuli; 3, drowsy but responsive to physical stimuli; 4, unresponsive to verbal and physical stimuli). The time to walking was assessed in every case. The patient was discharged when vital signs were stable, the motor block was completely resolved, and there was no severe pain or bleeding or vomiting after getting 18 as a recovery score . The score was explained to every patient in the induction room.
We would like to know how well you feel after recovery from anesthesia and operation.
Please circle the most appropriate responses (summary score 0-18).
Using PASS for sample size calculation, it was calculated that a sample size of 29 per group will achieve 80% power to detect a difference of 15 min in motor block between the two groups with a significance level (α) of 0.05, using a two-sided two-sample t-test; 35 patients per group were included to replace any dropouts.
The statistical analysis was performed using a standard SPSS software package version 17 (SPSS Inc., Chicago, Illinois, USA). Parametric data are presented as mean ± SD and compared using Student's t-test. Categorical data are presented as the number of patients, and differences between groups were compared using the Pearson χ2 -test.
Nonparametric data are presented as the median and range and compared using the Mann-Whitney U-test. All P-values are two-sided. P-value less than 0.05 is considered statistically significant.
| Results|| |
There was no statistically significant difference between the two groups with regard to age, weight, height, sex, the ASA physical status, and the duration of the procedure ([Table 1]).
The onset times of sensory and motor block were significantly shorter in group II than group I. The duration of sensory and motor blocks were significantly longer in group I than in group II. The duration of spinal analgesia was significantly shorter in group II ([Table 2]).
There was no statistically significant difference between the two groups with regard to hemodynamic variables ([Table 3]).
There was no statistically significant difference with regard to the side effects in both groups. No patients in both groups suffered from sedation, headache, or dissociative effects. However, seven patients suffered from shivering in group I compared with five patients in group II. Three patients suffered from hypotension in group I compared with five patients in group II. Seven patients suffered from nausea and vomiting in group I compared with 10 patients in group II. No patients suffered from hallucinations in group I compared with one patient in group II ([Table 4]).
There was no statistically significant difference between both groups with regard to the recovery score. The median recovery score was 11 in both groups at 2 h. It was 15 in group I and 14 in group II at 3 h and it was 18 in both groups at 4 h ([Table 5]).
| Discussion|| |
Ketamine exerts analgesic effects after epidural, caudal, or intrathecal administration [9,10]. These analgesic effects are mediated by a number of mechanisms. Ketamine binds to opiate receptors and interacts with cholinergic, adrenergic and 5-hydroxitryptamine systems [11-13]. It can block the N-methyl-d-aspartate excitation of central neurons . Ketamine prevents action potential conduction by its effect on the sodium and potassium channels in nerve membranes, and so it has local anesthetic properties .
In this study, ketamine added to bupivacaine in spinal anesthesia shortened the onset of sensory and motor block and shortened the duration of motor block. This is similar to the results of Kathirvel et al. , who found that ketamine added to bupivacaine intrathecally shortened the duration of motor blockade more than in the bupivacaine group. Togal et al.  found that ketamine with bupivacaine intrathecally causes less motor and sensory block. Yanli and Eren  have shown that extradural ketamine reduces the onset time of motor blockade. Gantenbein et al.  reported that the local anesthetic activity of bupivacaine was significantly enhanced by ketamine. They explained that this result is possibly due to the inhibiting effect of ketamine on the metabolism of bupivacaine.
In contrast to our results, Khezri et al.  reported that intrathecal ketamine with bupivacaine prolongs intraoperative anesthesia. However, the discrepancy in the results might be due to the different populations as their study was conducted on pregnant women.
In this study, there were no significant differences between the two groups regarding their hemodynamics. This is similar to the results of Bion , Beigom et al. , Kathirvel et al. , and Togal et al. .
In the present study, we did not find any incidence of behavioral, psychomimetic or neurological complications. This is in harmony with the findings by Bion  who reported that intrathecal ketamine acts locally on spinal cord nociceptors and does not act systemically. The other possible cause of this finding is that we used a small dose of ketamine. Similar to this result, Beigom and colleagues did not find any incidence of behavioral or neurological changes.
In contrast to our results, those who used higher doses of intrathecal ketamine found some behavioral changes in their results, such as Weir and Fee , who observed a significant sedation in patients who received extradural ketamine with bupivacaine and explained this to be due to the lipid solubility and the extensive intravascular absorption of ketamine from the epidural space.
However, it seems that it is a dose-dependent phenomenon.
In this study, the time to full motor power recovery and time to walking was shorter in the ketamine group.
| Conclusion|| |
It was found that intrathecal ketamine (25 mg) with low-dose bupivacaine produced a shorter onset of motor and sensory block and had minimal systemic side effects; hence, the patient can regain full motor power early, which is needed in day-case surgery.
| Acknowledgements|| |
| References|| |
Ben-David B, Solomon E, Levin H, Admoni H, Goldik Z. Intrathecal fentanyl with small-dose dilute bupivacaine: better anesthesia without prolonging recovery. Anesth Analg 1997; 85:560-565.
Chaney MA. Side effects of intrathecal and epidural opioids. Can J Anaesth 1995; 42:891-903.
Sakura S, Sumi M, Sakaguchi Y, Saito Y, Kosaka Y, et al.
The addition of phenylephrine contributes to the development of transient neurologic symptoms after spinal anesthesia with 0.5% tetracaine. Anesthesiology 1997; 87:771-778.
Eisenach JC, De Kock M, Klimscha W. Alpha (2)-adrenergic agonists for regional anesthesia. A clinical review of clonidine (1984-1995). Anesthesiology 1996; 85:655-674.
Liu SS, Hodgson PS, Moore JM, Trautman WJ, Burkhead DL. Dose-response effects of spinal neostigmine added to bupivacaine spinal anesthesia in volunteers. Anesthesiology 1999; 90:710-717.
Hirota K, Lambert DG. Ketamine: its mechanism(s) of action and unusual clinical uses. Br J Anaesth 1996; 77:441-444.
Bion JF. Intrathecal ketamine for war surgery. A preliminary study under field conditions. Anaesthesia 1984; 39:1023-1028.
Myles PS, Hunt JO, Nightingale CE, Fletcher H, Beh T, et al.
Development and psychometric testing of a quality of recovery score after general anesthesia and surgery in adults. Anesth Analg 1999; 88:83-90.
Hawksworth C, Serpell M. Intrathecal anesthesia with ketamine. Reg Anesth Pain Med 1998; 23:283-288.
Islas JA, Astorga J, Laredo M. Epidural ketamine for control of postoperative pain. Anesth Analg 1985; 64:1161-1162.
Finck AD, Ngai SH. Opiate receptor mediation of ketamine analgesia. Anesthesiology 1982; 56:291-297.
Pekoe GM, Smith DJ. Ketamine analgesia. Mediation by biogenic amine and endogenous opiate processes. Anesthesiology 1979; 51:S36.
White PF, Way WL, Trevor AJ. Ketamine: its pharmacology and therapeutic uses. Anesthesiology 1982; 56:119-136.
Way WL, Trevor AJ. Pharmacology of intravenous non-narcotic anesthetics. In: Miller RD, editor. Text book of Anesthesiology. New York: Churchill Livingstone; 1986. 813-817.
Peat SJ, Bras P, Hanna MH. A double-blind comparison of epidural ketamine and diamorphine for postoperative analgesia. Anaesthesia 1989; 44:555-558.
Kathirvel S, Sadhasivam S, Saxena A, Kannan TR, Ganjoo P. Effects of intrathecal ketamine added to bupivacaine for spinal anaesthesia. Anaesthesia 2000; 55:899-904.
Togal T, Demirbilek S, Koroglu A, Yapici E, Ersoy O. Effects of S(+) ketamine added to bupivacaine for spinal anaesthesia for prostate surgery in elderly patients. Eur J Anaesthesiol 2004; 21:193-197.
Yanli Y, Eren A. The effect of extradural ketamine on onset time and sensory block in extradural anaesthesia with bupivacaine. Anaesthesia 1996; 51:84-86.
Gantenbein M, Abat C, Attolini L, Pisano P, Emperaire N, et al.
Ketamine effects on bupivacaine local anaesthetic activity and pharmacokinetics of bupivacaine in mice. Life Sci 1997; 61:2027-2033.
Khezri MB, Ghasemi J, Mohammadi N. Evaluation of the analgesic effect of ketamine as an additive to intrathecal bupivacaine in patients undergoing cesarean section. Acta Anaesthesiol Taiwan 2013; 51: 155-160.
Weir PS, Fee JP. Double-blind comparison of extradural block with three bupivacaine-ketamine mixtures in knee arthroplasty. Br J Anaesth 1998; 80:299-301.
[Table 1], [Table 2], [Table 3], [Table 4], [Table 5]