Hostname: page-component-848d4c4894-ndmmz Total loading time: 0 Render date: 2024-05-12T21:41:40.049Z Has data issue: false hasContentIssue false

Hyperbaric bupivacaine affects the doses of midazolam required for sedation after spinal anaesthesia

Published online by Cambridge University Press:  25 November 2005

H. İ. Toprak
Affiliation:
Medical School of Inonu University, Department of Anaesthesiology, Malatya, Turkey
Z. Ozpolat
Affiliation:
Medical School of Inonu University, Department of Anaesthesiology, Malatya, Turkey
E. Ozturk
Affiliation:
Medical School of Inonu University, Department of Anaesthesiology, Malatya, Turkey
M. H. Ulger
Affiliation:
Medical School of Inonu University, Department of Anaesthesiology, Malatya, Turkey
O. Sagir
Affiliation:
Medical School of Inonu University, Department of Anaesthesiology, Malatya, Turkey
M. O. Ersoy
Affiliation:
Medical School of Inonu University, Department of Anaesthesiology, Malatya, Turkey
Get access

Extract

Summary

Background and objective: Patients having spinal anaesthesia with hyperbaric bupivacaine may become sensitive to sedative drugs but no data exists about any dose-related effect of the local anaesthetic on the sedative requirement. We aimed to investigate whether hyperbaric bupivacaine dose in spinal anaesthesia has any effect on midazolam requirements. Methods: Sixty unpremedicated patients were allocated to three equal groups. Patients in Groups I and II received hyperbaric bupivacaine 0.5% 10 and 17.5 mg respectively for spinal anaesthesia and Group III was a control group without spinal anaesthesia. In Groups I and II, after the evaluation of sensory block, patients received intravenous midazolam 1 mg per 30 s until the Ramsay sedation score reached 3 (drowsy but responsive to command). In Group III, general anaesthesia was induced after sedation score had reached 3 using midazolam. The total dose of midazolam (mg kg−1) given to each patient, the level of sensory block and complications were recorded. Results: The level of sensory block was higher in Group II (T7) than Group I (T9) (P < 0.01). The doses of midazolam were 0.063 mg kg−1 in Group I, 0.065 mg kg−1 in Group II and 0.101 mg kg−1 in Group III (P < 0.001). There was no correlation between level of sensory block and dose of midazolam in Group I (r = −0.293, P = 0.21) and Group II (r = 0.204, P = 0.39). Conclusions: Different doses of hyperbaric bupivacaine for spinal anaesthesia do not affect the midazolam requirements for sedation. However, spinal anaesthesia with hyperbaric bupivacaine with a maximum spread in the middle thoracic dermatomes may be associated with sedative effects and thus a reduced need for further sedation with midazolam.

Type
Original Article
Copyright
© 2005 European Society of Anaesthesiology

Access options

Get access to the full version of this content by using one of the access options below. (Log in options will check for institutional or personal access. Content may require purchase if you do not have access.)

References

Tverskoy M, Shifrin V, Finger J, Fleyshman G, Kissin I. Effect of epidural bupivacaine block on midazolam hypnotic requirements. Reg Anesth 1996; 21: 209213.Google Scholar
Eappen S, Kissin I. Effect of subarachnoid bupivacaine block on anesthetic requirements for thiopental in rats. Anesthesiology 1998; 88: 10361042.Google Scholar
Ben-David B, Vaida S, Gaitini L. The influence of high spinal anesthesia on sensitivity to midazolam sedation. Anesth Analg 1995; 81: 525528.Google Scholar
Benards CM. Epidural and spinal anesthesia. In: Barrash PG, Cullen BF, Stoelting RK, eds. Clinical Anesthesia. Philadelphia, PA: Lippincott Williams & Wilkins, 2001: 689713.
Tverskoy M, Fleyshman G, Backrak L, Ben-Shlomo I. Effect of bupivacaine induced spinal block on the hypnotic requirement of propofol. Anaesthesia 1996; 51: 652653.Google Scholar
Gentili M, Chau Huu P, Enel D, Hollande J, Bonnet F. Sedation depends on the level of sensory block induced by spinal anaesthesia. Br J Anaesth 1998; 81: 970971.Google Scholar
Caplan RA, Ward RJ, Posner K, Cheney FW. Unexpected cardiac arrest during spinal anesthesia: a closed claims analysis of predisposing factors. Anesthesiology 1988; 68: 511.Google Scholar
Smith DC, Crul JF. Oxygen desaturation following sedation for regional analgesia. Br J Anaesth 1989; 62: 206209.Google Scholar
Munoz HR, Dagnino JA, Rufs JA, Bugedo GJ. Benzodiazepine premedication causes hypoxemia during spinal anaesthesia in geriatric patients. Reg Anesth 1992; 17: 139142.Google Scholar
Ramsay MAE, Savege TM, Simpson BRJ, Goodwin R. Controlled sedation with alphaxolone–alphadione. BMJ 1974; 2: 656659.Google Scholar
Pollock JE, Neal JM, Liu SS, Burkhead D, Polissar N. Sedation during spinal anesthesia. Anesthesiology 2000; 93: 728734.Google Scholar
Antognini JF, Jinks SL, Atherley R, Clayton C, Carstens E. Spinal anaesthesia indirectly depresses cortical activity associated with electrical stimulation of the reticular formation. Br J Anaesth 2003; 91: 233238.Google Scholar