Chondrotoxic effects of intra-articular injection of local anaesthetics in the rabbit temporomandibular joint.

The aim of this study was to investigate the chondrotoxic effects of a single-dose intra-articular injection of articaine, lidocaine, and bupivacaine on the rabbit temporomandibular joint (TMJ). Twenty-four rabbits were divided into four groups: control (group 1), articaine (group 2), lidocaine (group 3), and bupivacaine (group 4). Synovial fluid samples and venous blood were taken to evaluate matrix metalloproteinase 3 (MMP-3) levels. One millilitre of local anaesthetic solution was injected in the study groups and saline solution in the control group. The rabbits were euthanized after 4 weeks and the mandibular condyles and articular discs were evaluated. On histological examination, the study group samples had irregular joint surfaces, decreased collagen, and a thinner cartilage layer. Apoptotic cells were evaluated with the TUNEL method. TUNEL-positive apoptotic cell counts were higher in all study groups compared to the control group, and the difference was significant (P < 0.001). The mean preoperative serum MMP-3 level for all groups was 5.71 ± 3.33 ng/mL, while the mean postoperative level was 22.61 ± 6.36 ng/mL; this difference was significant (P < 0.001). A single-dose intra-articular injection of local anaesthetic had apoptotic effects on chondrocytes, leading to degenerative changes in the TMJ articular structures. Articaine was found to have less harmful effects than lidocaine and bupivacaine. Intra-articular injection of local anaesthetics should be limited in the TMJ because of the potential toxic effects.

The effects of dexmedetomidine and fentanyl on emergence characteristics after adenoidectomy in children.

This randomised controlled study evaluated the effects of fentanyl and dexmedetomidine on emergence characteristics of children having adenoidectomy and anaesthetised with sevoflurane. Ninety children, two to seven years of age and ASA physical status I, were studied. Children were randomly assigned to one of three groups of 30 children, with the study intervention injection given intravenously after intubation. Children in Group F received fentanyl 2.5 microg x kg(-1), children in Group D received dexmedetomidine 0.5 microG x kg(-1) and children in Group C received saline solution. Anaesthesia was induced with 50% N2O and 8% sevoflurane in O2 by mask and atracurium 0.6 mg x kg(-1) was administered for tracheal intubation. All children received paracetamol 40 mg/kg rectally one hour preoperatively and dexamethasone 0.5 mg x kg(-1) intravenously. The time to extubation was shorter in Group D than Group F. The eye-opening time was longer in Group F (16.1 +/- 5.3 minutes) than in Groups C (12.0 +/- 4.2 minutes) and D (12.7 +/- 3.2 minutes). The proportion of pain-free children in early recovery was significantly higher in Groups D (47%) and F (43%) than Group C (13%) (P < 0.05). The proportion of children with agitation scores > 3 was lower in Groups D 17% (5/30) and F 13% (4/30) than in Group C 47% (14/30) (P < 0.05). Fentanyl 2.5 microg x kg(-1) and dexmedetomidine 0.5 microg x kg(-1) had similar haemodynamic effects and emergence characteristics. Fentanyl has been safely used in children for many years. Further studies of dexmedetomidine safety and its interaction with other anaesthetic agents are required before recommending its routine use during general anaesthesia in children.

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

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.