Epidural morphine injection after combined spinal and epidural anaesthesia.

BACKGROUND AND OBJECTIVE: Although combined spinal and epidural anaesthesia is efficient and easy to perform, the technique can be a double-edged sword having the potential risk that an increased flux of drugs across the meninges through the hole made in it may lead to severe adverse effects. The aim was to compare the incidence of adverse events when an epidural injection of morphine was given after combined spinal and epidural anaesthesia or after epidural anaesthesia. METHODS: Fifteen patients had an epidural catheter inserted at the L2-3 interspace, and then a spinal block administered via the L3-4 interspace. Another 15 patients only had an epidural catheter inserted. After the onset of spinal or epidural anaesthesia had been confirmed, morphine 2 mg was injected into the epidural space, and a continuous epidural infusion of morphine was started. At the end of the operation and at 4, 8 and 12 h after the administration of epidural morphine and on the next day, the following variables were examined: blood pressure, heart rate, respiratory rate, arterial blood-gas analysis, visual analogue scale pain scores, nausea/vomiting scores, and pruritus scores. RESULTS: In the study population, the epidural injection of morphine was not associated with a significantly higher incidence of adverse events when given after spinal anaesthesia than after epidural anaesthesia. CONCLUSIONS: The adverse effects associated with epidural morphine given after spinal anaesthesia did not increase significantly when a 27-G Whitacre needle was used. Thus, the morphine flux through the meningeal hole into the cerebrospinal fluid was trivial.

Localized airway anesthesia with lidocaine partially suppresses cardiovascular responses To lung inflation.

UNLABELLED: Lung inflation causes cardiovascular suppression via an increase in intrathoracic pressure and neural mechanisms. To examine the mechanisms involved, we mea-sured the heart rate (HR) and arterial blood pressure (AP) responses to lung inflation before and after spraying the bronchi with lidocaine to suppress airway reflex. Thirty women participated in the study. One group (n = 20, Group BT) had their tracheas intubated by using double-lumen tubes. The other group (n = 10, Group TT) received an ordinary endotracheal tube. They were all studied under general anesthesia by using nitrous oxide, isoflurane, and muscle relaxation after a thiopental induction. In each patient, airway pressure was increased for 3 s, and changes in HR and AP were measured. Lung inflation was repeated after 5 mL of 4% lidocaine had been sprayed into the main bronchi unilaterally in Group BT or bilaterally in Group TT. There were no significant differences in cardiovascular responses between left and right lung inflation with the pressure at 20 and 30 cm H(2)O. Both lungs inflated at 20 cm H(2)O caused an increase in HR with a significantly greater decrease in AP than with unilateral inflation. Anesthesia of the bronchi abolished the HR increase, but not the AP decrease. Lung inflation at 30 cm H(2)O caused significant decreases in HR and AP which were not affected with topical anesthesia. These results indicate that the cardiovascular responses elicited by lung inflation in anesthetized humans are predominantly the direct effect of the increase in intrathoracic pressure, although sympathetic afferent activity induced via stimulation of mechanoreceptors in the airways contributes. IMPLICATIONS: Localized airway anesthesia with lidocaine is unlikely to suppress the cardiovascular responses to lung inflation. This suggests that a limited number of neurogenic mechanisms are involved in the cardiovascular responses to lung inflation in anesthetized humans.