Anesthesia & Clinical Research
Open Access

Complications of Spinal Anesthesia in Central Nervous System

Harald Gabriel^{* *}Correspondence: Harald Gabriel, Department of Anesthesiology, The University of Newcastle, Callaghan, Australia, Email:

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Introduction

Spinal anesthesia has been shown to have sedative effects in the absence of intravenous sedation. Spinal anesthesia is a simple technique that provides a deep and fast surgical block through the injection of small doses of local anesthetic solution into the subarachnoid space. The purpose of this review is to provide an overview on recent developments on local anesthetic drugs, side effects, and special techniques of intrathecal anesthesia. Spinal anesthesia can be considered adequately safe, and severe complications are reasonably rare. The cardiovascular effects associated with sympathetic block are more frequent, but successfully treated with volume expansion and administration of vasoactive drugs. It is clear that the total dose of local anesthetic injected into the subarachnoid space is the most important determinant of both therapeutic and unwanted effects of spinal anesthesia. Several studies have also demonstrated the efficacy and safety of using small doses of long acting agents, such as bupivacaine or ropivacaine, to produce an adequately short spinal block in outpatients. Levopivacaine, the pure enantiomer of racemic bupivacaine showed a lower risk of cardiovascular and Central Nervous System (CNS) toxicity than bupivacaine. In the last years we have assisted important changes in the health care organization, with most of the surgical procedures performed on outpatients or on elderly patients with concomitant diseases. This forced us to change the indications and clinical use of intrathecal anesthesia techniques, which have been modified according to the changing needs of surgery. The development of new drugs and special techniques for spinal anesthesia will further improve the clinical use of this old but evergreen technique. Central neuraxial anesthesia has been reported to decrease the dose of both intravenous and inhalational anesthetics needed to reach a defined level of sedation. The mechanism behind this phenomenon is speculated to be decreased afferent stimulation of the reticular activating system. The authors performed a two-part study (nonrandomized pilot study and a subsequent randomized, double-blind, placebo-controlled study) using the Bispectral Index (BIS) monitor to quantify the degree of sedation in unmediated volunteers undergoing spinal anesthesia.

Description

Spinal anesthesia is accompanied by significant sedation progressively when compared with controls as measured by OAA/S and self-sedation scores. This effect was not related to block height. The proposed mechanism for this independent sedative effect of spinal anesthesia is a decrease in reticular activating system activity due to interruption of ascending afferent sensory input to the brain. Neurological complexities after obstetric focal brain blocks are uncommon occasions. Although central neural blockade does result in neurological complications, it is important to keep in mind that neurological deficits can occur either naturally or during labor and delivery. Both in vitro and in vivo evidence of multi potential cells has been found in the central nervous system of vertebrates. Multi potential cells from the adult central nervous system can be cultured with a similar signaling logic, and factors that control the differentiation of fetal stem cells into neurons and glia have been identified in vitro. The fact that neuro epithelial cells have the capacity to integrate into numerous brain regions is emphasized when cells are transplanted to new locations. Understanding the origin and stability of cell types in the central nervous system will guide the development of therapies for rebuilding damaged or diseased brains.

Conclusion

Spinal anesthesia results from local anesthetic depression of the cervical spinal cord and brainstem. Signs and symptoms include dysphonia, dyspnea, and upper extremity weakness, loss of consciousness, pupillary dilation, hypotension, bradycardia, and cardiopulmonary arrest. Early recognition is the key to management. Treatment includes securing the airway, mechanical ventilation, volume infusion, and pressor support. The patient should receive sedation once ventilation is instituted and the hemodynamics stabilizes. The effects of total spinal anesthesia usually resolve by the conclusion of the surgical procedure, and, unless otherwise contraindicated, the patient can be extubated.