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Adverse effects of neuraxial analgesia and anesthesia for obstetrics 1 de 20 Official reprint from UpToDate® Print | Back Adverse effects of neuraxial analgesia and anesthesia for obstetrics Author Gilbert J Grant, MD Section Editor David Hepner, MD Deputy Editor Vanessa A Barss, MD Last literature review for version 17.1: enero 1, 2009 | This topic last updated: enero 28, 2009 INTRODUCTION — Regional anesthetic techniques, such as epidural and spinal anesthesia, provide the most effective means of pain relief during labor, which is likely the most severe pain that a woman experiences during her lifetime [1]. The prevention and treatment of adverse effects of these techniques will be reviewed here. Specific issues related to pain management of labor and delivery and administration of neuraxial anesthesia are discussed separately. (See "Pharmacologic management of pain during labor and delivery" and see "Neuraxial analgesia and anesthesia for labor and delivery: Techniques"). SYSTEMIC TOXICITY — Systemic toxicity of local anesthetics is related to high plasma drug concentrations. The most common etiology is accidental injection of local anesthetic into a blood vessel. Systemic toxicity manifests in the central nervous system (CNS) as tinnitus, disorientation, and (ultimately) seizures; in the cardiovascular system toxicity manifests as hypotension, dysrhythmias, and cardiac arrest. CNS toxicity typically precedes cardiovascular toxicity, thus patients may experience cerebral signs without hemodynamic compromise. Bupivacaine toxicity does not adhere to this sequence; cardiac toxicity may occur in the absence of CNS toxicity [2]. High plasma drug levels may cause systemic toxicity after epidural administration, but are unlikely after spinal administration because lower doses of drug are given. The likelihood of systemic toxicity can be reduced by aspirating the catheter before injecting to help ascertain that its distal aperture(s) is (are) not located within a blood vessel. Other measures to reduce the risk of toxicity include adding epinephrine to the solution to delay intravascular absorption, using a test dose, injecting a local anesthetic with a lower toxicity profile, reducing the total dose injected, and administering the dose incrementally. If CNS signs of local anesthetic toxicity develop, the injection should be stopped immediately. Seizures cay be treated with a small dose of benzodiazepine (eg, midazolam 2 to 5 mg) or barbiturate (eg, thiopental 50 to 75 mg). Oxygen should be administered, as seizure activity increases maternal oxygen consumption, which will decrease oxygen delivery to the fetus. The patient should be protected from injuring herself during the seizure. In the event of cardiovascular toxicity, advanced cardiac life support (ACLS) should be provided with certain considerations specific to local anesthetic toxicity. Airway management is critical, as cardiotoxicity is exacerbated by hypercapnia, hypoxia, and acidosis. Dysrhythmias are difficult to control, especially those resulting from bupivacaine toxicity. Currently, amiodarone, a primary drug in the ACLS arrhythmia treatment algorithm, is the favored treatment for severe bupivacaine-induced arrhythmias [3]. Early administration of lipid emulsion is another component in resuscitation of bupivacaine-induced cardiotoxicity. However, the dysrhythmias are often recalcitrant to therapy; emergency cardiopulmonary bypass may be lifesaving until the drug dissociates from cardiac tissue [4]. Treatment of hypotension with vasopressin, 40 units IV, rather than epinephrine is preferred because epinephrine may exacerbate local anesthetic-induced arrhythmias. Other drugs that should be avoided in the management of local anesthetic induced cardiotoxicity include calcium channel 12/06/2009 22:21

Adverse effects of neuraxial analgesia and anesthesia for obstetrics

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