Consider Chloroprocaine for Regional Blockade When Appropriate—It Is a Rapid-Onset Local Anesthetic with Low Systemic Toxicity
Joshua M. Zimmerman MD
Randal O. Dull MD, PhD
2-Chloroprocaine is an ester local anesthetic introduced into clinical practice in 1951; the initial paper described >200 successful spinal anesthetics. Despite its initial use in spinal anesthetics, 2-chloroprocaine found its greatest use in labor epidurals because of its rapid metabolism and low toxicity to both mother and fetus. The widespread use and availability of intrathecal lidocaine, however, apparently prevented most anesthesiologists from adopting 2-chloroprocaine as their spinal drug of choice. After decades of use, a report of 8 patients who suffered neurologic deficits after “epidural” anesthesia with 2-chloroprocaine was published. It appears that at least half of these patients had inadvertently received intrathecal administration, and this raised the question of neurotoxicity. It was not clear at the time whether the etiology was the local anesthetic or the sodium bisulfite preservative. A flurry of publications have attempted to address this issue of toxicity, establish a dose-response curve, and evaluate various adjuncts to 2-chloroprocaine as an effective spinal anesthetic and as a replacement for intrathecal lidocaine.
CHEMICAL PROPERTIES
2-Chloroprocaine contains a lipophilic aromatic ring bound to a hydrophilic tertiary amine by an ester linkage.
CLINICAL PHARMACOLOGY
Like all local anesthetics, chloroprocaine inhibits the generation and propagation of nerve impulses by increasing the threshold for electrical excitation, slowing conduction, and reducing the rate of rise of the action potential. Being an ester, 2-chloroprocaine is metabolized by plasma cholinesterase (and red cell esterase, to a lesser extent) into an alcohol and a para-aminobenzoic acid. Chloroprocaine is metabolized much more quickly than procaine or tetracaine, contributing to its low systemic toxicity. Its plasma half-life is approximately 21 seconds in adults and 43 seconds in neonates. Any condition, however, that inhibits the activity or quantity of pseudocholinesterase will prolong action and increase toxicity (e.g., liver disease,
atypical cholinesterase). The kidney is the primary route of excretion for chloroprocaine metabolites.
atypical cholinesterase). The kidney is the primary route of excretion for chloroprocaine metabolites.
CLINICAL USE
Intrathecal Use.
Though chloroprocaine was initially described as a spinal anesthetic, it has fallen into disfavor in the past two decades because of concerns about neurotoxicity. This notion has recently been challenged by a series of studies. The future of 2-chloroprocaine as a medication for intrathecal use is currently in flux, and further studies are underway to further define its use. It was initially shown that 2-chloroprocaine was an appropriate substitute for intrathecal lidocaine, providing similar quality, height, and duration of block when compared to equal doses of lidocaine. A later study showed that 30, 45, and 60 mg of 2-chloroprocaine yielded mean maximal block heights of T7, T5, and T2 and block duration of 98, 116, and 132 minutes, respectively. When 20 mcg of fentanyl was added, the duration of sensory but not motor blockade was lengthened (by 25 minutes). When epinephrine was added to 2-chloroprocaine, a transient flulike syndrome was reported, leading to the recommendation to avoid this combination. When compared to other local anesthetics for ambulatory surgery, 2-chloroprocaine provides adequate duration and quality of blockade, with significantly faster resolution than bupivacaine and less risk of transient neurological syndrome (TNS) than lidocaine. Considerable controversy still surrounds the issue of potential neurotoxicity of spinal 2-chloroprocaine. The prevailing conclusion of a series of animal studies was that the preservative sodium bisulfite, possibly in combination with low pH, was responsible for several early episodes of irreversible blockade. However, at least one study suggests that 2-chloroprocaine may itself be neurotoxic, and that sodium bisulfite may actually be neuroprotective.
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