• M A Rosen, C L Baysinger, S M Shnider, P A Dailey, M Norton, J D Curtis, M Collins, and R L Davis.
• Anesth. Analg. 1983 Sep 1;62(9):802-8.

AbstractRecent case reports describing prolonged neurologic deficit after accidental spinal anesthesia with large volumes of 2-chloroprocaine have led to the suggestion that chloroprocaine may be more likely to cause such complications than other local anesthetics. We evaluated the neurologic effects of lumbar puncture alone and of large-volume subarachnoid administration of 2-chloroprocaine (3%), bupivacaine (0.75%), lidocaine (2%), Elliott's solution B (which is similar to CSF), or the carrier solution of 2-chloroprocaine (Nesacaine) in 48 sheep and 8 monkeys. Cerebrospinal fluid of sheep was collected on days 1 and 7 for biochemical and biological analyses, and CSF pressures of monkeys were recorded before and after injection. Animals were observed for neurologic deficits for seven days. Twelve sheep were unable to stand. Monkeys, on the other hand, had no apparent neurologic deficits. Autopsies revealed that 5 of the 12 sheep had lumbar subpial demyelination with macrophage infiltration: two of the five had received lidocaine; two received 2-chloroprocaine; and one had only a lumbar puncture. Two other sheep also had subpial demyelination: one had received lidocaine and one received 2-chloroprocaine. Three of the eight monkeys had lumbar subpial demyelination with macrophage invasion; two had received bupivacaine, and one received 2-chloroprocaine. No solution produced significant abnormalities in sheep CSF composition. We conclude that no local anesthetic or solution was more neurotoxic than another when injected in large volumes into the subarachnoid space of sheep or monkeys.

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