This study was designed to determine whether systemic absorption plays any role in the antinociceptive effect of epidural (EP) sodium S(+)-ibuprofen (IB). One week after surgical implantation of EP catheters, six rabbits were given EP injections with either normal saline (NS) 0.4 mL or IB 10 mg in 0.4 mL NS (Group 1) on separate days. Each animal was injected with IB 10 mg intravenously (IV) on another day. Six control rabbits (Group 2) had neither surgery nor any injection. Analgesic testing was performed using electric stimulation through two electrocardiogram (ECG) skin electrodes with built-in adhesive, attached to shaved hip areas using 50 V, 1 Hz, 3 ms, before and 0.5, 1, 2, and 3 h after injection in Group 1, and in similar times in controls. The 95% confidence intervals (CI) of the mean difference between baseline and maximal nociceptive response latency of all groups were compared using analysis of covariance (ANCOVA) adjusted for baseline measurements. This comparison covered all possible pairs among all groups. Significant antinociceptive effects were seen after EP IB but not after control or IV IB. Neither motor dysfunction nor evidence of systemic toxicity or neurotoxicity was observed in any animal. (Anesth Analg 1995;80:92-6)

This study was undertaken to illustrate the potential for subarachnoid injection during retrobulbar block as a cause of respiratory arrest. Cadaver orbits were used to document the connection between the optic nerve sheath and the subarachnoid space. Following dissections of the orbits on one side of 24 cadavers, the optic nerve sheaths were identified and injected with 0.5 ml of water for measurement of pressure generated during injection. This was followed by intrasheath injection of equal volume of methylene blue for demonstrating the subarachnoid space surrounding the optic nerves. All injections were performed with a 1-ml syringe with a one-and-one-half-inch 22-G needle over a period of 10 s. The blue dye was found to track along the subarachnoid space of the optic nerve sheath to the chiasmatic cistern in the middle cranial fossa. Retrobulbar injections were performed on the contralateral undissected orbits and intrascleral injections were performed on undissected eyes. The size of the syringes, the gauge of the needles, and the speed of injection were uniform for all injections. The pressure generated by injection into the optic nerve sheath or intrascleral injection (approximately 138 mmHg) was three- to fourfold that produced by injection into the retrobulbar adipose tissue (approximately 35 mmHg) (P less than 0.05). The authors conclude that any resistance encountered during retrobulbar block should serve as a warning signal, mandating redirection of the needle, in order to prevent subarachnoid injection.

Chronic neurological deficits have been described in patients after presumed accidental subarachnoid injection of 2-chloroprocaine-CE (Nesacaine-CE; N-CE) intended for epidural block. This study investigated the possible role of pure 2-chloroprocaine (2-CP) and sodium bisulfite, two components of Nesacaine-CE, in causing these complications when injected separately into the lumbar subarachnoid space of neurologically intact awake rabbits. Repeated 2–4-mg spinal anesthetic doses of pure 2-CP in lactated Ringer's solution did not produce chronic hindlimb paralysis even though accumulated doses reached 50 mg. However, 1.2–2.4 mg of sodium bisulfite, the antioxidant in N-CE added to prolong shelf-life, resulted in irreversible hindlimb paralysis in 12 out of 14 animals. This amount of bisulfite is contained in 12–24 mg of 2% N-CE. The demonstration that persistent paralysis resulted from low dosages of sodium bisulfite contained in commercially available 2-CP requires revaluation of the suitability of this antioxidant for products prepared for intrathecal use.