Potential neurotoxic effect of dexamethasone used as adjuvant to local anesthetics during peripheral nerve blockade

Background: The use of peripheral nerve blocks for anesthesia and postoperative analgesia has increased siginificantly in recent years. Many additives to local anesthetics to prolong the duration of analgesia for peripheral nerve blocks have been studied. Dexamethasone has been studied as an effective adjuvant to prolong the analgesia duration of local anesthetics in peripheral nerve block. However, the route of action for dexamethasone and its potential neurotoxicity are still unclear. The aim of this study is to determine possible toxic effects of dexamethasone on peripheral nerve tissue and the dependence of these effects on the place of intraneural applications. Methods and Materials: A rat sciatic nerve block model was used.  The study was conducted in accordance with the principles of laboratory animal care and was approved by the Laboratory Animal Care and Use Committee. Fifty adult Wistar rats (300 g) both sexes were studied. After induction of general anesthesia, the sciatic nerve was exposed bilaterally. Sciatic nerves were randomly assigned by the method of sealed envelopes to recive: intraneural, intrafascicular 2 mL of lidocaine with dexamethasone  (n=25), intraneural, extrafascicular injection  2 mL of lidocaine with dexamethasone (n=25),  perineural 2 mL of lidocaine with dexamethasone  (n=25) and perineural 2 mL of saline 0.9%  (n=25). Injection pressure was continuosly recorded using an in-line digital manometer. Increased injection pressure was used to distinguish intrafascicular from extrafascicular inrtaneural injections. After injection, the rats were awakened and subjected to serial neurologic examinations. Neurologic examination protocol was followed to determine proprioception by tactile placement response, motor function by extensor postural thrust and nociception by withdrawal reflex. On day 3 of the experiment, the animals were sacrificed and the neural tissue histologically examined. Results: Intraneural injections (intrafasciculary and extrafasciculary) of lidocaine in combination with dexamethasone caused neurological deficits and severe pathohistological damage to nerve fibers. All perineural injections (independent of the tested solution), combined with low injection pressure showed a uniform changes, with minimal histological deviation of the normal structure of the nerve fiber. Conclusions: When applied intraneuraly dexamethasone in combination with lidocaine caused nerve fiber damage. However, future studies are required to elucidate the most effective route and optimum dosing range for dexamethasone’s use in this field.