Aim: Through the analysis of two cases of serious neurological complications after triamcinolone acetonide use, this case study warns that the risk of serious neurological complications should be paid attention to when triamcinolone acetonide is used clinically. Presentation of Case: In this paper, we reported two cases of severe neurological complications caused by triamcinolone acetonide. One case was severe hearing loss on the same side after triamcinolone acetonide was injected around the ear to treat scars. After 2 months of treatment, the patient's nausea, vomiting and vertigo improved, but the hearing damage did not improve. The other case was severe complications of lower limb paralysis after triamcinolone acetonide was injected into the spinal canal. Two hours after the injection of the drug, the patient developed paraplegia of both lower limbs. After three months of treatment, it still did not improve. Discussion and Conclusion: Triamcinolone acetonide is a suspension, insoluble in water, with a large number of particles gathering, and the largest particle is greater than 500μm. It has been reported that the medium-sized particles of adrenocortical hormone with a diameter of 51-1000μm can easily block the blood vessels, especially the anterior spinal artery. In clinical practice, we should pay attention to the disastrous neurological complications caused by triamcinolone acetonide hydrochloride, and take relevant preventive and coping measures.

Peripheral neurotoxicity injury caused by local anesthetics is a common complication of clinical anesthesia. The study of its mechanism is helpful to prevent and treat the neurotoxic injury of local anesthetics. Previous studies on peripheral neurotoxicity injury caused by local anesthetics have mainly focused on in vitro cell experiments. Due to the lack of an animal model of peripheral neurotoxicity damage caused by local anesthetics, there are few in vivo experimental studies regarding this topic. Herein, 1% ropivacaine hydrochloride was injected into the sciatic nerve by direct incision and exposure of the sciatic nerve to create a local anesthetic neurotoxic injury model. The results showed that 1% ropivacaine hydrochloride could reduce the lower limb motor score and mechanical paw withdrawal threshold in mice 48 hours after injection. Pathological sections showed that 48 hours after treatment with 1% ropivacaine hydrochloride, the sciatic nerve showed increased axonal edema and degeneration, edema between nerve fiber bundles, increased degeneration of axon and myelin sheath vacuoles, edema of nerve bundle membrane and local degeneration and necrosis, and a large number of inflammatory cells around the nerve adventitia were soaked. The above results show that under open vision, 1% ropivacaine hydrochloride can cause injury to the sciatic nerve after 48 h of treatment, which can simulate the neurotoxic damage of local anesthetics. This animal model provides a research tool for studying the mechanism of neurotoxic injury caused by local anesthetics.