Rationale:Ropivacaine and lidocaine are amide local anesthetics (LAs) commonly used for brachial plexus block, and with lower central nervous system (CNS) toxicity and cardiovascular toxicity than bupivacaine. However, emerging evidence suggests that neurotoxicity associated with these LAs may still occur, particularly in high-risk populations such as uremic patients, who may exhibit altered drug metabolism and increased susceptibility to adverse effects. Therefore, we aimed to report and analyze 2 cases of CNS toxicity following ropivacaine and lidocaine administration in this population. The findings will contribute to a better understanding of the safety profile of these LAs in uremic patients.Patient concerns:We describe 2 cases of CNS toxicity in uremic patients following brachial plexus blocks induced by a total of 20 mL 0.375% ropivacaine mixed with 1% lidocaine. Both patients became unconscious and failed to respond to verbal after brachial plexus blocks. However, their vital signs were stable and no signs of cardiovascular toxicity were observed.Diagnoses:The 2 patients were diagnosed with CNS toxicity following brachial plexus block. The diagnosed of CNS toxicity was based on:(1) Unconscious and failed to respond to verbal after LAs injection.(2) Exclusion of alternatives: no hypoglycemia; normal arterial blood gases; absence of focal neurological signs suggesting stroke or epilepsy.(3) Supporting factors: reduced renal clearance may lead to larger plasma concentrations of LAs in uremic patients; hypertension likely resulted from sympathetic activation during CNS toxicity.Diagnoses:The 2 patients were diagnosed with CNS toxicity following brachial plexus block. The diagnosed of CNS toxicity was based on:(1) Unconscious and failed to respond to verbal after LAs injection.(2) Exclusion of alternatives: no hypoglycemia; normal arterial blood gases; absence of focal neurological signs suggesting stroke or epilepsy.(3) Supporting factors: reduced renal clearance may lead to larger plasma concentrations of LAs in uremic patients; hypertension likely resulted from sympathetic activation during CNS toxicity.Diagnoses:The 2 patients were diagnosed with CNS toxicity following brachial plexus block. The diagnosed of CNS toxicity was based on:(1) Unconscious and failed to respond to verbal after LAs injection.(2) Exclusion of alternatives: no hypoglycemia; normal arterial blood gases; absence of focal neurological signs suggesting stroke or epilepsy.(3) Supporting factors: reduced renal clearance may lead to larger plasma concentrations of LAs in uremic patients; hypertension likely resulted from sympathetic activation during CNS toxicity.Diagnoses:The 2 patients were diagnosed with CNS toxicity following brachial plexus block. The diagnosed of CNS toxicity was based on:(1) Unconscious and failed to respond to verbal after LAs injection.(2) Exclusion of alternatives: no hypoglycemia; normal arterial blood gases; absence of focal neurological signs suggesting stroke or epilepsy.(3) Supporting factors: reduced renal clearance may lead to larger plasma concentrations of LAs in uremic patients; hypertension likely resulted from sympathetic activation during CNS toxicity.Interventions:Both patients were given oxygen via a mask at a rate of 3 L/min, standard monitoring, and close observation. Arterial blood gas analysis was immediately conducted.Outcomes:They were both fully conscious 2 hours after the brachial plexus block. Vascularized injection sites, uremic status, preexisting cardiac dysfunction, and the mixing of the 2 local anesthetics may be the reasons for the occurrence of the CNS toxicity.Lessons:When performing peripheral nerve block, it is necessary to identify whether there are risk factors that increase the incidence of local anesthetic systemic toxicity.