Many patients ask: Why do waist and leg pain occur after semi-anaesthesia surgery? Because of the neurotoxicity of partial anesthesia. Lidocaine has been considered to have a good safety profile when used for spinal anesthesia. In 1991, Rigler first reported 4 cases of cauda equina syndrome after continuous subarachnoid anesthesia with a high proportion of 5% lidocaine. In 1993, Schneider et al reported 4 cases of transient neurotoxic symptoms in patients receiving subarachnoid anesthesia with 5% lidocaine. Neurotoxic syndrome occurs within a few hours to 24 hours after the neuraxial anesthesia wears off and neurological function is fully restored. The clinical symptoms are buttock pain that radiates to both lower limbs. The degree of pain ranges from mild to severe. Usually Disappears naturally within 5 days. The difference from cauda equina syndrome is that cauda equina syndrome presents with lower limb weakness and impaired rectal and bladder function. No abnormal findings were found in neurological examination, MRI and electrophysiological examination in patients with neurotoxic syndrome. The incidence of neurotoxic syndrome caused by lidocaine is much higher than that of other local anesthetics. All local anesthetics have more or less potential neurotoxicity, which depends on the dose and exposure time of the drug. In clinical practice, different local anesthetics (lidocaine, mepivacaine, procaine, tetracaine, bupivacaine, ropivacaine), different concentrations, different specific gravity, and different surgical positions are used for spinal anesthesia. Neurotoxic syndrome has been reported. The reason is not completely clear, but it may be related to the following factors: the inherent spinal neurotoxicity of local anesthetics, especially lidocaine, radiculitis caused by spinal anesthesia can stimulate the nerve roots; puncture injury ; Nerve ischemia; excessive stretch of the sciatic nerve caused by surgical position; puncture needle tip position, adding glucose to cause uneven distribution or redistribution of local anesthetic; muscle spasm and myofascial trigger points caused by early movement of the patient and excitement of spinal dorsal root neurons ; The sacrococcygeal puncture needle tip may be a sensitive site for local anesthetic neurotoxicity. The occurrence of neurotoxic syndrome has nothing to do with local anesthetic concentration, drug specific gravity and osmotic pressure. The mechanism of neurotoxicity of local anesthetics: 1. Direct toxicity of local anesthetics to spinal nerves: Local anesthetics injected into the epidural space and subarachnoid space directly act on nerve cells, causing potential damage to cell membranes and destroying the phospholipids of nerve fiber membranes. and protein structure, which can cause irreversible membrane rupture, also damage the cellular oxidative phosphorylation process, affect mitochondrial transmembrane action potential, and promote programmed death of neurons. After intrathecal injection of local anesthetics of different concentrations, the concentration of glutamate in the cerebrospinal fluid increased, and histopathological changes occurred in the spinal motor neurons, suggesting damage to the anterior and posterior roots of the spinal nerves; it was also observed under the microscope that the formation of vacuoles in the notochord of the spinal cord and movement Neuronal chromatin disintegration. This histopathological change is closely related to sensory function scores and has nothing to do with peak glutamate concentration. Lidocaine is the most neurotoxic, and ropivacaine is the least toxic. The order of neurotoxicity of local anesthetics from low to high is procaine = mepivacaine < ropivacaine = bupivacaine < lidocaine < tetracaine < dibucaine. When regenerated nerves are exposed to local anesthetics, the nerve trunks (growth cones) are rapidly damaged. 2. Nerve ischemia and destruction of the blood-brain barrier: Long-term exposure of neurons to high concentrations of local anesthetics can cause neuronal blood flow to decrease. Adding epinephrine to local anesthetics can further prolong the contact time between spinal nerves and local anesthetics, further reducing blood flow. . Therefore, some people have proposed that local ischemia is the mechanism of nerve damage caused by local anesthesia. Some people believe that local anesthetics inhibit endothelium-dependent vasodilation, interfere with prostaglandin synthesis, cause vasoconstriction, and cause neuronal ischemia and hypoxia, which is considered a type of hypoxic injury. 3. Increase in intracellular calcium ion concentration: Increasing intracellular calcium ion concentration can fully induce delayed nerve death within 5 minutes. In experiments on the electrophysiological changes of local anesthetics on acutely isolated rat spinal dorsal root ganglia, it was found that the toxicity of spinal dorsal root ganglia caused by local anesthetics has nothing to do with the cell membrane sodium channels blocked by local anesthetics. Local anesthetics can cause intracellular calcium ions to increase. The concentration increased, and the degree of increase was consistent with the neurotoxicity of local anesthetics; adding CAPTA to the extracellular fluid resulted in calcium-free extracellular fluid, and the degree of spinal dorsal root ganglion damage caused by local anesthetics was significantly reduced. Therefore, it is believed that , intracellular calcium overload is the cause of local anesthetic spinal neurotoxicity.
4. Lack of neurotrophic factors: Local anesthetics interfere with the axonal transmission of neurotrophic factors, resulting in a lack of neurotrophic factors in the cell body, which may cause delayed nerve damage. Due to the action of enzymes during the process of nuclear fragmentation, it may be the mechanism of delayed nerve damage. The clinical symptoms of neurotoxic syndrome mainly include pain in the lower limbs (including buttocks, thighs and calves) within 24 hours after surgery, after the spinal anesthesia has completely recovered. Most of this pain disappeared on the second day of surgery, and the longest one lasted for 5 days, with only one patient lasting as long as 10 days; no neurological sequelae occurred in any patient; the nature of the pain was burning pain, squeezing pain, or radiating pain. 50% of the patients believe that the pain radiates to the lower limbs, and 50% to 100% of the patients complain of low back pain. These may cause difficulties in the differential diagnosis of neurotoxic syndrome, epidural hematoma, and nerve root injury. Neurotoxic Syndrome and Permanent Neurological Complications Permanent neurological dysfunction, which is different from radicular symptoms, paralysis, and cauda equina syndrome, has been reported after both general and regional anesthesia. Most cases are related to a variety of factors, and there is no significant difference between anesthesia methods. It may be related to existing neuropathological changes, or it may be caused by improper patient positioning. Neurological sequelae associated with regional anesthesia are rare. Possible causes include: intrathecal hematoma caused by the use of anticoagulants, including low molecular weight heparin; spinal cord ischemia; mechanical injury and neurotoxicity. Prevention and Treatment In view of the risk factors for TNS, attention should be paid to the correct positioning of the patient during surgery. For patients who are ambulatory and active early after surgery, intraspinal lidocaine needs to be selected with comprehensive consideration of its efficacy, action time and risk factors. Other local anesthetics such as ropivacaine, levobupivacaine, and chloroprocaine should be the drugs of choice for subarachnoid anesthesia, and treatment with tromethamine and nonsteroidal anti-inflammatory drugs may be effective.