Good morning or good afternoon. My name is Dr. Michael Beldoestel. I'm a PM&R resident at the University of Louisville. Our case today is paraplegia and chemical meningitis after spinal anesthesia. Our patient is a 69-year-old female with no prior neurologic disease. She was undergoing a right knee replacement and had spinal anesthesia. It was anatomy-guided block at L3-4 with bupivacaine. The patient tolerated the anesthesia and the procedure went well. However, after the procedure and the hours to come, she began to complain of chest pain, bilateral arm pain, numbness tingling, and lack of movement in her lower extremities. Her physical exam was notable for absent lower extremity reflexes and profound weakness. She underwent extensive workup at the acute care facility, including blood work, brain and spine imaging, and lumbar puncture, all of which was largely unremarkable. She remained at the acute care facility for further workup. On post-op day 8, she had a repeat brain MRI that showed multiple areas of acute ischemia consistent with meningitis. On post-op day 10, she had a repeat MRI thoracolumbar spine that showed abnormal T2 cord signal, T3L2, secondary to meningiomyelitis. The patient was discharged with a spinal cord injury to inpatient rehab. When she came to inpatient rehab, she was determined to be a T2-AISC. After three weeks of inpatient rehab and therapy, she was discharged as a T7-ASD. She had marked functional improvement, but still had deficits. If we move to the center of the screen, we can review some of her imaging. Looking at A and B, we see thoracolumbar, MR, T2, sagittal fascia, and addiction with images. Looking at A, we see the thoracic spine, and B, we see the lumbar spine. The yellow arrows indicate the abnormal signal changes that are seen in our patient's spinal cord. Moving to images C and D on the right of the poster, we see MR, T2, transverse trace cuts. Image C is the right temporal lobe, and D shows the right frontal lobe. The areas marked are the areas of ischemia consistent with meningitis. Reviewing our case now, our patient had chemical meningitis, and this is an uncommon adverse drug reaction due to spinal anesthesia, specifically with Vivacaine. Its incidence is less than 0.01. Chemical meningitis is a diagnosis of exclusion. The workup includes a lumbar puncture with CSF analysis, appropriate imaging studies, and, as always, a thorough history, specifically of medications and surgeries. If you are clinically suspicious of chemical meningitis, discontinue the possible offending drug. Treat for suspected bacterial meningitis until the cultures have resulted, and provide supportive care. Two thoughts for causing chemical meningitis are a delayed hypersensitivity reaction in a direct chemical meningeal irritation. More commonly, offending drugs are NSAIDs, antibiotics, and IVIG. Common presenting symptoms are meningeal signs such as headache, nausea, vomiting, and nuchal rigidity. Neurologic symptoms and deficits only occur about 18% of the time. Symptoms typically improve when sensation of the drug occurs. However, the severity and duration of the symptoms will vary widely among patients. Recovery can happen as quickly as a few days or as slow as several weeks. Unfortunately, our patient is about one year from her accident and still has persistent and profound neurologic deficits. Specifically, she still has some left-sided weakness. She still has neurogenic bowel and bladder requiring intermittent caths, and she still has neuropathic pain that require medication. Chemical meningitis is a rare but severe pathology, and a high level suspicion is required to diagnose and treat this to prevent long-term functional deficits. Thank you everyone for your time, and if you have any questions, you can email me at michael.delbusto at louisville.edu. Thank you. Have a great day. you

paraplegia

chemical meningitis

spinal anesthesia

knee replacement

functional improvement