Title : Transient neurological symptoms and abnormal Magnetic Resonance Imaging (MRI) changes of the brain, following Sugammadex (SUG) reversal of Neuromuscular Blockade (NMB).
Abstract:
Introduction: SUG revolutionized anesthesia by offering rapid, effective reversal of non-depolarizing neuromuscular blocking agents (NMBAs). SUG works by encapsulating NMBAs, thereby reducing their free plasma concentration. However, post-marketing surveillance identified rare occurrences of early awakening, paradoxical prolonged NMB, and anaphylaxis. Neurological side effects, including anxiety, depression, dizziness, headaches, numbness and throat spasms have been reported. To our knowledge, this is the first reported case of transient neurological symptoms and abnormal MRI changes, following SUG administration.
Case Presentation: 65-year-old female underwent endoscopic resection of gastric lesion under general anesthesia. The anesthetic regimen included Rocuronium. During the procedure, moderate bleeding occurred, systolic blood pressure subsequently dropped, necessitating the use of phenylephrine. SUG was used to reverse the NMB. Preoperatively, she was alert, oriented with intact neurological function. However, postoperatively she developed a rightward head turn, gaze deviation, incomprehensible speech, inability to follow commands, left-sided hemineglect and motor weakness. Differential diagnosis included acute ischemic stroke, seizures or medication affect. Day 1, Unchanged neurological exam with Midazolam challenge followed by continuous EEG (cEEG) ruled out seizures. MRI with diffusion-weighted imaging (DWI) showed faint hyperintensity in the right temporal cortex. Days 2 and 3, her neurological status continued to improve On Day 4, despite an improved neurological exam repeat DWI MRI revealed evolving hyperintensity in bi-temporal cortex. By Day 5, she returned to baseline without residual deficits. A follow-up MRI on Day 21 showed complete resolution. Notably, five months earlier, she underwent another procedure, which was the first instance when SUG was used as a reversal agent. A prolonged wake-up period, right-sided ocular drift, right-sided head tilt, and impaired speech were reported. However, these symptoms were short-lived.
Discussion: Cortical-based DWI and T2 alterations can result from hypoxia, ischemia, metabolic dysfunction, infections, seizures, neuroinflammation, and neurotoxins. However, the absence of hemodynamic instability or anoxic events, transient nature of the DWI changes and the rapid reversal of symptoms makes global anoxia unlikely. Phenylephrine-induced local vasospasm could be another possibility, although the large areas of restricted diffusion seen in this would be expected from a proximal vasospasm, which was not evident on imaging. The post-anesthetic presentation, rapid symptom resolution without immunomodulatory therapy, and the overall clinical context argue against neuroinflammation or infectious etiology. Naranjo score of 6 suggests a probable association between SUG and the adverse neurological reaction. The post-anesthetic presentation and resolution of symptoms upon discontinuation of the drug strengthens the argument. Notably, neurological symptoms occurred following the only two occasions in which SUG was used to reverse Rocuronium. In contrast, no adverse effects were reported when Rocuronium was reversed using neostigmine in previous procedures. The mechanism of SUG causing transient neurological symptoms with MRI changes is unclear, rat nerve cell culture studies indicate possibility of neurotoxicity.
