Enzymatic Evaluation of General Anesthesia-Induced Neurotoxicity in Aneurysmal Subarachnoid Hemorrhage Patients

Keywords

CSF - SAH - caspase-3

Introduction: Animal and observational human studies suggest that general anesthetics cause neurotoxic changes in developing brain. No direct evidence of neurotoxicity in adults exposed to general anesthetics is available. Proposed mechanism of neurotoxicity is neuroapoptosis. Caspase-3 is the biomarker.

Aim: Estimation of changes in cerebrospinal fluid (CSF) and serum caspase-3 in subarachnoid hemorrhage (SAH) patients exposed to general anesthetics.

Methodology/Description: Prospective randomized double-blind study—from January 2016 to May 2017. Thirty-two patients with good grade aneurysm—clipping and endovascular coiling were recruited and randomized to four groups for the maintenance of anesthesia—propofol, isoflurane, sevoflurane, and desflurane. Lumbar drain preoperatively was inserted for CSF sampling. Standard monitors and induction techniques were used. Concentrations of anesthetic agents were compared using state entropy-maintained bet ween 40 and 60. CSF and serum samples collected at base line, 1 hour after exposure to anesthesia, after the cessation of anesthesia. Samples were centrifuged, stored and later analyzed using ELISA.

Results: CSF caspase-3 levels significantly decreased from baseline to 1 hour after exposure to anesthetic agents, which then reached to baseline levels after the cessation of anesthesia. These changes were statistically significant and comparable between all the groups. Serum caspase-3 levels significantly increased from baseline to 1 hour after exposure to anesthetic agents, which then reached to baseline levels after the cessation of anesthesia. These changes were statistically significant and comparable between all the groups.

Conclusion: Intravenous and inhalational anesthetic agents have same effect on the serum and CSF caspase-3 levels. The reduction in CSF caspase-3 levels suggests the role of anesthesia in reduction of apoptotic mechanism. Increase in serum caspase-3 levels after exposure may be due to caspase-dependent apoptosis in peripheral mononuclear cells secondary to inflammatory stress response.

• References

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