Abstract
The aim of this study is to find out the neuroprotective mechanism of lidocaine in epidural haematoma (EDH) in moderate brain injury. The effects are measured by the level of interleukin-6 (IL-6) and phospholipase A2 (PLA2). This study is done in forty epidural haematoma patients with moderate brain injury. The objects are divided into two groups, group A with NaCl 0.9% infusion only (control) and group B with NaCl 0.9% infusion combined with lidocaine 1 mg/kg/hr. The blood samples were taken right before induction and two hours after infusion. The result shows that the level of IL-6 and PLA2 is significantly low in group B (p<0.005) with Mann Whitney and Dependent t test. The decreasing level of IL-6 and PLA2 is related with the dose of lidocaine. The inhibition mechanism of IL-6 and PLA2 secretion by lidocaine is considered as a responsible factor in inflammation and brain cells damage. Summary • Infusion of lidocaine 1 mg/kg/hr will decrease the level of IL-6 in moderate brain injury • Infusion of lidocaine 1 mg/kg/hr will decrease the level of PLA2 in moderate brain injury
Highlights
Traumatic Brain Injury (TBI) is considered as a daily case
In a severe TBI, there is excessive inflammation process and so many pro-inflammation cytokines are released (TNF-α & IL-6) that will lead to cellular apoptosis and necrosis
The treatment group is the group that gained in the lidocaine infusion fluids 0.9% NaCl and the control group only received 0.9% NaCl infusions without lidocaine. 2 hours post infusion, serum lidocaine levels examined in both groups
Summary
Traumatic Brain Injury (TBI) is considered as a daily case. Traumatic Brain Injury is defined as non-degenerative and non-congenital disorder that is caused by an outer mechanical mass. This injury will result in whether temporary or permanent impairment in cognitive or even psychosocial function that will lead to unconsciousness status. The recent management is just to impede to secondary brain injury that will activate series of ischemic cascades along with pro-inflammation cytokine release and free radicals [3]. In a severe TBI, there is excessive inflammation process and so many pro-inflammation cytokines are released (TNF-α & IL-6) that will lead to cellular apoptosis and necrosis. Many drugs had been proposed as a potent drug in bringing down the permanent neuronal damage, but only few are proven clinically [4]
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