Effects of Apolipoprotein E Polymorphism on Cerebral Oxygen Saturation After Traumatic Brain Injury.

Zhimin Wu,Li Jiang,Senjie Xiong,Xiaochuan Sun,Yan Zhan,Quanhong Shi,Wei Dan,Yanfeng Xie

doi:10.3389/fneur.2020.539627

Abstract

Objective: To investigate the effects of the apolipoprotein E gene (APOE) on the cerebral oxygen saturation of patients after traumatic brain injury (TBI).Methods: Clinical data of 114 patients with TBI and 54 normal people were collected. The APOE genotypes of all subjects were determined by quantitative fluorescent polymerase chain reaction (QF-PCR). The regional cerebral oxygen saturation (rScO2) of TBI patients and normal people were monitored by near-infrared spectroscopy (NIRS).Results: The mean rScO2 of patients was (55.06 ± 7.60)% in the early stage of TBI, which was significantly lower than that of normal people (67.21 ± 7.80)% (P < 0.05). Single-factor and multifactor logistic regression analyses showed APOEε4 was an independent risk factor that caused the early decline of rScO2 in TBI patients. Furthermore, in the TBI group, the rScO2 of APOEε4 carriers (52.23 ± 8.02)% was significantly lower than that of non-ε4 carriers (60.33 ± 7.12)% (P < 0.05). But in the normal group, no significant differences in rScO2 were found between APOEε4 carriers and non-carriers.Conclusion: The rScO2 may be significantly decreased after TBI, and APOEε4 may be a risk factor for decreased rScO2 in the early stage of TBI.

Highlights

Traumatic brain injury (TBI) is a common disease with high disability and mortality in the neurointensive care unit (NICU) [1,2,3]
Cerebral blood flow often decreased after TBI, which may lead to ischemia and hypoxia in brain tissue and result in irreversible brain damage
We found the level of GCS and Marshall CT Class were the risk factors affecting rScO2 in the early stage of TBI, indicating that rScO2 was related to the severity of TBI

Summary

Introduction

Traumatic brain injury (TBI) is a common disease with high disability and mortality in the neurointensive care unit (NICU) [1,2,3]. Cerebral blood flow often changes after TBI, which may lead to a series of pathological responses and irreversible brain damage [4, 5]. TBI is often followed by ischemia and hypoxia, resulting in severe neurological impairment and death. Previous studies have shown that ischemia and hypoxia are strongly associated with poor outcomes [6, 7], and a decrease of cerebral oxygen saturation usually indicates the possibility of cerebral ischemia and hypoxia. Cerebral oxygen saturation monitoring is an important method to evaluate the condition of TBI patients during neurointensive care [8].

Methods

Results

Discussion

Conclusion