International Journal of Clinical Case Reports, 2025, Vol.15, No.6, 259-270 http://medscipublisher.com/index.php/ijccr 260 This study will analyze the value of brain injury biomarkers in addressing the nursing challenges after cardiopulmonary resuscitation. Some biomarkers can detect hypoxic-ischemic brain injury at an early stage and predict recovery. They not only often appear earlier than physical symptoms but also reflect the severity and changing trend of the injury. Biomarkers such as Nf-L and NSE have a good predictive effect on the poor recovery of neurological function within a specific period after the recovery of heartbeat and respiration. If molecular biomarker monitoring is incorporated into the post-cardiopulmonary resuscitation diagnosis and treatment process in the emergency department, it is expected to more accurately classify the risk level of patients, provide guidance for treatment, and also help doctors and family members communicate about the recovery prospects of patients. There are still many difficulties in achieving standardization of detection and analysis, eliminating interfering factors to interpret the results, and converting biomarker data into actual treatment plans. As research progresses, the role of biomarker monitoring in post-cardiopulmonary resuscitation care will become increasingly significant, providing new ideas for improving the rehabilitation outcomes of such high-risk patients. 2 The Mechanism and Biomarker Basis of Brain Injury after Cardiopulmonary Resuscitation 2.1 Ischemia-reperfusion and biomarkers The pathophysiology of brain injury after cardiopulmonary resuscitation (CPR) is mainly driven by ischemia-reperfusion injury. When cardiac arrest occurs, cerebral blood flow is interrupted, oxygen and glucose are rapidly depleted, energy-dependent ion pumps fail, cells depolarize and cytotoxic edema appears. After the circulation was restored, reperfusion further exacerbated neuronal damage through a series of biochemical events such as calcium overload, excitotoxicity, and reactive oxygen species (ROS) production (Perkins et al., 2024; Jiang et al., 2025). This biphasic process not only leads to the death of direct neurons but also lays the foundation for the secondary injury mechanism that occurs several hours to several days after resuscitation. Biomarkers released during ischemia-reperfusion can reflect the degree and type of damage to nerve cells and glial cells. Neuron-specific enolase (NSE) is a kind of glycolase specific to nerve cells. It enters the blood after the death of nerve cells and is closely related to the poor recovery of the nervous system in adults and children (Fink et al., 2022; Kaminoska et al., 2025). Similarly, neural filament light chain (Nf-L) is a marker of axonal injury and has a strong predictive effect on poor prognosis, especially within 48 hours after the restoration of spontaneous circulation (Hoiland et al., 2022). Proteomic studies have also identified some candidate markers, such as calcitonin-2, which is associated with neurodegeneration and may become a new indicator of early neurological prognosis after cardiac arrest (Yao et al, 2025; Zhu et al., 2025). The dynamic changes of these biomarkers can reflect the pathological conditions of ischemia-reperfusion and provide assistance for clinical monitoring and prognosis prediction. 2.2 Inflammation, oxidative stress and biomarkers Restoring blood flow after ischemia can trigger a strong inflammatory response, specifically manifested as the activation of glial cells originally present in the brain, the entry of immune cells from other parts of the body into the brain, and the massive release of pro-inflammatory factors such as IL-6 and TNF-α (Wang et al., 2023; Angulo et al., 2025). This kind of neuroinflammation can aggravate nerve cell damage through programmed cell death such as microglial activation, oxidative stress, necroptosis, and pyroptosis (Wang et al., 2021; Jiang et al., 2025). Excessive reactive oxygen species (ROS) in the body can lead to oxidative stress, further damaging cell structure and disrupting oxidative balance, making the initial ischemic damage even more severe. Some studies use biomarkers that can reflect inflammation and oxidative stress to assess recovery. In the early stage of cardiac arrest, high mobility histone 1 (HMGB1) and IL-6 increase significantly and are associated with neurological recovery, indicating that they are related to secondary brain injury. When astrocytes are damaged, they release glial fibrillary acidic protein (GFAP). S100 calcium-binding protein B (S100B) is associated with abnormal functions of astrocytes and blood-brain barrier (BBB), and it also increases when there is inflammation and oxidative stress in the nerves (Fink et al., 2022; Hoiland et al., 2022; Kaminoska et al., 2025). The newly discovered biomarker calcitonin-2 is closely associated with neurodegeneration and inflammation, enriching the types of biomarkers for brain injury after cardiopulmonary resuscitation (Yao et al., 2025). These markers not only reflect the underlying pathological changes but also provide clear targets for treatment and monitoring.
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