Abstract
Traumatic Spinal Cord Injury (TSCI) is debilitating and often results in a loss of motor and sensory function caused by an interwoven set of pathological processes. Oxidative stress and inflammatory processes are amongst the critical factors in the secondary injury phase after TSCI. The essential trace element Zinc (Zn) plays a crucial role during this phase as part of the antioxidant defense system. The study aims to determine dynamic patterns in serum Zn concentration in patients with TSCI and test for a correlation with neurological impairment. A total of 42 patients with TSCI were enrolled in this clinical observational study. Serum samples were collected at five different points in time after injury (at admission, and after 4 h, 9 h, 12 h, 24 h, and 3 days). The analysis of the serum Zn concentrations was conducted by total reflection X-ray fluorescence (TXRF). The patients were divided into two groups—a study group S (n = 33) with neurological impairment, including patients with remission (G1, n = 18) and no remission (G0, n = 15) according to a positive AIS (American Spinal Injury Association (ASIA) Impairment Scale) conversion within 3 months after the trauma; and a control group C (n = 9), consisting of subjects with vertebral fractures without neurological impairment. The patient data and serum concentrations were examined and compared by non-parametric test methods to the neurological outcome. The median Zn concentrations in group S dropped within the first 9 h after injury (964 µg/L at admission versus 570 µg/L at 9 h, p < 0.001). This decline was stronger than in control subjects (median of 751 µg/L versus 729 µg/L, p = 0.023). A binary logistic regression analysis including the difference in serum Zn concentration from admission to 9 h after injury yielded an area under the curve (AUC) of 82.2% (CI: 64.0–100.0%) with respect to persistent neurological impairment. Early Zn concentration dynamics differed in relation to the outcome and may constitute a helpful diagnostic indicator for patients with spinal cord trauma. The fast changes in serum Zn concentrations allow an assessment of neurological impairment risk on the first day after trauma. This finding supports strategies for improving patient care by avoiding strong deficits via adjuvant nutritive measures, e.g., in unresponsive patients after trauma.
Highlights
Traumatic spinal cord injury (TSCI) is considered as one of the most severe injuries in traumatology.As it predominantly affects young patients [1,2], it requires a lot of experience, practice, and knowledge to assure the best possible care and increase the chances of a fortunate outcome for the patient.The physical and psychosocial [3] consequences for patients are debilitating as well as the economic consequences, which are a concern for the patient, his or her environment, society, and health care institutions [4]
A total of 42 patients with a traumatic spinal cord injury were studied over 3 months
Data from the current study indicate some considerable alterations in the neuronal damage after the TSCI
Summary
Traumatic spinal cord injury (TSCI) is considered as one of the most severe injuries in traumatology.As it predominantly affects young patients [1,2], it requires a lot of experience, practice, and knowledge to assure the best possible care and increase the chances of a fortunate outcome for the patient.The physical and psychosocial [3] consequences for patients are debilitating as well as the economic consequences, which are a concern for the patient, his or her environment, society, and health care institutions [4]. Traumatic spinal cord injury (TSCI) is considered as one of the most severe injuries in traumatology. As it predominantly affects young patients [1,2], it requires a lot of experience, practice, and knowledge to assure the best possible care and increase the chances of a fortunate outcome for the patient. Traumatic damage to the spinal cord proceeds in several sequential phases. The primary injury phase is defined by the immediate mechanical damage to the tissue mostly due to shearing, laceration, acute stretching, and sudden acceleration-deceleration events causing spinal shock [5,6]. A more prolonged secondary injury phase is set in motion that involves complex inflammatory responses. The chronic phase is characterized by autonomic dysregulations [6,7,8,9]
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