| Autor: |
Visagan R; Academic Neurosurgery Unit, St. George's, University of London, London, United Kingdom., Kearney S; Academic Neurosurgery Unit, St. George's, University of London, London, United Kingdom.; Neuro Anesthesia and Neuro Intensive Care Unit, St. George's Hospital, London, United Kingdom., Blex C; Department of Neurology and Experimental Neurology, Spinal Cord Injury Research (Neuroparaplegiology), Charité - Universitätsmedizin Berlin, Berlin, Germany., Serdani-Neuhaus L; Department of Neurology and Experimental Neurology, Spinal Cord Injury Research (Neuroparaplegiology), Charité - Universitätsmedizin Berlin, Berlin, Germany., Kopp MA; Department of Neurology and Experimental Neurology, Spinal Cord Injury Research (Neuroparaplegiology), Charité - Universitätsmedizin Berlin, Berlin, Germany., Schwab JM; Department of Neurology and Experimental Neurology, Spinal Cord Injury Research (Neuroparaplegiology), Charité - Universitätsmedizin Berlin, Berlin, Germany.; The Belford Center for Spinal Cord Injury, The Ohio State University, Wexner Medical Center, Columbus, Ohio, USA.; Departments of Neurology, Physical Medicine and Rehabilitation, and Neurosciences, The Ohio State University, Columbus, Ohio, USA., Zoumprouli A; Neuro Anesthesia and Neuro Intensive Care Unit, St. George's Hospital, London, United Kingdom., Papadopoulos MC; Academic Neurosurgery Unit, St. George's, University of London, London, United Kingdom., Saadoun S; Academic Neurosurgery Unit, St. George's, University of London, London, United Kingdom. |
| Abstrakt: |
This study aims to determine the effect of neurogenic, inflammatory, and infective fevers on acutely injured human spinal cord. In 86 patients with acute, severe traumatic spinal cord injuries (TSCIs; American Spinal Injury Association Impairment Scale (AIS), grades A-C) we monitored (starting within 72 h of injury, for up to 1 week) axillary temperature as well as injury site cord pressure, microdialysis (MD), and oxygen. High fever (temperature ≥38°C) was classified as neurogenic, infective, or inflammatory. The effect of these three fever types on injury-site physiology, metabolism, and inflammation was studied by analyzing 2864 h of intraspinal pressure (ISP), 1887 h of MD, and 840 h of tissue oxygen data. High fever occurred in 76.7% of the patients. The data show that temperature was higher in neurogenic than non-neurogenic fever. Neurogenic fever only occurred with injuries rostral to vertebral level T4. Compared with normothermia, fever was associated with reduced tissue glucose (all fevers), increased tissue lactate to pyruvate ratio (all fevers), reduced tissue oxygen (neurogenic + infective fevers), and elevated levels of pro-inflammatory cytokines/chemokines (infective fever). Spinal cord metabolic derangement preceded the onset of infective but not neurogenic or inflammatory fever. By considering five clinical characteristics (level of injury, axillary temperature, leukocyte count, C-reactive protein [CRP], and serum procalcitonin [PCT]), it was possible to confidently distinguish neurogenic from non-neurogenic high fever in 59.3% of cases. We conclude that neurogenic, infective, and inflammatory fevers occur commonly after acute, severe TSCI and are detrimental to the injured spinal cord with infective fever being the most injurious. Further studies are required to determine whether treating fever improves outcome. Accurately diagnosing neurogenic fever, as described, may reduce unnecessary septic screens and overuse of antibiotics in these patients. |
