ABSTRACT
STUDY DESIGN: Systematic review. OBJECTIVE: To determine the incidence, pathogenesis, and clinical outcomes related to neurogenic fevers following traumatic spinal cord injury (SCI). METHODS: A systematic review of the literature was performed on thermodysregulation secondary to acute traumatic SCI in adult patients. A literature search was performed using PubMed (MEDLINE), Cochrane Central Register of Controlled Trials, and Scopus. Using strict inclusion and exclusion criteria, seven relevant articles were obtained. RESULTS: The incidence of fever of all origins (both known and unknown) after SCI ranged from 22.5 to 71.7% with a mean incidence of 50.6% and a median incidence of 50.0%. The incidence of fever of unknown origin (neurogenic fever) ranged from 2.6 to 27.8% with a mean incidence of 8.0% and a median incidence of 4.7%. Cervical and thoracic spinal injuries were more commonly associated with fever than lumbar injuries. In addition, complete injuries had a higher incidence of fever than incomplete injuries. The pathogenesis of neurogenic fever after acute SCI is not thoroughly understood. CONCLUSION: Neurogenic fevers are relatively common following an acute SCI; however, there is little in the scientific literature to help physicians prevent or treat this condition. The paucity of research underscored by this review demonstrates the need for further studies with larger sample sizes, focusing on incidence rate, clinical outcomes, and pathogenesis of neurogenic fever following acute traumatic SCI.
ABSTRACT
The authors endeavor to highlight the surgical management of severe neurological deficit resulting from cement leakage after percutaneous vertebroplasty and to systematically review the literature on the management of this complication. A patient presented after a vertebroplasty procedure for traumatic injury. A CT scan showed polymethylmethacrylate leakage into the right foramina at T-11 and L-1 and associated central stenosis at L-1. He underwent decompression and fusion for removal of cement and stabilization of the fracture segment. In the authors' systematic review, they searched Medline, Scopus, and Cochrane databases to determine the overall number of reported cases of neurological deficit after cement leakage, and they collected data on symptom onset, clinical presentation, surgical management, and outcome. After surgery, despite neurological recovery postoperatively, the patient developed pneumonia and died 16 days after surgery. The literature review showed 21 cases of cement extravasation with neurological deficit. Ultimately, 15 patients had resolution of the postoperative deficit, 5 had limited change in neurological status, and 2 had no improvement. Cement augmentation procedures are relatively safe, but certain precautions should be taken to avoid such complications including high-resolution biplanar fluoroscopy, considering the use of a local anesthetic, and controlling the location of cement spread in relationship to the posterior vertebral body. Immediate surgical intervention with removal of cement provides good results with complete recovery in most cases.
