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To observe anatomic relationships between lumbar bicortical pedicle screws (BPSs) at 2 sagittal section angles (SSAs) and lumbar artery (LA). We observed 2 SSAs, vertical angle and cephalic angle, of the BPS. The positions at which the BPS breaks through the anterior vertebral cortex were defined as point A and point B. Distances from point A and point B to LAs were measured. The percentage of risk of injury to LAs was calculated according to these distances. At the same transverse section angle on the left and right side in L1 and L2, distance from point A to LA was significantly greater than distance from point B to LA (P < 0.001) except at a transverse section angle of 0° on the right side in L2 (P > 0.05). At the same transverse section angle on the left in L3 and L4, distance from point B to LA was significantly greater than distance from point A to LA (P < 0.001). The percentages of high risk of injury to the LA resulting from BPSs at the vertical angle in L1 and L2 were 0%–6.2%. The percentages of high risk of injury to the LA resulting from BPSs at the cephalic angle on the left side in L3 and L4 were 0%–18.5%. Lumbar BPSs present a risk of injury to the LA. The vertical angle is the recommended SSA for BPSs in L1 and L2, and the cephalic angle is the recommended SSA in L3 and L4. [ABSTRACT FROM AUTHOR]

Background We reviewed the reported data related to iatrogenic lumbar artery injury (ILAI) in spine surgery with a focus on which iatrogenic procedure might cause lumbar artery injury. Methods We conducted a comprehensive search in the Web of Science, PubMed, EMBASE, and Chinese biomedical databases in July 2018. Results A total of 20 reports on ILAI were selected for the present study. Most of these were case reports, with a total of 26 cases. The causes of ILAI were as follows: puncture injury in 9 cases, transforaminal endoscopic operation in 5 cases, pedicle screw injury in 3 cases, intervertebral foramen decompression in 2 cases, disc rongeur injury during discectomy in 2 cases, lumbar artery tear caused by transverse process fracture in 1 case, vertebral fracture restoration in 1 case, retractor injury in 1 case, cage insertion or pedicle screw injury in 1 case, and drainage tube stimulation in 1 case. The treatment methods included transarterial embolization in 20 cases, percutaneous embolization in 2 cases, surgical ligation in 1 case, and steroid and cyclophosphamide treatment in 1 case. All patients were treated successfully. One patient died during antishock therapy, and another patient died because her family refused any further intervention. Conclusions Attention should be given to the surgical procedures that are likely to cause ILAI, such as percutaneous vertebroplasty/percutaneous kyphoplasty, vertebral biopsy, pedicle screw implantation, discectomy, transforaminal endoscopic operation, and intervertebral foramen decompression. Once a diagnosis of ILAI has been confirmed, selective endovascular transarterial embolization is the preferred treatment. [ABSTRACT FROM AUTHOR]

Objective Traumatic brain injury (TBI) is a devastating neurologic injury and remains a major cause of death in the world. Secondary injury after TBI is associated with long-term disability in patients with TBI. This study evaluated adrenomedullin (AM) on secondary injury and neurologic functional outcome in rats after TBI. Methods Forty-eight Sprague Dawley rats were randomly assigned into 3 groups: sham, TBI, and TBI with AM groups. TBI was induced by fluid percussion injury, and AM was intravenously injected. Neurologic function was examined at 2, 3, and 7 days after TBI. Enzyme-linked immunosorbent assay was used to test tumor necrosis factor (TNF)-α, interleukin (IL)-1β, and IL-8 levels in the brain. Brain edema and blood–brain barrier (BBB) permeability in brain tissue were tested. Western blot was used to examine the expression of aquaporin-4, phosphorylated myosin light-chain, and cleaved caspase-3. Terminal deoxynucleotidyl transferase dUTP nick end labeling was used to test the apoptosis. Results Compared with the sham group, TNF-α, IL-1β, and IL-6 levels, brain edema, BBB permeability, neurologic examination scores, terminal deoxynucleotidyl transferase dUTP nick end labeling-positive cells, and expression of aquaporin-4, phosphorylated myosin light-chain, and cleaved caspase-3 significantly increased in the TBI group. AM treatment significantly inhibited TBI-induced effects. Conclusions AM can improve neurologic function and ameliorate brain injury in rats with TBI. AM exerts its neuroprotective effect via its anti-inflammatory and antiapoptotic effect. Highlights • The role of AM was studied in rats with traumatic brain injury. • AM inhibited inflammation, brain edema, BBB permeability, and apoptosis. • AM reduced brain injury and improved neurologic function. • AM reduced secondary injury via anti-inflammatory and antiapoptotic effects. [ABSTRACT FROM AUTHOR]