scholarly journals 11 femoral fractures with vascular injury: Good outcome with early vascular repair and internal fixation

1996 ◽  
Vol 67 (2) ◽  
pp. 161-164 ◽  
Author(s):  
Martinus Bråten ◽  
Per Helland ◽  
Hans O Myhre ◽  
Anders Mølster ◽  
Terje Terjesen
1995 ◽  
Vol 08 (03) ◽  
pp. 159-162 ◽  
Author(s):  
L. Susan ◽  
R. T. O’Brien ◽  
K. A. Johnson

SummaryTwo young dogs examined for hindlimb lameness were found to have healed femoral fractures, 2-4 cm of femoral shortening, and 1 cm of compensatory ipsilateral tibial overgrowth. Neither dog had had surgery or internal fixation. Although tibial overgrowth partially corrected for limb shortening, both dogs had chronic intermittent lameness due to malformation of the femoral condyles and secondary stifle osteoarthritis.Compensatory tibial overgrowth was found in two young dogs with femoral fractures which had healed without any surgical reduction or internal fixation. Tibial overgrowth of approximately 1 cm in each case partially compensated for 2-4 cm of femoral shortening.


2016 ◽  
Vol 16 (1) ◽  
Author(s):  
Hang Wang ◽  
Yang-Guang Yin ◽  
Hao Huang ◽  
Xiao-Hui Zhao ◽  
Jie Yu ◽  
...  

2018 ◽  
Vol 08 (04) ◽  
pp. 258-262
Author(s):  
Ahsin Manzoor Bhatti ◽  
Junaid Mansoor ◽  
Haroon Sabir Khan

Objective: To analyze errors in primary treatment of vascular injuries and delayed presentations of missed vascular injuries as a surrogate indicator of need for improved vascular surgical training of upcoming general surgeons. Materials and methods: This retrospective observational study was carried out at vascular surgery department of two tertiary care hospitals of Armed Forces from Jan 2012 to June 2017. Hospital records of all patients with vascular trauma were analyzed for presence of pitfalls in primary treatment and delayed presentation of missed vascular injuries which resulted in redo surgeries or adverse outcomes. Results: Out of 256 patients with vascular injury sequel 41 had either a problem in primary treatment or presented with delayed complications of missed injuries. The omissions can be divided into: missed injuries (24/41), technical errors in initial repair (12/24), reperfusion of mangled Extremity (3/41) and non availability of a surgeon capable of undertaking vascular repair. The commonest operative fault was failure to debride the vessel adequately and vascular repair under tension. The commonest primary assessment problem was failure to timely appreciate hard signs of vascular injury. Conclusion: With better training and emphasizing the need of thorough clinical examination outcome of vascular trauma can be improved.


2018 ◽  
Vol 29 (4) ◽  
pp. 365-372
Author(s):  
Ahmed Saeed Younis ◽  
Shady Mahmoud ◽  
Ahmed Salem Eid ◽  
Amr Khairy Mahmoud

Author(s):  
Jing Yan ◽  
Wen-Bin Wang ◽  
Yang-Jing Fan ◽  
Han Bao ◽  
Na Li ◽  
...  

Endothelial progenitor cells (EPCs) play a vital role in endothelial repair following vascular injury by maintaining the integrity of endothelium. As EPCs home to endothelial injury sites, they may communicate with exposed vascular smooth muscle cells (VSMCs), which are subjected to cyclic stretch generated by blood flow. In this study, the synergistic effect of cyclic stretch and communication with neighboring VSMCs on EPC function during vascular repair was investigated. In vivo study revealed that EPCs adhered to the injury site and were contacted to VSMCs in the Sprague–Dawley (SD) rat carotid artery injury model. In vitro, EPCs were cocultured with VSMCs, which were exposed to cyclic stretch at a magnitude of 5% (which mimics physiological stretch) and a constant frequency of 1.25 Hz for 12 h. The results indicated that stretched VSMCs modulated EPC differentiation into mature endothelial cells (ECs) and promoted angiogenesis. Meanwhile, cyclic stretch upregulated the mRNA expression and secretion level of connective tissue growth factor (CTGF) in VSMCs. Recombinant CTGF (r-CTGF) treatment promoted endothelial differentiation of EPCs and angiogenesis, and increased their protein levels of FZD8 and β-catenin. CTGF knockdown in VSMCs inhibited cyclic stretch-induced EPC differentiation into ECs and attenuated EPC tube formation via modulation of the FZD8/β-catenin signaling pathway. FZD8 knockdown repressed endothelial differentiation of EPCs and their angiogenic activity. Wnt signaling inhibitor decreased the endothelial differentiation and angiogenetic ability of EPCs cocultured with stretched VSMCs. Consistently, an in vivo Matrigel plug assay demonstrated that r-CTGF-treated EPCs exhibited enhanced angiogenesis; similarly, stretched VSMCs also induced cocultured EPC differentiation toward ECs. In a rat vascular injury model, r-CTGF improved EPC reendothelialization capacity. The present results indicate that cyclic stretch induces VSMC-derived CTGF secretion, which, in turn, activates FZD8 and β-catenin to promote both differentiation of cocultured EPCs into the EC lineage and angiogenesis, suggesting that CTGF acts as a key intercellular mediator and a potential therapeutic target for vascular repair.


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