ABSTRACT
PURPOSE: The aim of this study was to radiologically evaluate the risk of reduction loss after locking plate fixation of proximal humerus fractures. METHODS: From September 2007 to April 2009, 71 patients (28 males, 43 females) with unstable proximal humeral fracture were treated with open reduction and internal fixation by locking plate. The mean follow-up time was 31.2 months (range: 26-47). The head-shaft angulation (HSA) and the humeral head height (HHH) in true anteroposterior (AP) were recorded and compared over time. All complications were noted. Shoulder function was measured by the Constant score. RESULTS: Patients with ΔHSA >10° (t=2.740, P=0.008) and ΔHHH >5mm (t=2.55, P=0.019) were more likely to have impaired shoulder function. Varus collapse occurred most frequently in patients with initial reduction of HSA <125° (χ(2)=19.17, P<0.001, Fisher's exact test F<0.001). Patients with >5mm HHH decrease were strongly associated with loss of reduction (χ(2)=24.23, P<0.001, F<0.001). CONCLUSIONS: Dynamic change of HSA >10° and HHH >5mm were radiological factors that indicated poor shoulder function. Intra-operative HSA >125° should be achieved to avoid reduction loss following locking plate fixation of proximal humerus fracture. LEVEL OF EVIDENCE: level IV.
Subject(s)
Bone Plates , Fracture Fixation, Internal/instrumentation , Imaging, Three-Dimensional , Shoulder Fractures/surgery , Shoulder Joint/diagnostic imaging , Tomography, X-Ray Computed/methods , Adult , Aged , Aged, 80 and over , Female , Follow-Up Studies , Fracture Healing , Humans , Male , Middle Aged , Range of Motion, Articular , Retrospective Studies , Shoulder Fractures/diagnostic imaging , Shoulder Fractures/physiopathology , Shoulder Joint/physiopathology , Time Factors , Trauma Severity IndicesABSTRACT
Prourokinase (proUK) is a zymogenic plasminogen activator that at pharmacological doses is prone to nonspecific activation to urokinase. This has handicapped therapeutic exploitation of its fibrin-specific physiological properties. To attenuate this susceptibility without compromising specific activation of proUK on a fibrin clot, a Lys300-->His mutation (M5) was developed. M5 had a lower intrinsic activity and, therefore, remained stable in plasma at a 4-fold higher concentration than did proUK. M5 had a higher 2-chain activity and induced more rapid plasminogen activation and fibrin-specific clot lysis in vitro. Sixteen dogs embolized with radiolabeled clots were infused with saline, proUK, tissue plasminogen activator, or M5. The lower intrinsic activity allowed a higher infusion rate with M5, which induced the most rapid and efficient clot lysis (50% clot lysis by approximately 600 microg/kg M5 versus approximately 1200 microg/kg proUK). In association with this, M5 caused neither a significant increase in the primary bleeding time nor secondary bleeding (total blood loss). By contrast, these measurements increased 4-fold and 5-fold, respectively, with proUK and >5-fold and 8-fold, respectively, with tissue plasminogen activator. Clot lysis by M5 and hemostasis were further evaluated in 6 rhesus monkeys. M5 again induced rapid clot lysis without a significant increase in the primary bleeding time, and secondary bleeding did not occur. In conclusion, a site-directed mutation designed to improve the stability of proUK in blood at therapeutic concentrations induced superior clot lysis in vitro and in vivo without causing significant interference with hemostasis.
