Common peroneal nerve palsy complicating knee dislocation and bicruciate ligaments tears

SummaryIntroductionThe occurrence rate of common peroneal nerve (CPN) palsy associated with knee dislocation or bicruciate ligament injury ranges from 10 to 40%. The present study sought first to describe the anatomic lesions encountered and their associated prognoses and second to recommend adequate treatment strategy based on a prospective multicenter observational series of knee ligament trauma cases.Material and methodsTwelve out of 67 knees treated for dislocation or bicruciate lesion presented associated CPN palsy: two females, 10 males; mean age, 32 years. Four sports injuries, three traffic accidents and five other etiologies led to seven complete dislocations and five bicruciate ruptures. Four cases involved associated popliteal artery laceration ischemia; one of the dislocations was open. Paralysis was total in eight cases and partial in four. There were two complete ruptures, three contusions with CPN in continuity stretch lesions and three macroscopically normal aspects.ResultsAt a minimum 1 year's follow-up, regardless of the initial surgical technique performed, recovery was complete in six cases, partial (in terms of motor function) in one and absent in five. Without specific CPN surgery, spontaneous recovery was partial in one case, complete in two and absent in none. Following simple emergency or secondary neurolysis, remission was total in four cases and absent in one. Three nerve grafts were all associated with non-recovery.DiscussionThe present results agree with literature findings. Palsy rates varied with trauma circumstances and departmental recruitment. Neurologic impairment was commensurate to ligamentary damages. The anatomic status of the CPN, subjected to violent traction by dislocation, was the most significant prognostic factor for neurologic recovery. In about 25% of dislocations, contusion-elongation over several centimeters was associated with as poor a prognosis as total rupture. CPN neurolysis is recommended when early clinical and EMG recovery fails to progress and/or in case of lateral ligamentary reconstruction. Possible peripheral nerve impairment needs to be included in the overall functional assessment of treatment for severe ligaments injuries and knee dislocation.Level of evidenceLevel IV, prospective study

A computed tomography based study on rotational alignment accuracy of the femoral component in total knee arthroplasty using computer-assisted orthopaedic surgery

Rotation of the femoral component in total knee arthroplasty (TKA) is of high importance in respect of the balancing of the knee and the patellofemoral joint. Though it is shown that computer assisted surgery (CAOS) improves the anteroposterior (AP) alignment in TKA, it is still unknown whether navigation helps in finding the accurate rotation or even improving rotation. Therefore the aim of our study was to evaluate the postoperative femoral component rotation on computed tomography (CT) with the intraoperative data of the navigation system. In 20 navigated TKAs the difference between the intraoperative stored rotation data of the femoral component and the postoperative rotation on CT was measured using the condylar twist angle (CTA). This is the angle between the epicondylar axis and the posterior condylar axis. Statistical analysis consisted of the intraclass correlation coefficient (ICC) and Bland-Altman plot. The mean intraoperative rotation CTA based on CAOS was 3.5° (range 2.4–8.6°). The postoperative CT scan showed a mean CTA of 4.0° (1.7–7.2). The ICC between the two observers was 0.81, and within observers this was 0.84 and 0.82, respectively. However, the ICC of the CAOS CTA versus the postoperative CT CTA was only 0.38. Though CAOS is being used for optimising the position of a TKA, this study shows that the (virtual) individual rotational position of the femoral component using a CAOS system is significantly different from the position on a postoperative CT scan

Does the activation of poly (ADP-ribose) synthetase mediate tissue injury in the sepsis induced by cecal ligation and puncture?

Poly (ADP-ribose) synthetase (PARS) is a DNA protective enzyme activated by single-strand breakage. It is suspected that exaggerated PARS activation related to biochemical stress by reactive oxygen and nitrogen species contributes to cellular injury in sepsis. The main hypothesis is that PARS activation leads to massive ATP and NAD consumption and consequent cellular energy depletion. The PARS inhibitor 3-amino-benzamide (3AB) is protective in rodents challenged with either endotoxin or intraperitoneal zymozan. The present experiment was designed to test the effect of 3AB in a more clinically relevant model of sepsis, namely polymicrobial sepsis induced by cecal ligature and puncture (CLP). Adult male Wistar rats were anesthetized, instrumented with catheters in the jugular vein and in the carotid artery, and then randomized into three groups: Sham (no laparotomy, n = 13), CLP (n = 15), and CLP/3AB (n = 18). All animals were allowed to recover and they received a continuous intravenous infusion of saline (20 mL/kg/h) and fentanyl (20 microg/kg/h). 3AB was administered to the CLP/3AB group as an intravenous bolus (10 mg/kg) followed by a continuous intravenous infusion (10 mg/kg/h). After 24 h, blood was drawn for the determination of biological indicators of organ injury. Rats were then anesthetized and biopsies of the liver were quickly frozen into liquid nitrogen for the subsequent determination of NAD and ATP levels. Further organ samples were collected for the assay of myeloperoxidase (MPO) to indicate tissue infiltration by leukocytes, and nitrotyrosine to indicate the level of biochemical stress by reactive nitrogen species. Twenty-four-hour mortality was 0/13 (Sham), 1/15 (CLP), and 5/18 (CLP/3AB; p = NS). In the surviving rats, CLP induced a clear elevation of liver enzymes, bilirubin, and pancreatic lipase, but not creatinine in the plasma, as well as a marked increase of MPO activity in liver, jejunum, and lung, but not kidney or heart. None of these variables was affected by treatment with 3AB. Furthermore, CLP did not cause depletion of NAD or ATP in the liver, nor any change in the nitrotyrosine content of any organ. These data argue against a general role of PARS activation in the pathogenesis of sepsis-induced tissue injury