The prevalence of septic arthritis after an ACL reconstruction in this series was 1.8 %. Arthroscopic lavages along with antibiotic treatment led us to preserve all but one graft. Functional outcomes in the infected patients were not as good as those obtained in patients without infection.

The aim of this study was to investigate pretreatment prognostic factors that could be useful in predicting the response to plasma exchange in thrombotic thrombocytopenic purpura/hemolytic uremic syndrome (TTP/HUS). Thirty-two patients with TTP/HUS, treated with plasma exchange at our institution from 1980 to 1994, were studied. The main clinical and laboratory data at the beginning of plasma exchanges were analyzed by the Cox stepwise logistic regression, applied to either treatment failure or death. Seventeen (53%) patients attained a complete remission and 22 (69%) survived (five in advanced renal failure and long-term hemodialysis). Longer delay in initiating plasma exchanges, presence of stupor or coma, and higher creatinine levels at the beginning of plasma exchanges were independent predictors of treatment failure. Stupor or coma at the beginning of plasma exchanges was the only predictor of mortality from unremitted TTP/HUS. Hemoglobin levels, platelet count, and LDH activity, traditionally envisaged as markers of disease activity, neither correlated with previous duration of TTP/HUS nor had any prognostic value. Early diagnosis of TTP/HUS and prompt initiation of intensive plasma exchange emerged from this study as the most effective interventions for improving the prognosis of TTP/HUS patients.

Background:The diagnosis of Morton's neuroma is based primarily on clinical findings. Ultrasonography (US) and magnetic resonance image (MRI) studies are considered complementary diagnostic techniques. The aim of this study was to establish the correlation and sensitivity of both techniques used to diagnose Morton's neuroma.Materials and Methods:Thirty seven patients (43 intermetatarsal spaces) with Morton's neuroma operated were retrospectively reviewed. In all cases MRI or ultrasound was performed to complement clinical diagnosis of Morton's neuroma. In all cases, a histopathological examination confirmed the diagnosis. Estimates of sensitivity were made and correlation (kappa statistics) was assessed for both techniques.Results:Twenty seven women and 10 men participated with a mean age of 60 years. Double lesions presented in six patients. The second intermetatarsal space was affected in 10 patients and the third in 33 patients. An MRI was performed in 41 cases and a US in 23 cases. In 21 patients, both an MRI and a US were performed. With regard to the 41 MRIs performed, 34 were positive for Morton's neuroma and 7 were negative. MRI sensitivity was 82.9% [95% confidence interval (CI): 0.679–0.929]. Thirteen out of 23 US performed were positive and 10 US were negative. US sensitivity was 56.5% (95% CI: 0.345–0.768). Relative to the 21 patients on whom both techniques were carried out, the agreement between both techniques was poor (kappa statistics 0.31).Conclusion:Although ancillary studies may be required to confirm the clinical diagnosis in some cases, they are probably not necessary for the diagnosis of Morton's neuroma. MRI had a higher sensitivity than US and should be considered the technique of choice in those cases. However, a negative result does not exclude the diagnosis (false negative 17%).

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SummaryProthrombin fragment 1+2 (F1+2) and thrombin-antithrombin complexes (TAT), as well as other coagulation and fibrinolysis parameters, were studied in a series of 13 patients affected by thrombotic thrombocytopenic purpura (TTP) or hemolytic-uremic syndrome (HUS). Fragment F1+2 was found to be increased in all patients at diagnosis (patients' range, 1.21-19.03 nmol/1; normal limits, 0.28-1.08 nmol/1), and remained also higher than normal after treatment with plasma exchange (patients' range, 1.5-4.01 nmol/1). Even though the analysis of fibrinolysis markers did not show a definite state of hypo or hyperfibrinolysis in the systemic circulation, enhanced circulating D-dimer levels (0.53-12.6 ug/ml, normal levels of 0.03-0.29 εg/ml) indicated that a certain grade of fibrin lysis was present at previously formed thrombi. Plasma PAI-1 activities either on admission (9.2-38.2 U/ml) and after plasma exchange therapy (2.6-38.6 U/ml) showed a behavior irrespective of t-PA: Ag changes, and post-plasmapheresis values remained high only in patients with fatal neurological outcome. Nevertheless, no correlations between clinical and laboratory data could be established useful for the TTP/HUS prognosis. We conclude that increased thrombin generation occurring in damaged areas is appropriately inhibited by antithrombin III in the systemic circulation, avoiding consumption coagulopathy to develop in uncomplicated patients. In addition, fibrinolysis data suggest that elevated PAI-1 may decisively favor the development of microvascular thrombi.