Dynamic Fixation versus Static Screw Fixation for Syndesmosis Injuries in Pronation External Rotation Ankle Fractures: A Retrospective Case Control Study

@#Introduction: The current standard treatment for ankle syndesmosis injury is static screw fixation. Dynamic fixation was developed to restore the dynamic function of the syndesmosis. The purpose of this study was to determine that which of static screw fixation and dynamic fixation is better for treatment of ankle syndesmosis injury in pronationexternal rotation fractures. Materials and methods: Thirty patients were treated with dynamic fixation (DF group) and 28 patients with static screw fixation (SF group). The primary outcome was Olerud–Molander Ankle Outcome Score. The secondary outcome were Visual Analogue Scale score and American Orthopedic Foot and Ankle Society score, radiographic outcomes, complications and cost effectiveness. To evaluate the radiographic outcome, the tibiofibular clear space, tibiofibular overlap, and medial clear space were compared using the pre-operative and last follow-up plain radiographs. To evaluate the cost effectiveness, the total hospital cost was compared between the two groups Results: There was no significant difference in primary outcome. Moreover, there were no significant difference in secondary outcome including Visual Analogue Scale score and American Orthopedic Foot and Ankle Society score and radiographic outcome. Two cases of reduction loss and four cases of screw breakage were observed in the SF group. No complication in the DF group was observed. Dynamic fixation was more cost effective than static screw fixation with respect to the total hospital cost. Conclusion: Although dynamic fixation provided similar clinical and radiologic outcome, dynamic fixation is more cost effective with fewer complications than static screw fixation in ankle syndesmosis injury of pronation-external rotation fractures.

Clinical significance of enzymatic lysophosphatidylcholine (LPC) assay data in patients with sepsis.

Lysophosphatidylcholine (LPC) has been suggested to serve as a useful prognostic marker for sepsis. However, existing LPC assays are complicated, time-consuming, and of limited application in real clinical situations. Thus, we investigated the serum LPC levels in sepsis patients using an enzymatic assay and analyzed the correlations between the serum LPC concentration and clinical characteristics. We prospectively collected blood samples from suspected sepsis patients, commencing on day 1 of sepsis. We analyzed all samples using an enzymatic assay. Additionally, we analyzed the serum LPC concentrations in a control group of 21 healthy blood donors. A total of 105 patients who fulfilled the sepsis criteria were included. The mean serum LPC concentration was 43.49 ± 33.09 µmol/L in sepsis patients, which was much lower than that of 21 healthy controls (234.68 ± 30.33 µmol/L, p<0.001). Bacteremic sepsis was associated with a lower serum LPC concentration than non-bacteremic sepsis (34.8 ± 26.85 vs. 49.05 ± 35.63 µmol/L, p<0.05). No difference in serum LPC concentration was evident between survivors and non-survivors. The serum LPC concentration tended to decrease with the severity of sepsis. The day 1 serum LPC concentration was decreased in patients with sepsis, especially when bacteremia was present. However, the serum LPC level did not correlate with disease severity and did not predict mortality from sepsis.

Acute exacerbation of idiopathic pulmonary fibrosis: incidence, risk factors and outcome.

Although acute exacerbation of idiopathic pulmonary fibrosis (IPF) has become well recognised, the reported incidence and outcomes are highly variable, and risk factors are unknown. The aim of this study was to estimate the incidence, risk factors and impact of acute exacerbations, and other known causes of rapid deterioration. This was a retrospective review of 461 patients with IPF (269 cases were biopsy-proven). The median follow-up period was 22.9 months. Rapid deterioration requiring hospitalisation occurred in 163 (35.4%) patients, with multiple episodes in 42 patients. Acute exacerbation was the most frequent cause (55.2%), followed by infection. The 1- and 3-yr incidences of acute exacerbation were 14.2 and 20.7%, respectively. Never having smoked and low forced vital capacity (FVC) were significant risk factors. The in-hospital mortality rate was 50.0%, and the 1- and 5-yr survival rates from the initial diagnosis were 56.2 and 18.4%, respectively. Acute exacerbation was a significant predictor of poor survival after the initial diagnosis, along with increased age, low FVC and diffusing capacity of the lung for carbon monoxide, and steroid use with or without cytotoxic therapy. 1- and 3-yr incidences of acute exacerbation were 14.2 and 20.7%, respectively. Never having smoked and low FVC were risk factors. Acute exacerbation had a serious impact on the overall survival of the patients with IPF.

Clinical course and lung function change of idiopathic nonspecific interstitial pneumonia.

Most studies of idiopathic nonspecific interstitial pneumonia (NSIP) have primarily studied mortality. In order to clarify the detailed outcome and prognostic markers in idiopathic NSIP, the clinical course with initial radiological and clinical features was analysed. The clinical course of 83 patients who were classified with idiopathic NSIP (72 fibrotic, 11 cellular; 27 males and 56 females; mean+/-sd age 54.4+/-10.1 yrs) was retrospectively analysed. In fibrotic NSIP, 16 (22%) patients died of NSIP-related causes with a median (range) follow-up of 53 (0.3-181) months. Despite the favourable survival (5-yr 74%), patients with fibrotic NSIP were frequently hospitalised with recurrence rate of 36%. Reduced forced vital capacity at 12 months was a predictor of mortality. On follow-up, lung function was improved or stable in approximately 80% of the patients. The extent of consolidation and ground-glass opacity on initial high-resolution computed tomography correlated significantly with serial changes of lung function, and the presence of honeycombing was a predictor of poor prognosis. During follow-up, eight (10%) patients developed collagen vascular disease. In conclusion, the overall prognosis of fibrotic nonspecific interstitial pneumonia was good; however, there were significant recurrences despite initial improvement and a subset of the patients did not respond to therapy. Some patients developed collagen vascular diseases at a later date.

Comparison of two commercial interferon-gamma assays for diagnosing Mycobacterium tuberculosis infection.

The clinical usefulness of ex vivo interferon-gamma assays may largely depend on the assay format and epidemiological status of tuberculosis (TB) in the region studied. From July 2004 to June 2005 a prospective comparison study was undertaken at a tertiary referral hospital in South Korea. The results of tuberculin skin tests (TST) and the commercially available QuantiFERON-TB Gold (QFT-G) and T SPOT-TB (SPOT) assays were compared in an intermediate TB-burden country. Of the 224 participants studied, results from all three tests (TST, QFT-G, and SPOT) were available in 218; 87 with active TB and 131 at a low risk for TB. Using 10 mm as a cut-off for TST, SPOT sensitivity (96.6%) was significantly higher than that seen for TST (66.7%) and QFT-G (70.1%). QFT-G showed superior specificity over TST (91.6 versus 78.6%). Although the specificity of QFT-G was higher than that of SPOT (91.6 versus 84.7%), the difference was not statistically significant. Whilst some differences were found in the performance of the two commercialised interferon-gamma assays, they seemed to be superior in their detection of Mycobacterium tuberculosis infection compared with tuberculin skin tests. The most appropriate choice of interferon-gamma assay to use may depend on the clinical setting.

Hypothermia attenuates vascular manifestations of ventilator-induced lung injury in rats.

Alveolar hemorrhage and pulmonary edema induced by mechanical ventilation are partly dependent on cardiac output. Because cardiac output is low during hypothermia, we hypothesized that hypothermia may protect against these vascular manifestations of ventilator-induced lung injury. Twenty-seven Sprague-Dawley rats were assigned to either normothermia (37 +/- 1 degrees C)-injurious ventilation (NT; n = 10), hypothermia (27 +/- 1 degrees C)- injurious ventilation (HT; n = 10), or nonventilated control ( n = 7). The two ventilated groups were subjected to injurious ventilation of peak airway pressure 30 cm H(2)O with zero end-expiratory pressure for 20 min. Compared with the NT group, the hemorrhage/congestion score of the lung (11.2 +/- 1.5 vs. 4.7 +/- 1.6; p < 0.001) and the ratio of wet/dry lung weight (6.1 +/- 0.8 vs. 5.0 +/- 0.1; p = 0.046) of the HT group were lower. Compared with the NT group, protein concentration (3,471 +/- 1,985 micro g/ml vs. 1,374 +/- 726 micro g/ml; p = 0.003) and lactate dehydrogenase level (0.43 +/- 0.22 U/ml vs. 0.18 +/- 0.1 U/ml; p = 0.046) in bronchoalveolar lavage fluid of the HT group were lower. Whereas pressure-volume curve was shifted to the right in the NT group after injurious ventilation, it was not shifted in the HT group. In conclusion, hypothermia in rats attenuated the degrees of vascular manifestations and alveolar epithelial injuries induced by injurious ventilation, and preserved the mechanical properties of the lung.