Post-thrombotic syndrome: current prevention and management strategies.

The post-thrombotic syndrome (PTS) is the most commonly occurring long-term complication of deep vein thrombosis (DVT) with a cumulative incidence of up to 50% within the first 2 years after the thrombotic event. It is characterized by the development of various symptoms and signs related to chronic venous disease in a limb previously affected by DVT. PTS is a condition that significantly impairs quality of life and results in substantial burden to patients and society. So far, treatment options for PTS are limited, and strategies that prevent PTS occurrence are therefore of pivotal importance. These include compression therapy, prevention of recurrent ipsilateral DVT and possibly endovascular catheter-directed thrombolytic procedures. Clinical predictors of PTS are progressively characterized, but the ability to predict which patient with DVT is likely to develop PTS remains limited.

Serial limited versus single complete compression ultrasonography for the diagnosis of lower extremity deep vein thrombosis.

The diagnostic approach to deep vein thrombosis (DVT) has evolved during the last 3 decades. Contrast venography has been replaced by noninvasive tests. Compression ultrasonography (CUS) is currently the most widely used diagnostic test. Whereas CUS has a high accuracy for proximal DVT (thrombosis of the popliteal and more proximal veins), it has been shown to lack sensitivity and specificity for distal DVT. Ultrasonography can either be limited to the proximal veins and repeated within 1 week (serial limited CUS) or extended to both proximal and distal veins and performed on one occasion (single complete CUS). Both strategies are reliable diagnostic options for the management of patients with suspected DVT. The main limitation of proximal CUS is the need to repeat the test once in patients with initial negative findings. Conversely, complete CUS detects many distal DVTs for which systematic anticoagulation therapy is debatable and exposes patients to potentially unnecessary anticoagulation. Incorporation of D-dimer testing and clinical pretest probability assessment in the diagnostic algorithm is beneficial because it allows excluding DVT without the need for diagnostic imaging in about a third of patients.

Quorum sensing-dependent virulence during Pseudomonas aeruginosa colonisation and pneumonia in mechanically ventilated patients.

BACKGROUND: Pseudomonas aeruginosa frequently colonises intubated patients and causes life-threatening ventilator-associated pneumonia (VAP). The role of quorum sensing (QS), regulating virulence in this pathogen, during colonisation and development of VAP is unknown. METHODS: P aeruginosa isolates and tracheal aspirates were prospectively collected from intubated patients. Genotypes and QS-independent virulence traits (exoU, exoS, PAPI-1 and PAPI-2) harboured by colonising isolates were identified in vitro with the CLONDIAG array. The production of elastase and rhamnolipids was measured to assess QS-dependent virulence. To monitor QS activity 'in patient', total RNA was extracted directly from tracheal aspirates and expression of QS genes was measured. RESULTS: 320 P aeruginosa isolates and tracheal aspirates were obtained from 29 patients of whom 6 developed VAP (20%). Seven patients (24%) were initially colonised by QS-proficient isolates; 57% of them developed VAP as compared with 9% of patients colonised by QS-deficient isolates (p=0.018). Of all tested virulence traits from the initial colonising isolates, only rhamnolipids were associated with development of VAP (p=0.003). VAP occurred more frequently in patients colonised during the entire observation period by isolates producing high levels of rhamnolipids (p=0.001). 'In patient' monitoring of QS genes showed non-induced expression profiles in patients without VAP. In contrast, exponential induction of QS circuit and target gene expression was observed for two patients with VAP, and an 'in patient' QS gene expression profile and hierarchy similar to those in vitro was measured for one patient with VAP. CONCLUSIONS: Production of the QS-dependent virulence factor rhamnolipids by colonising P aeruginosa isolates is associated with development of VAP.