Stalenhoef J.E.,Leiden University |
Van Dissel J.T.,Leiden University |
Van Nieuwkoop C.,Haga Hospital
Current Opinion in Infectious Diseases | Year: 2015
Purpose of review: To review the recent advances in the diagnostic and therapeutic approach to adults presenting with febrile urinary tract infection (UTI) in the emergency department (ED). Recent findings: Recent research suggests overdiagnosis and therefore overtreatment of UTI in the ED, especially in the elderly. Antimicrobial pretreatment, an indwelling catheter, and malignancy are independent risk factors for bacteremia with uropathogens that cannot be cultured from urine. A simple clinical prediction rule can predict clinically relevant radiologic findings in patients with invasive UTI. Procalcitonin is a marker for bacteremia; pro-adrenomedullin predicts a complicated course and 30-day mortality in complicated UTI. Several reports have identified the risk factors for resistant uropathogens in community-acquired febrile UTI. Adherence to the guidelines and early culture-guided intravenous-to-oral switch reduces the length of hospitalization. Summary: An effective strategy is needed to improve the diagnosis of UTIs in acute care. Further research regarding biomarker-guided triage might improve the management of patients with febrile UTI. Future efforts should be directed toward the improvement of adherence to UTI treatment guidelines. Copyright © 2015 Wolters Kluwer Health, Inc. All rights reserved.
Hogervorst T.,Haga Hospital |
Eilander W.,Leiden University |
Fikkers J.T.,Leiden University |
Meulenbelt I.,Leiden University
Clinical Orthopaedics and Related Research | Year: 2012
Background: Developmental hip disorders (DHDs), eg, developmental dysplasia of the hip, slipped capitis femoris epiphysis, and femoroacetabular impingement, can be considered morphology variants of the normal hip. The femoroacetabular morphology of DHD is believed to induce osteoarthritis (OA) through local cumulative mechanical overload acting on genetically controlled patterning systems and subsequent damage of joint structures. However, it is unclear why hip morphology differs between individuals with seemingly comparable load histories and why certain hips with DHD progress to symptomatic OA whereas others do not. Questions/Purposes: We asked (1) which mechanical factors influence growth and development of the proximal femur; and (2) which genes or genetic mechanisms are associated with hip ontogenesis. Methods: We performed a systematic literature review of mechanical and genetic factors of hip ontogeny. We focused on three fields that in recent years have advanced our knowledge of adult hip morphology: imaging, evolution, and genetics. Where Are We Now?: Mechanical factors can be understood in view of human evolutionary peculiarities and may summate to load histories conducive to DHD. Genetic factors most likely act through multiple genes, each with modest effect sizes. Single genes that explain a DHD are therefore unlikely to be found. Apparently, the interplay between genes and load history not only determines hip morphotype, but also joint cartilage robustness (''cartilotype'') and resistance to symptomatic OA. Where Do We Need to Go?: We need therapies that can improve both morphotype and cartilotype. How Do We Get There?: Better phenotyping, improving classification systems of hip morphology, and comparative population studies can be done with existing methods. Quantifying load histories likely requires new tools, but proof of principle of modifying morphotype in treatment of DDH and of cartilotype with exercise is available. © The Association of Bone and Joint Surgeons® 2012. © The Association of Bone and Joint Surgeons® 2012.
Melsen W.G.,Julius Center for Health science and Primary Care |
Rovers M.M.,Julius Center for Health science and Primary Care |
Koeman M.,Haga Hospital |
Bonten M.J.M.,Julius Center for Health science and Primary Care |
Bonten M.J.M.,University Utrecht
Critical Care Medicine | Year: 2011
Objective: To assess the attributable mortality of ventilator-associated pneumonia using results from randomized controlled trials on ventilator-associated pneumonia prevention. Data Sources: A systematic search was performed in PubMed, Embase, Web of Science, and Cochrane Library from their inception until July 2010. In addition, a reference and related article search was performed. Study Selection: Randomized ventilator-associated pneumonia prevention studies in which all patients were mechanically ventilated and from which ventilator-associated pneumonia and mortality rates of intervention and control group could be extracted were included. Data Extraction/Synthesis: Fifty-three papers were identified describing 58 comparisons. Statistical significant reductions in ventilator-associated pneumonia incidences were reported in 20 of the 58 comparisons, whereas none of these trials reported a significant reduction of mortality. Pooled estimates of the relative risk reductions of both ventilator-associated pneumonia and mortality were calculated and the attributable mortality was estimated as the ratio between the relative risk reductions of mortality and ventilator-associated pneumonia. Effects of study quality, diagnostic methods used, and effectiveness of preventing ventilator-associated pneumonia on the mortality rate of ventilator-associated pneumonia were assessed in subgroup analyses. The overall attributable mortality of ventilator-associated pneumonia was estimated as 9%. In subgroup analyses, the attributable mortality varied between 3% and 17%. Conclusion: Based on the results of 58 randomized studies on ventilator-associated pneumonia prevention, the attributable mortality rate of ventilator-associated pneumonia was estimated to be 9% and ranged between 3% and 17% in subgroup analyses. Together with the results of other recent studies, there is cumulative evidence that the attributable mortality resulting from ventilator-associated pneumonia is approximately 10%. © 2011 by the Society of Critical Care Medicine and Lippincott Williams & Wilkins.
Hirdes M.M.C.,University Utrecht |
Siersema P.D.,University Utrecht |
Houben M.H.M.G.,Haga Hospital |
Weusten B.L.A.M.,St. Antonius Hospital |
Vleggaar F.P.,University Utrecht
American Journal of Gastroenterology | Year: 2011
Objectives:Partially covered self-expanding metal stents (SEMSs) are regularly used for malignant and occasionally for benign esophageal disorders. Safe removal of these stents can be challenging due to embedding of the uncovered stent ends. Our aim is to report the results of removal of embedded, partially covered SEMSs by induction of pressure necrosis using the stent-in-stent technique.Methods:Consecutive patients referred to three endoscopy units in 2007-2009, treated by the stent-in-stent technique, were reviewed. The partially covered SEMSs were inserted for malignant (n3) or benign (n16) conditions and were left in situ for a median of 42 days (14-189). When SEMSs were found to be embedded, a fully covered self-expanding plastic stent (SEPS) or fully covered SEMS was placed inside the partially uncovered SEMS. Subsequent removal of both stents was planned after a period of 10-14 days.Results:In total, 23 stent-in-stent procedures were performed in 19 patients (10 males). Placement of a fully covered stent (SEPS: n9 and SEMS: n14) was technically successful in all patients. In 21 of 23 (91%) procedures, both stents were successfully removed in one procedure after a median of 12 days (5-18). In two patients, a repeat stent-in-stent procedure was needed for persistent embedding of the partially uncovered SEMSs. One (5%) procedure was complicated by severe bleeding, which could be treated endoscopically. In seven (36%) patients, the initial disorder had resolved after stent removal and no further endoscopic interventions were needed. Two (10%) patients were treated with chemoradiation or surgery for esophageal cancer after stent removal. In 10 (53%) patients, a repeat endoscopic intervention was required during follow-up because of progressive dysphagia or a persisting leak or fistula.Conclusions:The stent-in-stent technique is safe and effective for the removal of partially covered SEMSs that are embedded in the esophageal wall. © 2011 by the American College of Gastroenterology.
Van De Stolpe A.,Philips |
Kauffmann R.H.,Haga Hospital
RSC Advances | Year: 2015
Autoimmune diseases are exclusively human diseases with a complex genetic background and variable clinical presentation, of which the underlying pathophysiology is insufficiently understood. Current treatment is mainly empirical with limited efficacy and significant side effects. To develop more effective targeted therapy for personalized treatment, understanding of the human pathophysiology is crucial, implying a high need for human investigational disease models. Using the example of anti-neutrophil cytoplasmic antibody (ANCA) autoimmune vasculitis, the concept of building an in vitro organ-on-chip type human disease model, consisting of cultured organ-specific vascular tissue in interaction with relevant immune system components (e.g. lymph node and thymus tissue) is presented. This in vitro approach makes use of advances in engineering and human stem cell technologies, enabling derivation of pluripotent stem cell lines from patients, differentiation to required cell types, and incorporation in microfluidic chip-based culture systems to optimally mimic in vivo disease conditions. Knowledge-based computational disease modeling is introduced as a valuable complementary tool to generate an integral mechanistic picture of the disease. Combining these multidisciplinary developments promises breakthroughs in understanding autoimmune disease and targeted drug development, while simultaneously reducing use of animal models. Current state of the art and issues remaining to be solved are discussed. © The Royal Society of Chemistry 2015.