Management of the Urologic Sepsis Syndrome

In approximately one-third of patients with sepsis, the source of infection is the urinary tract. The management of sepsis has rapidly changed over the past two decades, and a review of urosepsis management is paramount. It is estimated that in 30% of patients with severe sepsis and septic shock, the underlying reason is a urinary tract infection (UTI). The prevalence of microbiologically proven urosepsis in urology departments has been reported as 1.5% (quarter of health care–associated UTIs). On a global level, it has been postulated that 5.4 million deaths occur due to sepsis. The main causes of urosepsis are indwelling urinary catheters and urologic interventions (stone treatment, prostate biopsies, and endoscopic urethral stricture treatment). Urosepsis-causative pathogens are primarily gram-negative bacteria; this is different from sepsis overall, which is dominated by gram-positive bacteria. Its been reported that the resistance rates of pathogens in urosepsis are >10% for almost all antibiotics. The main principles of management of urosepsis and sepsis are the same, including early goal-directed treatment and antibiotic administration within the first 45 min. Early goal-directed therapy was recently shown not to be superior to standard care; however, these results may not be applicable to settings in which standard care needs improvement. Selection of an appropriate antibiotic for the initial empirical treatment in urosepsis requires knowledge of previous interventions, antibiotic usage, and local resistance rates. Future research on the management of urosepsis should be directed toward identification of groups at risk of developing urosepsis, antibiotic selection, and value of biomarkers in treatment response (eg, lactate, procalcitonin).Patient summaryIn approximately one-third of patients with sepsis, the source of infection is the urinary tract. This review assessed causes and management of urosepsis and directions for future research.     

脓毒症患者血浆乳酸水平轻度升高与病死率相关性研究

目的既往的研究表明，乳酸水平高于2mmol／L与预后不良相关，但目前还不清楚当乳酸水平在正常范围内升高对预后的影响。本研究拟比较存活组与死亡组乳酸水平的差异，从而明确乳酸相对增高与死亡率的关系，同时寻找提示预后不良的最佳乳酸值。方法采用回顾性分析，研究对象为107例脓毒症患者，所有患者入院时血乳酸水平均波动在0．5—2．0mmol／L范围。首先根据患者住院期间临床结局将患者分为存活与死亡2组，采用独立样本t检验明确两者乳酸水平是否有统计学差异。用ROC曲线寻找预测患者死亡率的最佳乳酸值，进一步根据该值将患者分为高、低乳酸血症2组，再比较2组患者死亡率是否有统计学差异。结果107例患者中32例死亡75例存活。存活组患者血浆乳酸平均值为（0．8347±0．2310）mmol／L，而死亡组为（1．2188±0．3881），t=14．377，P〈0．001，乳酸水平大于1．15mmol／L时预测患者死亡率的敏感性为59．4％，特异性为90．7％（AUC=0．79，P〈0．001，95％CI=0．687～0．893）。高乳酸血症组患者26例，死亡19例，低乳酸血症患者81例，死亡13例，差异有统计学意义（P〈0．001）。结论入院时患者乳酸水平即使轻度升高（1．16—2．00mmoL／L）也与脓毒症患者死亡率增高相关。当乳酸水平大于1．15mmol／L时提示患者预后不良。     

The impact of trauma on neutrophil function

A well described consequence of traumatic injury is immune dysregulation, where an initial increase in immune activity is followed by a period of immune depression, the latter leaving hospitalised trauma patients at an increased risk of nosocomial infections. Here, we discuss the emerging role of the neutrophil, the most abundant leucocyte in human circulation and the first line of defence against microbial challenge, in the initiation and propagation of the inflammatory response to trauma. We review the findings of the most recent studies to have investigated the impact of trauma on neutrophil function and discuss how alterations in neutrophil biology are being investigated as potential biomarkers by which to predict the outcome of hospitalised trauma patients. Furthermore, with trauma-induced changes in neutrophil biology linked to the development of such post-traumatic complications as multiple organ failure and acute respiratory distress syndrome, we highlight an area of research within the field of trauma immunology that is gaining considerable interest: the manipulation of neutrophil function as a means by which to potentially improve patient outcome.     

Treatment of impaired perfusion in septic shock

Severe sepsis and septic shock are relatively common problems in intensive care. The mortality in septic shock is still high, and the main causes of death are multiple organ failure and refractory hypotension. Impaired tissue perfusion due to hypovolemia, disturbed vasoregulation and myocardial dysfunction contribute to the multiple organ dysfunction. Treatment of hemodynamics in septic shock consists of appropriate fluid therapy guided by invasive monitoring combined with vasoactive drugs aiming to correct hypotension and inappropriately low cardiac output. The drug of choice for low vascular resistance is norepinephrine, while insufficient myocardial contractility is commonly treated with dobutamine. The use of norepinephrine seems to be associated with better prognosis as compared to results from the use of dopamine or epinephrine. In septic shock, vasopressin levels are low, and therefore, vasopressin has been advocated as a vasopressor. Its effectiveness and safety have not yet been documented, and so far it is regarded as an experimental treatment. Recent data support the use of corticosteroid, at least in some of the patients with septic shock. Also, activated protein C, a drug with anti-inflammatory and antithrombotic properties, decreases mortality in patients with septic shock.     

Die extrakorporale Therapie septischer Patienten

Zusammenfassung Trotz zahlreicher Fortschritte in der Intensivmedizin stellt die Behandlung von Patienten mit schwerer Sepsis und septischem Schock eine medizinische Herausforderung dar. In der Pathogenese der systemischen Inflammation (SIRS) kommt es zur exzessiven Freisetzung von multiplen endogenen und exogenen inflammatorischen Mediatoren [z. B. Lipopolysaccharid (LPS), Tumor-Nekrose-Faktor (TNF)-α, Interleukin (IL)-1, IL-6] und zur Entwicklung eines Multi- Organ-Versagen (MOV). Dies führt bekannterma?en zu schlechten überlebenszahlen septischer Patienten. Ein komplexes dynamisches Kontrollsystem führt in der Abfolge meist zur zeitnahen gegen-regulatorischen antiinflammatorischen Antwort mittels Induktion anti-inflammatorischer Mediatoren (IL-10, transforming growth factor-beta [TGF-β]). In einer gro?en Anzahl septischer Patienten kommt es durch eine Persistenz des inflammatorischen Reizes zu einer Deaktivierung von antigenpr?sentierenden Zellen bzw. zu einem Versagen des zellvermittelten Immunsystems („Immunparalyse“). Unselektive und selektive intermittierende und kontinuierliche extrakorporale Therapieverfahren wurden evaluiert, ob diese in der Lage sind, in inflammatorische durch den klinischen Verlauf günstig zu beeinflussen. Technologische Fortschritte im Hinblick auf die Entwicklung von extrakorporalen Plasmapherese- bzw. Adsorptionsverfahren bieten heute neue, effektive M?glichkeiten, Mediatoren aus der Blutbahn septischer Patienten zu entfernen. In der vorliegenden übersichtsarbeit werden aktuell verfügbare und zukünftige adjunktive extrakorporale Therapiestrategien vorgestellt und vor dem Hintergrund aktueller Studien diskutiert.