作者: Paul Ellis Marik , Paul Ellis Marik , None
DOI: 10.1007/978-3-319-11020-2_41
关键词:
摘要: Acute kidney injury (formally known as acute renal failure) is a common problem in the ICU. AKI syndrome characterized by rapid loss of kidney’s excretory function and typically diagnosed accumulation end products nitrogen metabolism (urea creatinine) or decreased urine output both [1, 2]. Although serum creatinine (Scr) not perfect marker GFR, it frequently used surrogate to estimate GFR. Currently, additional biomarkers are undergoing investigation more sensitive indicators (cystatin C, IL-18, neutrophil gelatinase-associated lipocalin, molecule 1, etc.) [2, 3]. defined twofold greater increase Scr, GFR decrease >50 % <0 mls/kg/h for 12 h [2]. represents spectrum from risk failure complete function. The RIFLE criteria have been define classify (see Table 41.1) [4]. In critically ill patients usually result extrarenal insults, most commonly sepsis, trauma, hypovolemic “shock”, rhabdomyolysis. pathophysiology with sepsis complex poorly understood; however blood flow does appear play role occurs up two-thirds ICU that increasing severity associated mortality [5]. Even modest degrees resulting dialysis treatment death approximately fivefold [6]. Coca colleagues demonstrated elevations Scr less than classification short-term [7]. this study 10–24 had relative 1.8 (95 CI, 1.3–2.5). who require has remained excess 50 despite improvements renal-replacement therapy aggressive supportive care [8]. It therefore essential all efforts be made avoid complication; i.e. appropriate fluid resuscitation avoidance potentially nephrotoxic drugs. therapeutic intervention choice intravascular volume depletion oliguria furosemide/Lasix™. However, discussed Chap. 9, excessive high central venous pressure will “paradoxically” impair 8). A rational evidence-based approach reduce dysfunction patients.