脓毒症致急性肾损伤的处理

S. Rajapakse, C. Rodrigo, Eranga S. Wijewickrema
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引用次数: 1

摘要

12.00 Normal 0 false false false EN-US X-NONE X-NONE 12.00 Normal 0 false false false false EN-US X-NONE X-NONE /* Style Definitions */表。mso-style-name:"Table Normal";mso-tstyle-rowband-size: 0;mso-tstyle-colband-size: 0;mso-style-noshow:是的;mso-style-priority: 99;mso-style-qformat:是的;mso-style-parent:“”;mso- font - family:宋体;mso-para-margin: 0;mso-para-margin-bottom: .0001pt;mso-pagination: widow-orphan;字体大小:11.0分;字体类型:“Calibri”、“无衬线”;mso-ascii-font-family: Calibri;mso-ascii-theme-font: minor-latin;mso-fareast-font-family:宋体;mso-fareast-theme-font: minor-fareast;mso-hansi-font-family: Calibri;mso-hansi-theme-font: minor-latin;mso-bidi-font-family:宋体;} /*样式定义*/mso-style-name:"Table Normal";mso-tstyle-rowband-size: 0;mso-tstyle-colband-size: 0;mso-style-noshow:是的;mso-style-priority: 99;mso-style-qformat:是的;mso-style-parent:“”;mso- font - family:宋体;mso-para-margin: 0;mso-para-margin-bottom: .0001pt;mso-pagination: widow-orphan;字体大小:11.0分;字体类型:“Calibri”、“无衬线”;mso-ascii-font-family: Calibri;mso-ascii-theme-font: minor-latin;mso-fareast-font-family:宋体;mso-fareast-theme-font: minor-fareast;mso-hansi-font-family: Calibri;mso-hansi-theme-font: minor-latin;mso-bidi-font-family:宋体;急性肾损伤(Acute kidney injury, AKI)在严重脓毒症患者中发生的比例相当大,是严重脓毒症患者死亡的重要原因。目前关于AKI发病机制的概念正在从血管收缩-缺血诱导的损伤转向毒性和免疫介导的损伤以及导致肾细胞凋亡的充血性损伤。肾脏替代疗法是AKI治疗的主要手段。充分的透析可能与更好的结果有关,但对透析的时间、方式、强度或频率仍没有明确的共识。血流动力学不稳定的患者通常需要持续的肾脏替代治疗模式。生物相容性透析膜可能比旧的纤维素膜更安全。碳酸氢盐优于醋酸盐和乳酸盐作为透析液缓冲液。抗凝必须小心地进行,以防止在已经紊乱的止血情况下过度出血。充分的容量复苏和使用血管加压剂维持肾灌注是有益的;去甲肾上腺素是首选的血管加压剂。在脓毒症引起的AKI中,没有使用低剂量或肾剂量多巴胺、甘露醇或氟塞胺的地方,事实上它们可能是有害的。预防肾毒性药物和造影剂对肾脏的损害是至关重要的。仔细管理肾毒性药物的剂量可以防止肾损伤。在给予造影剂之前进行水化可防止肾毒性,但n -乙酰半胱氨酸的益处尚不清楚。严格的血糖控制可能有保护肾的作用,尽管其在严重败血症治疗中的地位目前尚有争议。没有明确的证据表明其他新疗法有益。关键词:重症监护;急性肾损伤;透析;引用本文:Rajapakse S, Rodrigo C, Wijewickrema ES。脓毒症致急性肾损伤的处理。斯里兰卡重症监护杂志2009;1:3-14 DOI: 10.4038/sljcc.v1i1.937
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Management of Sepsis-Induced Acute Kidney Injury
12.00 Normal 0 false false false EN-US X-NONE X-NONE 12.00 Normal 0 false false false EN-US X-NONE X-NONE /* Style Definitions */ table.MsoNormalTable {mso-style-name:"Table Normal"; mso-tstyle-rowband-size:0; mso-tstyle-colband-size:0; mso-style-noshow:yes; mso-style-priority:99; mso-style-qformat:yes; mso-style-parent:""; mso-padding-alt:0in 5.4pt 0in 5.4pt; mso-para-margin:0in; mso-para-margin-bottom:.0001pt; mso-pagination:widow-orphan; font-size:11.0pt; font-family:"Calibri","sans-serif"; mso-ascii-font-family:Calibri; mso-ascii-theme-font:minor-latin; mso-fareast-font-family:"Times New Roman"; mso-fareast-theme-font:minor-fareast; mso-hansi-font-family:Calibri; mso-hansi-theme-font:minor-latin; mso-bidi-font-family:"Times New Roman"; mso-bidi-theme-font:minor-bidi;} /* Style Definitions */ table.MsoNormalTable {mso-style-name:"Table Normal"; mso-tstyle-rowband-size:0; mso-tstyle-colband-size:0; mso-style-noshow:yes; mso-style-priority:99; mso-style-qformat:yes; mso-style-parent:""; mso-padding-alt:0in 5.4pt 0in 5.4pt; mso-para-margin:0in; mso-para-margin-bottom:.0001pt; mso-pagination:widow-orphan; font-size:11.0pt; font-family:"Calibri","sans-serif"; mso-ascii-font-family:Calibri; mso-ascii-theme-font:minor-latin; mso-fareast-font-family:"Times New Roman"; mso-fareast-theme-font:minor-fareast; mso-hansi-font-family:Calibri; mso-hansi-theme-font:minor-latin; mso-bidi-font-family:"Times New Roman"; mso-bidi-theme-font:minor-bidi;} Acute kidney injury (AKI) occurs in a significant proportion of patients with severe sepsis, and is an important cause of mortality in such patients. Current concepts of pathogenesis of AKI are shifting from vasoconstriction-ischaemia induced injury to toxic and immune mediated injury and hyperaemic injury resulting in apoptosis of renal cells.  Renal replacement therapy is the mainstay of management of AKI. Adequacy of dialysis is likely to be linked to better outcome, but there is still no clear consensus on the timing, modality, intensity or frequency of dialysis. Haemodynamically unstable patients usually require modes of continuous renal replacement therapy. Biocompatible dialyser membranes are likely to be safer than older cellulose membranes. Bicarbonate is preferred to acetate and lactate as dialysate buffer.  Anticoagulation has to be undertaken with care to prevent excessive haemorrhage in the setting of already deranged  haemostasis.  Adequate volume resuscitation and maintenance of renal perfusion by the use of vasopressors is beneficial; norepinephrine is the vasopressor of choice. There is no place for the use of low- or renal-dose dopamine, mannitol or frusemide in the setting of sepsis-induced AKI, and in fact they may be detrimental. Prevention of kidney damage by nephrotoxic drugs and radio-contrast media is of vital importance. Careful dose management of nephrotoxic drugs will prevent renal injury. Hydration prior to administration of contrast media prevents nephrotoxicity, but the benefit of N-Acetylcysteine is unclear. Tight glycaemic control may have renoprotective effects, though its place in the management of severe sepsis is now controversial. No clear evidence of benefit is seen with other newer therapies. Keywords: Critical care; acute kidney injury; dialysis; renal replacement Citation: Rajapakse S, Rodrigo C, Wijewickrema ES. Management of Sepsis-Induced Acute Kidney Injury. Sri Lanka Journal of Critical Care 2009;1:3-14 DOI: 10.4038/sljcc.v1i1.937
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