Purpose This review provides a focused and comprehensive update on emerging evidence related to acute kidney injury (AKI).Principal findings Acute kidney injury is a significant clinical problem that increasingly complicates the course of hospitalization and portends worse clinical outcome for sick hospitalized patients. The recent introduction of consensus criteria for the diagnosis of AKI (i.e., RIFLE/AKIN classification) have greatly improved our capacity not only to standardize the diagnosis and classification of severity of AKI, but also to facilitate conducting comparative epidemiologic studies in an effort to better understand the burden of adult and pediatric AKI and its syndromes (i.e., septic, cardio-renal, hepato-renal). The characterization of several novel AKI-specific biomarkers (i.e., neutrophil gelatinase-associated lipocalin, kidney injury molecule-1, and interleukin-18) is extending our understanding of the pathophysiology of AKI. Moreover, these biomarkers appear to have clinical relevance for early detection and they provide prognostic value. These innovations are aiding in the design of epidemiologic surveys and randomized trials of therapeutic interventions. Strategies for prevention Editor's Note: This article is the first of two linked special review articles published in this issue of the Journal. The concept of these articles emerged from the scientific content of the 2010 Acute Kidney Injury (AKI) and Renal Support in Critical Illness Symposium, hosted in Edmonton, Alberta. This review (Part 1) provides a focused and comprehensive update on emerging evidence in the diagnosis and classification of AKI, on specific AKI syndromes, and on the prevention and conservative management of hospitalized patients with AKI. Abstracts presented at this meeting were selected on the basis of peer review by the Scientific Committee and were accepted for presentation at the AKI 2010 Symposium, and appear as Electronic Supplementary Material at
Fluid therapy is perhaps the most common intervention received by acutely ill hospitalized patients; however, a number of critical questions on the efficacy and safety of the type and dose remain. In this review, recent insights derived from randomized trials in terms of fluid type, dose and toxicity are discussed. We contend that the prescription of fluid therapy is context-specific and that any fluid can be harmful if administered inappropriately. When contrasting ''crystalloid vs colloid'', differences in efficacy are modest but differences in safety are significant. Differences in chloride load and strong ion difference across solutions appear to be clinically important. Phases of fluid therapy in acutely ill patients are recognized, including acute resuscitation, maintaining homeostasis, and recovery phases. Quantitative toxicity (fluid overload) is associated with adverse outcomes and can be mitigated when fluid therapy based on functional hemodynamic parameters that predict volume responsiveness and minimization of non-essential fluid. Qualitative toxicity (fluid type), in particular for iatrogenic acute kidney injury and metabolic acidosis, remain a concern for synthetic colloids and isotonic saline, respectively. Physiologically balanced crystalloids may be the ''default'' fluid for acutely ill patients and the role for colloids, in particular hydroxyethyl starch, is increasingly unclear. We contend the prescription of fluid therapy is analogous to the prescription of any drug used in critically ill patients.© 2014 Baishideng Publishing Group Co., Limited. All rights reserved.Key words: Fluid therapy; Resuscitation; Critical illness; Peri-operative; Toxicity; Saline; Crystalloid; Colloid Core tip: Fluid therapy is exceedingly common in acutely ill patients; however, numerous questions on the efficacy and safety of fluid therapy in terms of the type and dose remain. Fluid therapy prescription is contextspecific and any fluid type can be harmful if administered inappropriately. When considering crystalloids versus colloids, differences in efficacy are modest but the risk of kidney toxicity and bleeding complications with hydroxyethyl starch appear more significant. The differences in chloride load across crystalloid solutions appears to have physiologic and clinically important effects, in particular for contributing to hyperchloremic metabolic acidosis, kidney injury and greater utilization of renal replacement therapy associated with 0.9% saline. Fluid therapy should be viewed as analogous to the prescription of any drug in acutely ill patients.McDermid RC, Raghunathan K, Romanovsky A, Shaw AD, Bagshaw SM. Controversies in fluid therapy: Type, dose and toxicity.
Heart failure is one of the most common chronic medical conditions in the developed world. It is characterized by neurohormonal activation of multiple systems that can lead to clinical deterioration and significant morbidity and mortality. In this regard, hyponatremia is due to inappropriate and continued vasopressin activity despite hypoosmolality and volume overload. Hyponatremia is also due to diuretic use in an attempt to manage volume overload. When hyponatremia occurs, it is a marker of heart failure severity and identifies patients with increased mortality. The recent introduction of specific vasopressin-receptor antagonists offers a targeted pharmacological approach to these pathophysiological derangements. Thus far, clinical trials with vasopressin-receptor antagonists have demonstrated an increase in free-water excretion, improvement in serum sodium, modest improvements in dyspnea but no improvement in mortality. Continued clinical trials with these agents are needed to determine their specific role in the treatment of both chronic and decompensated heart failure.
We aimed to describe the pre-operative incidence of hyponatremia in patients undergoing liver transplantation (LTx), as well as the rate and consequences of rapid perioperative sodium rises in these patients. Methods: This was a retrospective before and after observational study performed at a University-affiliated LTx center between January 2007 and June 2013. The primary exposure was pre-operative hyponatremia, defined as a serum sodium (SNa) 5133 mmol/L. The primary outcome was occurrence of a rapid SNa shift, defined as 10 mmol/L in the first 24 h following LTx. The rates of rapid peri-operative SNa shift were compared before and after a focused quality assurance (QA) initiative performed in July 2009. Results: Of 366 LTx, 69 (18.9%) had pre-operative hyponatremia, 6 (8.7%) of whom had a rapid rise in serum sodium (SNa). Rapid rise was associated with a greater intra-operative positive fluid balance (p50.001) and use of intra-operative continuous renal replacement therapy (CRRT) (p ¼ 0.017). A rapid rise in SNa was associated with more neurological investigations in the post-transplant period (brain computed tomography, electroencephalogram, swallow studies), increased neurological deficits (p ¼ 0.006), more abnormal swallowing assessments (p ¼ 0.003), a tendency for more neurology consultations (p ¼ 0.058), increased discharge to a rehabilitation or long-term care facility (p50.001), and increased 6-month mortality (p50.001). Following a QA initiative, rapid peri-operative rises in SNa among hyponatremic patients was significantly reduced (20% vs. 0%, p50.003). Conclusion: Pre-operative hyponatremia and rapid peri-operative SNa shifts are associated with a more complicated post-operative course and worse outcomes following LTx. Increased education and awareness, along with process changes, such as standardizing CRRT prescription, can reduce iatrogenic rapid peri-operative shifts in SNa.
IntroductionSodium chlorite is a powerful oxidizing agent with multiple commercial applications. We report the presentation and management of a single case of human toxicity of sodium chlorite.Case reportA 65-year-old man presented to hospital after accidentally ingesting a small amount of a sodium chlorite solution. His principal manifestations were mild methemoglobinemia, severe oxidative hemolysis, disseminated intravascular coagulation, and anuric acute kidney injury. He was managed with intermittent hemodialysis, followed by continuous venovenous hemofiltration for management of acute kidney injury and in an effort to remove free plasma chlorite. Concurrently, he underwent two red cell exchanges, as well as a plasma exchange, to reduce the burden of red cells affected by chlorite. These interventions resulted in the cessation of hemolysis with stabilization of serum hemoglobin and platelets. The patient survived and subsequently recovered normal renal function.DiscussionThis is only the second case of sodium chlorite intoxication reported in the medical literature and the first to report the use of renal replacement therapy in combination with red cell exchange in its management.
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