23 de setembro de 2011

Artigo recomendado: Clinical consequences of red cell storage in the critically ill


Alan Tinmouth, Dean Fergusson, Ian Chin Yee, and Paul C. Hébert for the ABLE Investigators and the Canadian Critical Care Trials Group

TRANSFUSION 2006;46:2014-2027

Over the past 25 years, we have witnessed a dramatic “paradigm shift” whereby red blood cell (RBC) transfusions, once regarded as “one of the great advances in modern medicine,” are now considered harmful in some clinical situations. This paradigm shift has focused attention on the quality of stored transfused blood. Changes accompanying the storage of red cells (RBCs) are known as the “storage lesion,” which can be defined as a series of biochemical and biomechanical changes in the RBC and storage media during ex vivo preservation that reduce RBC survival and function. Although the storage lesion has been well documented for decades,1 our understanding of the mechanisms involved in these changes and clinical consequences remains incomplete. Recent clinical trials and animal experiments have raised fundamental questions about the efficacy of stored RBCs, 2,3 which may haveimportant implications for the future of transfusion research.

In critically ill patients, clinical studies have reported an association between RBC transfusions and increased morbidity and mortality, an effect that may increase with the age of the transfused RBCs. Anemia is very common in the critically ill with 95 percent of patients admitted to the intensive care unit (ICU) experiencing a hemoglobin (Hb) level below normal by the third day 4,5 and 40 percent to 45 percent of critically ill patients receive 5 units of RBCs during their ICU admission.4,5 More recently, a seminal multicenter randomized controlled clinical trial in critically ill patients (TRICC, Transfusion Requirements in Critical Care) demonstrated a lower 30-day mortality rate in the patients randomly assigned to the restrictive transfusion strategy6 (23.3% vs. 18.7%, p = 0.11; Fig. 1). Plausible explanations for the increased morbidity and mortality seen in TRICC may be that prolonged storage renders RBCs ineffective oxygen (O2) carriers and/or modifies RBCs, which cause harm when transfused into vulnerable patients via either a proinflammatory effect or the direct toxic effects of by-products of RBC storage. To date, the mechanisms of action accounting for increased morbidity and mortality remain unknown. In this article, we will review the laboratory and clinical studies evaluating changes to RBCs with prolonged storage followed by a review of studies evaluating the clinical consequences of prolonged RBC storage.

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