الفهرس 
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Abstract
The etiology of anemia in critically ill patient is likely multifactorial, and may be the result of hemodilution, active bleeding, hemolysis, inflammation, phlebotomy, or more commonly combination of these factors. Other important contributing factors that exacerbate anemia in the critically ill include coagulopathies, pathogen-associated hemolysis, and nutrition deficiencies.
Red blood cell production in critically ill patients is often abnormal and is involved in the development and maintenance of anemia. The pathophysiology of this anemia is complex and includes decreased production of erythropoietin (EPO), impaired bone marrow response to EPO, and reduced RBC survival. Critically ill patients have an inappropriately low EPO concentration irrespective of the presence of acute renal failure.
Blood transfusions are frequently given to patients in intensive care units to treat low hemoglobin levels due to either acute blood loss or subacute anemia associated with critical illness. Although blood transfusion is a life-saving therapy, evidence suggests that it may be associated with an increased risk of morbidity and mortality.
Transfusion risks can be categorized into infectious and noninfectious risks, with the latter further grouped into immunogenic and non-immunogenic risks. Today’s blood supply is safer from infectious risks than ever. But, risk has not been eliminated completely, because many infections have window periods during which they are not detectable by assays beside risk of emerging new pathogen that is not recognized.
Noninfectious risks are more common, exceeding infectious risks by many factors. Noninfectious risks, include febrile, allergic/anaphylactic and hemolytic transfusion reactions, transfusion-related acute lung injury (TRALI) and transfusion-associated circulatory overload (TACO). They can lead to greater morbidity and mortality.
Erythropoietin has been used to treat anemia and avoid risks of blood transfusions. Also it has a cytoprotective agent as Epo receptors were found in many cell types. EPO can increase iron absorption by suppressing the hormone hepcidin. EPO also may be beneficial in treatment of patients with acute coronary syndromes. High levels of endogenous EPO in patients with a first MI who underwent successful primary coronary intervention were found to be associated with smaller infarcts, which were interpreted by the investigators as a possible endogenous, protective mechanism.
A number of problems have been associated with administration of high dose EPO. Erythropoietin has a range of adverse actions including vasoconstriction-dependent hypertension, stimulating angiogenesis, and inducing proliferation of smooth muscle fibers. Also, high doses of EPO raise hematocrite which increases the chance of increased thrombosis, seizures and hypertension. Recent experimental work indicates that lower dosages of Epo may in fact be effective.