The symptoms of iron-deficiency anemia may resemble other blood conditions or medical problems. Always consult your doctor for a diagnosis. Iron-deficiency anemia may be suspected from general findings on a complete medical history and physical examination, such as complaints of tiring easily, abnormal paleness or lack of color of the skin, or a fast heartbeat tachycardia.
Iron-deficiency anemia is usually discovered during a medical examination through a blood test that measures the amount of hemoglobin number of red blood cells present, and the amount of iron in the blood. In addition to a complete medical history and physical examination, diagnostic procedures for iron-deficiency anemia may include the following:. This test is usually not necessary. These tests may help rule out a source of blood loss. Iron-rich diet. Eating a diet with iron-rich foods can help treat iron-deficiency anemia.
Good sources of iron include the following:. Legumes, such as lima beans and green peas; dry beans and peas, such as pinto beans, black-eyed peas, and canned baked beans. Iron supplements. Iron supplements can be taken over several months to increase iron levels in the blood.
Iron supplements can cause irritation of the stomach and discoloration of bowel movements. They should be taken on an empty stomach, or with orange juice, to increase absorption. They are much more effective than dietary interventions alone.
In cases of malabsorption or intolerance, IV iron may be needed. Evaluation for a source of blood loss. Heart failure caused directly by severe anemia is relatively rare, according to Amsterdam. But if you have heart disease already, Amsterdam notes that even less severe cases of iron deficiency anemia can contribute to noticeable heart-related symptoms like shortness of breath or angina chest pain.
Possible loss of blood from your gastrointestinal tract may also be investigated. Most of the time, though, Amsterdam says, an infusion or two will need to be followed up by oral iron supplements, which will result in slow and steady progress rather than an instant improvement.
According to an article published in August in the journal Cardiovascular Therapeutics , among people with heart failure and iron deficiency, IV iron infusions were shown to improve symptoms, exercise capacity, and overall quality of life, both immediately and over time.
But proper treatment of iron deficiency, according to Landau, can make a big difference for people with heart conditions. A standard procedure in the workup of any anemia is the examination of the peripheral blood smear. The potential presence of multiple causes of anemia in HF dictates the assessment of the iron profile, the measurement of vitamin B 12 folic acid, and the assessment of thyroid function tests.
Iron profile includes transferrin saturation, transferrin total iron binding capacity , serum iron, and ferritin. In the presence of inflammation, however, ferritin levels are increased because it is an acute phase reactant.
The ratio of serum transferring receptors reflect tissue iron availability to ferritin has been proposed to distinguish between anemia due to iron deficiency versus inflammation anemia of chronic disease. Functional iron deficiency is characterized by inability to use available iron stores. To verify the presence of hemodilution, blood volume analysis with the chromium labeling technique or with I — tagged albumin could be considered; its use, however, has been restricted to research.
The etiology of anemia needs to be identified for the proper management of anemia. The causes of anemia in HF include the following Table 3 : hemodilution, inflammation Table 4 , renal impairment, iron deficiency, medications angiotensin-converting enzymes inhibitors [Table 5], angiotensin receptor antagonists and carvedilol [Table 6] , vitamin B 12 and folic acid deficiency, and thyroid function abnormalities.
The only consensus in the management of anemia in HF is in correcting hematinic deficiencies that include iron, vitamin B 12 , and folic acid. Iron deficiency is relatively common at least one third in patients with HF and may be caused by interference with iron absorption by hepcidin, poor dietary intake, an edematous gastrointestinal tract, or blood loss secondary to medications acetylsalicylic acid and warfarin.
Iron deficiency should be identified and is usually treated with oral supplementation Table 7. Hemoglobin rises within 2 weeks, the deficit is half corrected at 4 weeks, and fully corrected at 8 weeks.
On occasion, when a failure to respond to oral supplementation is noted, iron could be administered intravenously. Several preparations are available, such as ferric gluconate complex, iron sucrose, and ferric carboxymaltose Table 8. Despite the symptomatic improvement reported with intravenous iron in patients with HF, its role as a therapeutic intervention may await further classification of its impact on morbidity and mortality and long-term safety.
The only indication for blood transfusion is the presence of severe anemia. Red cell preparation and not whole blood should be selected to minimize volume overload, and concomitant diuretics need to be administered in the vast majority of patients with HF to avoid volume overload. The use of iron supplementation for the correction of iron deficiency anemia could be monitored by repeating hemoglobin in 4 weeks half way correction and 8 weeks Table 9.
Restoring iron stores requires a minimum of 6 months of treatment. In the occasional patient who fails to respond to oral supplementation, an intravenous preparation could be considered. Erythropoietin is a pleiotropic cytokine of renal origin produced in response to hypoxia to promote survival of red blood cells by inhibiting apoptosis of erythroblasts.
Increasing hemoglobin and thereby oxygen delivery could be achieved by the administration of erythropoiesis stimulating agents. However, their use in non-HF patients has been associated with undesirable affects, including elevated blood pressure, thrombotic events including stroke and increased risk of death. Hemodynamically they cause an increase in peripheral vascular resistance, a reduction in cardiac output, and lowering of left ventricular ejection fraction.
The use of erythropoiesis stimulating agents for the treatment of anemia in HF will be determined by the findings of the Reduction of Events with Darbepoetin Alfa in Heart Failure RED-HF trial in which patients with systolic HF and anemia were randomized to darbepoetin alfa or a placebo.
Oral iron supplementation may be associated with gastrointestinal side effects, including constipation or diarrhea, abdominal discomfort, or nausea and vomiting. The side effects of intravenous iron are related to the specific preparation.
In the Fair-HF trial, the adverse events in the group receiving ferric carboxymaltose were similar to the placebo group. There are no data that guide the management of anemia in patients with HF who have concomitant comorbidities including renal impairment and diabetes mellitus.
It would be useful, however, to review the available experience in the predominantly non-HF population.
Two studies have suggested that achievement of a higher hematocrit or hemoglobin target was associated with higher cardiovascular risk. The study was terminated prematurely because of a trend toward higher mortality and myocardial infarction in the higher hematocrit group. The higher hemoglobin target group experienced an increased incidence of the composite endpoint death, myocardial infarction, hospitalization for HF and stroke.
Based on these studies, the U. A subsequent analysis from TREAT demonstrated that a poor initial response to darbepoetin alfa requiring escalating doses was associated with increased risk of death or cardiovascular events, which raised concerns about the appropriateness and safety of targeting higher hemoglobin level as well as the need to assess responsiveness to ESAs.
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