Anemia associated with blood loss is the direct result of the decrease in circulating red blood cells (RBCs).The average adult has a total blood volume of approximately 5,000 to 6,000 ml (milliliters) and can usually lose 500 ml of blood without serious or lasting effects; but, if the loss reaches 1,000 ml or more, serious acute consequences may result.
Blood loss can be as a result of very heavy menstrual periods. Most women lose about 44 ml of blood per cycle, but some may lose considerably more. Blood loss also occurs during childbirth or during major surgical procedures.
Certain health issues may also contribute to iron loss, including chronic bleeding of the gums, hemorrhoids, or cancer of the stomach. In addition, prolonged treatment with certain drugs can cause gastrointestinal bleeding. Parasites can also cause anemia as they take blood and nutrients for themselves that are meant for the human host.
The restoration of the full complement of RBCs after blood loss is slower than repletion of other blood constituents. The effects are the same as those of iron deficiency, but may be more severe depending on the extent of the blood loss. The treatment is the same as for iron deficiency, except in severe cases where a transfusion of packed red cells may be necessary.
Early signs are weakness, cool moist skin, tachycardia, and hypotension. Later signs include decreased hemoglobin and hematocrit levels, which may not be evident until several hours after the blood loss has occurred.
Posthemorrhagic anemia is a normocytic-normochromic (see Types) anemia caused by sudden blood loss in an individual with normal iron stores. Hemorrhage may be obvious, that is, after surgery or before a trauma, as in the cases of malignancies or gastrointestinal disorders. It should be noted that minor prolonged hemorrhage does not result in classic posthemorrhagic anemia, but rather in iron deficiency anemia.
Within twenty-four hours of blood loss, there is a reduction in the number of circulating erythrocytes, which affects blood volume and its consistency. To compensate, water and electrolytes from tissues and interstitial spaces are mobilized to expand plasma volume and accelerate the formation and development of blood cells in the bone marrow (hematopoiesis).
While this action maintains adequate blood volume, it decreases the viscosity (thickness) of the blood. Diluted blood flows faster and more turbulently than normal blood and can cause heart problems (ventricular dysfunction, cardiac dilation, and heart valve insufficiency).
Clinical indications of anemia are likely to be obscured by the cardiovascular manifestations of acute hemorrhage. Severe shock, lactic acidosis, and death occur if blood loss exceeds 40% to 50% of plasma volume. Some of the apparent heart problems resulting from anemia are the result of hypoxia (decreased oxygen). This causes all blood vessels to dilate, speeding up the flow even more. As venus return to the heart increases, the heart pumps harder and faster to prevent cardiopulmonary congestion – all of which can cause congestive heart failure.
Tissue hypoxia has other effects on the heart and lungs. The rate and depth of breathing increase in an attempt to make more oxygen available to the remaining erythrocytes. Cardiac output increases to handle increased venus return and speed the remaining oxygen-carrying erythrocytes to and from hypoxic tissue cells. Hemoglobin in the erythrocytes releases its oxygen more readily than usual at the tissue level.
Treatment entails restoring blood volume through intravenous (IV) administration of saline, dextran, albumin, or plasma. For large blood losses, transfusion of fresh whole blood is the treatment of choice. The anemia itself does not require specific therapy unless it is associated with iron, folic acid (B9), or cobalamin (B12) deficiency.
A normal erythrocyte count is usually evident within four to six weeks, but hemoglobin restoration can take up to eight weeks.