Chapter 101. Hemolytic Anemias and Anemia Due to Acute Blood Loss (Part 18)

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Anemia Due to Acute Blood Loss Blood loss causes anemia by two main mechanisms: first, by the direct loss of red cells; second, because if the loss of blood is protracted, it will gradually deplete the iron stores, eventually resulting in iron deficiency. Iron-deficiency anemia is discussed in Chap. 98. Here we are concerned with post-hemorrhagic anemia, which follows acute blood loss. This can be external (as after trauma or due to postpartum hemorrhage) or internal (e.g., from bleeding in the gastrointestinal tract, rupture of the spleen, rupture of an ectopic pregnancy). In any of these cases—i.e., after the sudden...

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Chapter 101. Hemolytic Anemias and Anemia Due to Acute Blood Loss (Part 18) Anemia Due to Acute Blood Loss Blood loss causes anemia by two main mechanisms: first, by the direct loss of red cells; second, because if the loss of blood is protracted, it will gradually deplete the iron stores, eventually resulting in iron deficiency. Iron-deficiency anemia is discussed in Chap. 98. Here we are concerned with post-hemorrhagic anemia, which follows acute blood loss. This can be external (as after trauma or due to postpartum hemorrhage) or internal (e.g., from bleeding in the gastrointestinal tract, rupture of the spleen, rupture of an ectopic pregnancy). In any of these cases—i.e., after the sudden loss of a large amount of blood—three clinical/pathophysiologic stages are noted. 1. At first, the dominant feature is hypovolemia, which poses a threat particularly to organs that normally have a high blood supply, such as
the brain and the kidneys; therefore, loss of consciousness and acute renal failure are major threats. It is important to note that at this stage an ordinary blood count will not show anemia, as the hemoglobin concentration is not affected. 2. Next, as an emergency response, baroreceptors and stretch receptors will cause release of vasopressin and other peptides, and the body will shift fluid from the extravascular to the intravascular compartment, producing hemodilution. Thus, the hypovolemia gradually converts to anemia. The degree of anemia will reflect the amount of blood lost. If after 3 days the hemoglobin is, say, 7 g/dL, it means that about half of the entire blood volume had been lost. 3. Provided bleeding does not continue, the bone marrow response will gradually ameliorate the anemia if erythropoietin production, the erythroid progenitors, and iron supply are normal. Within about 2–3 days after acute hemorrhage, reticulocytes will increase in the blood and reach a maximum 7–10 days after the hemorrhage has been controlled. Reticulocyte counts of 20% may be achieved. The diagnosis of acute post-hemorrhagic anemia (APHA) is usually straightforward, although sometimes internal bleeding episodes—after a traumatic injury or otherwise—may not be immediately obvious, even when large.
Whenever an abrupt fall in hemoglobin has taken place, whatever history is given by the patient, APHA should be suspected. Supplementary history may have to be obtained by asking the appropriate questions, and appropriate investigations (e.g., a sonogram or an endoscopy) may have to be carried out. Internal bleeding may result in a rise in unconjugated bilirubin and a fall in serum haptoglobin. Anemia Due to Blood Loss: Treatment With respect to treatment, a two-pronged approach is imperative. First, in many cases the blood lost needs to be replaced promptly. With many chronic anemias, finding and correcting the cause of the anemia is the first priority, and blood transfusion may not be even necessary, because the body is adapted to the anemia; with acute blood loss the reverse is true. Since the body is not adapted to the anemia, blood transfusion takes priority. Although fluorocarbon synthetic chemicals have shown promise, no "blood substitute" has yet become standard treatment. Second, while the emergency is being confronted, it is imperative to stop the hemorrhage and to eliminate its source. Acknowledgment H. Frank Bunn and Wendell Rosse contributed this chapter in the last edition and material from that chapter has been used here Further Readings
Dacie J: The Haemolytic Anaemias, 5 volumes. London, Churchill Livingstone, 1995 Eber S, Lux SE: Hereditary spherocytosis—defects in proteins that connect the membrane skeleton to the lipid bilayer. Semin Hematol 41:118, 2004 [PMID: 15071790] Heier HE et al: Transfusion versus alternative treatment modalities in acute bleeding: A systematic review. Acta Anaesthesiol Scand 509:20, 2006 Hill A et al: Recent developments in the understanding and management of paroxysmal nocturnal hemoglobinuria. Br J Haematol 137:181, 2007 [PMID: 17408457] Hillmen P, et al: The complement inhibitor eculizumab in paroxysmal nocturnal hemoglobinuria. N Engl J Med 355:1233, 2006 [PMID: 16990386] Luzzatto L: Paroxysmal nocturnal hemoglobinuria, in Clinical Hematology, N Young, Gershon SL, High KA (eds). Philadelphia, Mosby, pp 326–339, 2006 Rosse WF, Hillmen P, Schreiber AD: Immune-mediated hemolytic anemia.
Hematology, Am Soc Hematol Educ Program pp. 48–62, 2004 Shapira Y et al: Erythropoietin can obviate the need for repeated heart valve replacement in high-risk patients with severe mechanical hemolytic anemia: Case reports and literature review. J Heart Valve Dis 10:431, 2001 [PMID: 11499585]