36 - 106 Anemia Due to Acute Blood Loss

106 Anemia Due to Acute Blood Loss

Loirat C et al: An international consensus approach to the manage­ ment of atypical hemolytic uremic syndrome in children. Pediatr Nephrol 31:15, 2016. Luzzatto L et al: Glucose-6-phosphate dehydrogenase deficiency. Blood 136:1225, 2020. Notaro R, Luzzatto L: Breakthrough hemolysis in PNH with proxi­ mal or terminal complement inhibition. N Engl J Med 387:160, 2022. Roy NBA et al: The use of next-generation sequencing in the diagnosis of rare inherited anaemias: A joint BSH/EHA Good Practice Paper. Br J Haematol 198:459, 2022. Uyoga S et al: Glucose-6-phosphate dehydrogenase deficiency and susceptibility to childhood diseases in Kilifi, Kenya. Blood Adv 4:5942, 2020. Dan L. Longo

Anemia Due to Acute

Blood Loss Blood loss causes anemia by two main mechanisms: (1) by the direct loss of red cells; and (2) if the loss of blood is protracted, it will gradu­ ally deplete iron stores, eventually resulting in iron deficiency. The latter type of anemia is covered in Chap. 102. Here, we are concerned

with the former type, that is, posthemorrhagic anemia, which follows acute blood loss. This can be external (e.g., after trauma or obstetric hemorrhage) or internal (e.g., from bleeding in the gastrointestinal tract, rupture of the spleen, rupture of an ectopic pregnancy, sub­ arachnoid hemorrhage, leaking aneurysm). In any of these cases, after the sudden loss of a large amount of blood, there are three clinical/ pathophysiologic stages. (1) At first, the dominant feature is hypovo­ lemia, which poses a threat particularly to organs that normally have a high blood supply, like 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 because the hemoglobin concentration is not affected. As hypovolemia is corrected with intravenous fluids acutely, the hemoglobin will gradu­ ally fall over several hours. On physical exam, tachycardia, tachypnea, decreased pulse pressure, cold skin that appears pale and mottled, and decreased urine output may be noted reflecting the efforts of the sympathetic nervous system to compensate. (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 hemodilu­ tion; thus, the hypovolemia gradually converts to anemia. The degree of anemia will reflect the amount of blood lost. If after 3 days the hemo­ globin is, for example, 7 g/dL, it means that about half of the entire blood has been lost. (3) Provided bleeding does not continue, the bone marrow response will gradually ameliorate the anemia. In this phase of the process, the reticulocyte count and erythropoietin levels will be ele­ vated. The physiologic increase in marrow red cell production reflected by the increase in reticulocytes is similar to the marrow response to hemolysis. Hemolysis and compensatory marrow increase in red blood cell (RBC) production are the two major mechanisms associated with anemia that is accompanied by an increase in reticulocyte count. The diagnosis of acute posthemorrhagic anemia (APHA) is usually straightforward, although sometimes internal bleeding episodes (e.g., after a traumatic injury), even when large, may not be immediately obvious. When the scene is bloody, often the estimate of the volume of blood loss is overestimated. Always check the patient carefully. Look for physical findings that may help localize the bleeding if the site of bleed­ ing is not obvious. Grey Turner sign (flank ecchymosis) may reflect retroperitoneal bleeding. Cullen sign (umbilical ecchymosis) may

suggest intraperitoneal or retroperitoneal bleeding. Dullness to chest percussion may suggest intrapleural bleeding. 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 investi­ gations (e.g., a sonogram or an endoscopy) may have to be carried out.

If blood loss is mild, enhanced O2 delivery is achieved through changes in the O2–hemoglobin dissociation curve mediated by a decreased pH or increased CO2 (Bohr effect). With acute blood loss, hypovolemia dominates the clinical picture, and the hematocrit and hemoglobin levels do not reflect the volume of blood lost. Signs of vascular instability appear with acute losses of 25% or more of the total blood volume. The donation of a unit of blood (~20% of the blood volume) is often minimally symptomatic. In patients who lose a larger percentage of the blood volume, the issue is not anemia but hypotension and decreased organ perfusion. When >30% of the blood volume is lost suddenly, patients are unable to compensate with the usual mechanisms of sympathetic nervous system increases in heart rate, vascular contraction, and changes in regional blood flow. The patient prefers to remain supine and will show postural hypotension and tachycardia. If the volume of blood lost is >40% (i.e., >2 L in the average-sized adult), signs of hypovolemic shock including confu­ sion, dyspnea, diaphoresis, hypotension, and tachycardia appear. Such patients have significant deficits in vital organ perfusion and require immediate volume replacement. CHAPTER 106 Symptoms associated with more chronic or progressive anemia depend on the age of the patient and the adequacy of blood supply to critical organs. Symptoms associated with moderate anemia include fatigue, loss of stamina, breathlessness, and tachycardia (particularly with physical exertion). However, because of the intrinsic compensa­ tory mechanisms that govern the O2–hemoglobin dissociation curve, the gradual onset of anemia—particularly in young patients—may not be associated with signs or symptoms until the anemia is severe (hemo­ globin <70–80 g/L [7–8 g/dL]). When anemia develops over a period of days or weeks, the total blood volume is normal to slightly increased, and changes in cardiac output and regional blood flow help compen­ sate for the overall loss in O2-carrying capacity. Changes in the posi­ tion of the O2–hemoglobin dissociation curve account for some of the compensatory response to anemia. With chronic anemia, intracellular levels of 2,3-bisphosphoglycerate rise, shifting the dissociation curve to the right and facilitating O2 unloading. This compensatory mechanism can only maintain normal tissue O2 delivery in the face of a 20–30 g/L (2–3 g/dL) deficit in hemoglobin concentration. Finally, further protec­ tion of O2 delivery to vital organs is achieved by the shunting of blood away from organs that are relatively rich in blood supply, particularly the kidney, gut, and skin. Anemia Due to Acute Blood Loss TREATMENT Anemia Due to Acute Blood Loss In patients who are hemodynamically unstable, the usual airway, breathing, and circulation assessments take priority. In the face of bleeding associated with hypotension, pharmacologic support with vasopressors is critical. With respect to anemia treatment, a twopronged approach is imperative. (1) In many cases, the blood lost needs to be replaced promptly. Unlike with many chronic anemias, when finding and correcting the cause of the anemia is the first pri­ ority and blood transfusion may not be even necessary because the body is adapted to the anemia, with acute blood loss, the reverse is true. Because the body is not adapted to the anemia, blood transfu­ sion takes priority. (2) While the emergency is being confronted, it is imperative to stop the hemorrhage and to eliminate its source. In an acute hemorrhage situation, plasma may be preferred to saline for volume expansion since dilution of clotting factors with crystalloid may interfere with hemostasis. Furthermore, trauma can lead to vascular and platelet abnormalities that enhance the bleeding risk. A special type of APHA is blood loss during and immediately after surgery, which can be substantial (e.g., up to 2 L in the case of a