# 36 - 106 Anemia Due to Acute Blood Loss

### 106 Anemia Due to Acute Blood Loss

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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