Transcript Page 52 Acquired Hemolytic Anemias

Acquired Anemia During Pregnancy
Reihaneh Pirjani, M.D.
Perinatologist, Assistant Professor,
Tehran University of Medical Sciences
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Hematologic changes in pregnancy
Physiologic anemia
Neutrophilia
Mild thrombocytopenia
Increased procoagulant factors
Diminished fibrinolysis
Plasma volume increases
Red blood cell mass increase
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A greater expansion of plasma volume relative to the
increase in hemoglobin mass and erythrocyte volume
is responsible for the modest fall in hemoglobin
levels.
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Physiologic anemia of pregnancy should resolve by
six weeks postpartum since plasma volume has
returned to normal by that time.
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Causes of Acquired Anemia during Pregnancy
Iron-deficiency anemia(most common)
Anemia caused by acute blood loss
Anemia of inflammation or malignancy
Megaloblastic anemia
Acquired hemolytic anemia
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‫از کم خونی های دوران بارداری ناشی ازفقر آهن است‬75%
The two most common causes of anemia during
pregnancy and the puerperium are iron
deficiency and acute blood loss
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If
The dietary iron intake is poor
The interval between pregnancies is short
The delivery is complicated by hemorrhage
Iron deficiency anemia readily and rapidly develops.
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Anemia has defined as hemoglobin levels of :
less than 11 g/dL (hematocrit less than 33 percent) in the
first and third trimesters
less than 10.5 g/dL (hematocrit less than 32 percent) in
the second trimester
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‫اولین قدم در بررسی آنمی در حاملگی این است که بتوانیم آنمی فیزیولوژیک‬
‫را از موارد پاتولوژیک افتراق دهیم‪.‬‬
‫برای این منظور‪:‬‬
‫‪ ‬اوأل باید نیاز طبیعی به آهن را در طی حاملگی بدانیم‪.‬‬
‫‪ ‬ثانیأ باید بتوانیم ازپارامترهای آزمایشگاهی استفاده مناسب کرده یا به‬
‫عبارت دیگر یافته های ازمایشگاهی را بتوانیم درست تفسیر کنیم‪.‬‬
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In a typical singleton gestation, the maternal need for
iron averages close to 1000 mg. Of this, 300 mg is for
the fetus and placenta; 500 mg for maternal
hemoglobin mass expansion; and 200 mg that is
shed normally through the gut, urine, and skin.
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patient should undergo a standard evaluation :
 complete blood count
 review of peripheral smear
 reticulocyte count
 serum Fe/TIBC, and ferritin
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Classical morphological evidence of iron-deficiency
anemia—erythrocyte hypochromia and microcytosis—is
less prominent in the pregnant.
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Classical morphological evidence of iron-deficiency
anemia—erythrocyte hypochromia and microcytosis—is
less prominent in the pregnant
Moderate iron-deficiency anemia during pregnancy
usually is not accompanied by obvious morphological
changes in erythrocytes
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If iron deficiency is combined with folate or
vitamin BI2 deficiency, normocytic and normochromic
RBCs are observed on the peripheral blood smear.
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pathologic change in iron deficiency anemia
1. The first pathologic change to occur in iron deficiency
anemia is the depletion of bone marrow, liver, and spleen
iron stores.
2. The serum iron level falls.
3. The total iron-binding capacity rises, because this is a
reflection of unbound transferrin.
4. A falling hemoglobin and hematocrit follow.
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In adult women, iron stores are located in
the bone marrow, liver and spleen in the form of ferritin.
Ferritin constitutes approximately 25 percent (500mg)
of the 2-g of iron stores found in the normal woman.
Approximately 65 percent of stored iron is located in the
circulating RBCs.
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Ferritin
 The ferritin level indicates the total status of her
iron stores.
 Serum ferritin levels normally decrease minimally
during pregnancy.
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Ferritin
 Ferritin levels are variable and can change 25
percent from one day to the next.
 However, a significantly reduced ferritin
concentration is indicative of iron deficiency
anemia and is the best parameter to judge the
degree of iron deficiency.
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Ferritin
Levels less than 10 to 15 mg/L confirm
iron-deficiency anemia
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Serum Transferrin Receptor
measuring serum transferrin receptors can give a
better index of true iron status.
A reduction in the iron supply increases TfR
synthesis.
In patients with iron deficiency anemia, the plasma
receptor is elevated threefold.
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Serum Transferrin Receptor
Ferritin can be elevated in acute and chronic infections,
whereas transferrin receptors do not change in response
to an infection.
Also receptor concentrations are not confounded by the
hemodynamic changes of pregnancy.
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Serum Transferrin Receptor
This test is not yet readily available but may help us
in the future to detect irondeficient patients.
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Serum Iron
A serum iron concentration less than 60 mg/dl
with less than 16 percent saturation of transferrin is
suggestive of iron deficiency.
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Serum Iron
A single normal serum iron concentration does not rule out
iron deficiency.
For example, a patient may take iron for several
days, and this may result in a transiently normal serum
iron concentration while iron stores are still negligible.
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Total Iron-Binding Capacity(TIBC)
TIBC rises in association with iron deficiency and
decreases in chronic inflammatory states.
It is increased in pregnancy because of the increase in
plasma volume.
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Total Iron-Binding Capacity(TIBC)
An increase in iron-binding capacity is not reliable,
because:
 15 percent of pregnant women without iron
deficiency show an increase in this parameter.
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Management Options
In pregnancy, iron absorption from the duodenum
increases.
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Management Options
Antacid medications, commonly used by many patients,
decreases the absorption of iron.
Chronic use of H2 blockers and proton pump inhibitors
also diminishes iron absorption.
Vitamin C, in addition to the iron, may increase the acid
environment of the stomach and increase absorption.
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Iron prophylaxis, however, is safe as only amounts that
can be used are absorbed.
With the exception of dyspepsia and constipation, side
effects are few.
If the iron is not needed, it will not be absorbed and will
be excreted in the feces.
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In iron-deficient patients, one iron tablet three
times daily has been recommended.
ferrous sulfate, fumarate, or gluconate—that
provide approximately 200 mg daily of elemental
iron.
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There are equivalent increases in hemoglobin
levels in women treated with either oral or
parenteral iron therapy.
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Parenteral iron is indicated in those who cannot or
will not take oral iron therapy and are not anemic
enough to require transfusion.
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Transfusions of red cells or whole blood seldom are
indicated unless hypovolemia from blood loss coexists
or an emergency operative procedure must be
performed on a severely anemic woman.
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To replenish iron stores, oral therapy should be
continued for 3 months after anemia has been
corrected
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Recombinant human erythropoietin has also been used
in difficult cases.
It does not cross the placenta but carries a risk of
hypertension and thrombosis.
Its role in pregnancy is not well established.
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Megaloblastic Anemia
megaloblastic anemia beginning during pregnancy
almost always results from folic acid deficiency.
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The earliest biochemical evidence is low plasma folic acid
concentrations.
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Early morphological changes usually include neutrophils that
are hypersegmented and newly formed erythrocytes that are
macrocytic.
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As the anemia becomes more intense, peripheral nucleated
erythrocytes appear and examination of the bone marrow
discloses megaloblastic erythropoiesis
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Treatment
The treatment of pregnancy-induced megaloblastic
anemia should include folic acid, a nutritious diet, and
iron.
As little as 1 mg of folic acid administered orally once daily
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Treatment
By 4 to 7 days after the beginning of treatment, the
reticulocyte count is increased, and leukopenia and
thrombocytopenia are corrected
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Megaloblastic anemia during pregnancy caused by lack
of vitamin B12, that is, cyanocobalamin, is exceedingly
rare.
During pregnancy, vitamin B12 levels are lower than
nonpregnant values because of decreased levels of
binding proteins
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vitamin B12 deficiency in pregnant women is more likely
encountered following partial or total gastric resection.
Other causes are Crohn disease, ileal resection, and
bacterial overgrowth in the small bowel.
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Women who have had a total gastrectomy require
1000 g of vitamin B12 intramuscularly at monthly
intervals.
Those with a partial gastrectomy usually do not need
such therapy, but vitamin B12 levels during pregnancy
should be measured.
.
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Addisonian pernicious anemia, a lack of intrinsic factor is
an extremely uncommon autoimmune disease
Typically has its onset after age 40 years.
Unless treated with vitamin B12, infertility may be a
complication.
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Anemia Associated with Chronic Disease
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renal insufficiency,
suppuration,
inflammatory bowel disease,
systemic lupus erythematosus,
granulomatous infections,
malignant neoplasms,
rheumatoid arthritis
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Bone marrow cellular morphology is not altered
Serum iron concentration is decreased
Ferritin levels usually are elevated.
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Chronic Renal Disease:
Chronic renal insufficiency may be accompanied by
anemia
 usually due to erythropoietin deficiency
 an element of anemia of chronic disease
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Women who have acute pyelonephritis with sepsis often
develop overt anemia.
This is caused by acute red cell destruction from
endotoxin-mediated sepsis, but with normal erythropoietin
production
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Treatment
Adequate iron stores must be ensured.
In pregnancies complicated by chronic renal insufficiency,
recombinant erythropoietin is usually considered when the
hematocrit approximates 20 percent.
One worrisome side effect is hypertension, which is already
prevalent in women with renal disease.
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Hemolysis
Positive antiglobulin test(coombs)
Spherocytosis and reticulocytosis
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Acquired Hemolytic Anemias
1-Autoimmune Hemolytic Anemia:
 primary (idiopathic)
 secondary due to underlying diseases
 induced by infectious etiologies like Mycoplasma
pneumoniae or Epstein-Barr viral mononucleosis
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Acquired Hemolytic Anemias
2-Drug-Induced Hemolytic Anemia:
Penicillin, cephalosporin, probenecid, quinidine,
rifampin and thiopental.
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Acquired Hemolytic Anemia
3-Pregnancy-Induced Hemolytic Anemia:
is rare
resolves within months after delivery.
There is no evidence of an immune mechanism or
intraerythrocytic or extraerythrocytic defects
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Treatment
drug withdrawal
can be prevented by avoidance of the drug
corticosteroid treatment ?
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