Download Anemia in Pregnancy

David M. Ellis
University of Gambia
Gynecology/Obstetrics 2
November, 2009
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Definition
Incidence
Etiology and Pathogenesis
Causes and Stages
Clinical characteristic/ Correlates in
Pregnancy
Diagnostic Approach
Management and Therapy/ Pregnancy
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Anemia is functionally defined as a decrease in
the competence of blood to carry oxygen to
tissues, thereby causing tissue hypoxia.
Clinically, it refers to a decrease in the normal
concentration of hemoglobin or erythrocytes.
However, anemia is not a disease per se but an
expression of an underlying disorder or disease.
Anemia in pregnancy is a condition of oxygen
delivery incompetence during the term of
pregnancy.
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Anemia in Africa has been defined by WHO
as Hb ≤10 g/dl.
Severity:
Moderate: 7-10.9 g/dl
Severe: 4-6.9 g/dl
Very severe: less than 4 g/dl
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According to one 1980s World Health
Organization, world incidence of anemia in
pregnancy is perhaps 51%.
Developed countries had an incidence of
14%.
However, Africa had an incidence of 63% for
all pregnant women ages 15-49.
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Hemoglobin is the intracellular protein of
erythrocytes responsible for transport of oxygen
from the lungs to the tissues. Its synthesis is
controlled by iron concentration within the cell.
Each Hb molecule is capable of carrying 4
molecules of O2, one molecule bound to each
of 4 iron-cored heme structures of hemaglobin.
Oxygen affinity (the ease with which Hb binds
and releases oxygen) is dependent on pO2, pH,
pCO2, 2,3-DPG, and temperature and can be
depicted by the oxygen dissociation curve.
Right-shifting of the
curve results in
decreased O2 affinity.
Increased CO2, heat,
and acid decrease O2
affinity.
 Left-shifting leads to
increased affinity. High
O2 concentrations
increase oxygen
affinity.
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Hemoglobin occupies
33% of the volume of
an erythrocyte and
accounts for 90% of
the cell’s dry weight.
Its concentration is
reported as mean
corpuscular
hemoglobin (MCH).
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In anemic states, the
erythrocyte may
contain less
hemoglobin and/or
there may be fewer
erythrocytes present,
often due to
compromises in the
erythrocyte membrane
or metabolic pathways.
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Red cell membranes are
supported by a protein
skeleton. Inherent
variants within these
proteins manifest as
abnormalities of shape,
as in sphero-, ellipto-,
and ovalocytosis.
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Erythrocytes obtain ATP
from breakdown of
glucose, 95% of which is
metabolized by
anaerobic glycolysis.
There are a number of
enzymyopathies
accounting for the
limitations in number of
RBCs and in optimal
delivery of O2.
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Based on a 5000 ml blood volume in a normal
adult, the total body mass of hemoglobin is
approximately 750 g. Since the normal
erythrocyte lifespan is about 120 d., and the
amount synthesized must be balanced with
amount lost, the body loses and produces
about 6.25 g of hemoglobin per day.
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If erythrocyte survival time is decreased by
hemolysis or hemorrhage, the bone marrow
producing them can be increased by a factor
of up to 10, so that erythrocyte life span may
decrease to about 18 days before marrow
compensation is inadequate and anemia
develops. If erythrocyte production cannot
be increased to match the erythrocyte loss,
anemia develops.
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Screening for anemia generally relies on the
relative hemoglobin and hematocrit (% of total
blood volume consisting of erythrocytes).
However, there are a few instances when the
hemoglobin or hematocrit concentration may be
misleading. One such case, common in
pregnancy, is hypervolemia, a total blood
volume increase caused by a plasma volume
increase while the erythrocyte mass remains
stable. In such case, Hb/Hct concentrations will
appear falsely decreased from hemodilution.
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On average, total red
cell mass increases
throughout pregnancy
by 25%. The
circulating plasma
volume increases by
about 40%. Thus,
there is a normal
dilutional drop in Hb
level.
Blood Loss- May be acute, as in trauma;
May be chronic, as in parasitic hookworm
infestation.
 Decreased Red Blood Cell Production May be nutritional, as in deficiency of iron,
folates, B12, vitamins;
 May be depressed bone marrow function:
 Secondary anemias (HIV, TB, Carcinomas)
 Aplastic anemias (Chemicals, Radiation, Drugs)
 Thalassemias
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Increased RBC Destruction-
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RBC Abnormalities
Hb (Sickle Cell Disease); Enzymatic (G6PD
Deficiency); Membrane-related
(Spherocytosis)
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Increased RBC Destruction-
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Abnormal Hemolysis continued
Immune Hemolysis (Autoimmune,
Fetomaternal, Incompatible Transfusion)
Non-Immune Hemolysis (Infection-i.e.,
Malaria, Venoms, Burns, Hypersplenism)
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Risk factors for anemia in pregnancy can be
drawn from causes of anemia often found in
pregnancy: excessive blood loss, poor diet,
malabsorption, chronic disease, thyroid
endocrinopathy.
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Anemia reduces the O2 carrying capacity of
the blood. The body compensates by 1)
increasing the release of O2 from Hb to the
tissues; 2) increasing cardiac output; 3)
enhancing blood flow to tissues with high O2
requirements; 4) increasing respiration. The
severity of the anemia may be considered as
passing through four stages:
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Compensated- in mild
to moderate anemia.
O2 curve shifts to right
(decreased O2
affinity), increasing O2
release to tissue by up
to 40%. Vasodilation of
myocardium as well as
skin and kidneys.
Breathlessness on
exertion only.
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Decompensatedoccurs when Hb falls
below 7 g/dl. Major
compensatory
mechanism is increased
cardiac output. Stroke
volume and heart rate
are raised at rest.
Patients are breathless
even at rest.
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Life threatening-If Hb
falls below 5 g/dl,
respiratory distress may
occur, showing as
tachyphnea and at
least one sign of nasal
flaring, chest
indrawing, or deep
breathing. Resulting
electrolyte changes:
acidosis.
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Anemic heart failureIf Hb falls below 3 g/dl,
O2 supply to the
myocardium becomes
insufficient, and no
further increase of
cardiac output is
possible. High-output
cardiac failure
develops.
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Many times, anemia
may be asymptomatic.
However, what we
usually associate with
anemia are signs like
pallor of the
conjunctiva and nail
beds as well as
spooning of the nails,
koilonychia.
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However, there are
other signs, including
the following: angular
stomatitis (often from
B12 or iron deficiency);
joint and bone pain
(sickle cell anemia);
and often late signs of
fatigue, palpitations,
dyspnea, exhaustion.
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In West Africa, the
most common
correlate causes to
anemia in pregnancy
are nutritional
deficiencies like iron,
folic acid, B12, and
vitamins. Parasitic
infections from malaria
and hookworm are
also common.
Pregnancy
conditions related
to anemia
Additionally, there are
numerous gynecological
conditions correlated with
blood loss and whose
outcome may lead to
anemia. Many of these
conditions are pregnancyrelated.
•Dysfunctional uterine
bleeding, encompassing a
number of conditions.
•Ectopic pregnancy
•Hemorrhoids
•Instrumentation
Look specifically
at the disorders of
pregnancy in Dysfunctional Uterine
Bleeding:
Ectopic pregnancy;
Placenta previa;
Hydatidiform mole;
Choroio-epithelioma; Abortion or
Premature sep.
of the placenta.
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Placental
Abruption
A premature separation
of an otherwise normally
implanted placenta
before delivery of the
fetus, one of the most
common risk factors of
which is pregnancyinduced hypertension.
There is bleeding into the
decidua basalia with
hematoma formation,
leading to progressive
separation of placenta.
There is a risk of acute
anemia as well as
evidence of clotting
activation.
Gestational
Trophoblastic
Disease
These include
choriocarcinoma and
molar pregnancy,
both of which arise
from abnormal
placental
proliferation. In 95%
of cases, painless
vaginal bleeding is
present, which can
lead to anemia.
Placenta Previa
A condition in which the
placenta is implanted in a
location that leaves part or
all of the cervical os
covered. It is associated
with potentially
catastrophic maternal
bleeding and obstruction of
the uterine outlet. There is
often painless vaginal
bleeding in about 70% of
the cases, generally not
until late second or early
third trimester. There may
be heavy or prolonged
bleeding after delivery. It
goes to reason that anemia
may be a sequelae.
Abortion
This is loss or failure of
early pregnancy in several
forms: complete;
incomplete; inevitable;
missed; septic, and
threatened.
General clinical
characteristics include
vaginal bleeding, which
may be bright red to dark
in color. Or there may be
bleeding that changes to
a dark brown discharge
that continues. Or, in
septic abortion, there
may be severe vaginal
hemorrhaging. All of
these conditions can
result in anemia for the
patient.
Uterine rupture
This is breech of the uterine
wall (new or after previous
cesarean delivery) that may
result in significant maternal or
fetal morbidity or mortality.
Often caused by abnormal
healing of a previous uterine
scar, mechanical disruption of
the uterine wall weakened by
previous surgery, congenital
anomalies, or abnormalities of
placentation. The uterus may
also be ruptured by injudicious
removal of the placenta or
manual exploration of the
uterus after placental delivery.
Vaginal bleeding may or may
not be present.
Ectopic
Pregnancy
Pregnancy that
implants outside of
the endometrial
cavity (fallopian tube,
ovary, abdominal
cavity, or cervix).
Signs and symptoms
often include vaginal
bleeding.
Hemorrhoids
These are
symptomatic dilation
of the hemorroidal
venous plexus resulting
in perianal swelling,
itching, pain, and
hematochezia.
Hemorrhoids are
extremely common as
pregnancy progresses
and have no effect on
pregnancy itself.
However, one possible
complication is
anemia.
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This is a condition that can cause anemia in
pregnancy but one not commonly listed in
books because for the most part it is
inexcusable and usually results from lack of
thoroughness and close observation by
medical personnel. Last week, the house
officer and I were called to the post-natal
ward to examine a woman who had
rechecked herself into the hospital after
giving birth two days previously….
24 yr old Fula; Grvda 2, para 1 plus 0. Previous full term SVD
delivery 6/07 at RVTH. Current pregnancy: booked at 20
wks. w early hyperemesis.
 12/9: Hb 8.8 g/dL w Dx: 3rd tri hemataemesis
 14/9: USS:Twin pregnancy 1st cephalic/2nd breech Normal
fetal heart beat, movement; normal fluid; anterior placenta.
 30/10: Dx: Placenta previa, schedule for C-S
 According to mother, she first went into labor before C-S was
done and was attempting to deliver breech. After, all she
remembered was that she had an operation.
 30/10: C-S for “occlusive placenta previa” completed. Alive
babies referred to neonatal unit where both died.
 31/10: Patient discharged to return for dressing change 6/11.
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Patient returned 1/11 for
admission with Hb of 7.5.
Called to exam at 1100 hrs.
 P/C: Abdominal pain and
dizziness
 Hx P/C: Patient had given
birth to twins via C-Section
that had resulted from
breech presentation. She
had been in active labor
before the C-S.
 What we saw O/E. What’s
your move? Rembr Hx.
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Instrumentation
On V/E, we noted a
vaginal tear of
approximately 7 cm
through the posterior
vaginal wall, and
through the
uterovaginal fascia.
The next morning, the
consultant discovered
no one had cleaned
this area and it was
filled with leaking
feces. She was
concerned the tear had
breeched the rectal
fascia as well as
compromised the
external and internal
sphincter muscles.
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How could this have happened? The best we
can speculate, a tear occurred between the
time the C-S was scheduled and then carried
out. Perhaps in labor, there was an
episiotomy instrumentation or a tear simply
from the breech presentation. Whatever the
case, there were presumable oversights.
Never assume anything. Always be
methodical and thorough.
Use your clinical skills. Rule out the obvious or
highly suspicious. Be skeptical of lab results. A
good history is 70% of the diagnosis.
 In West Africa, we are always suspicious of
nutritional and parasitic anemia. With distrust
for accurate lab results, we usually treat
empirically with Ferrous sulfate/folic acid tabs.
How many mg of iron and folic acid are in one
tab? How much does a pregnant woman need
daily? And for how long?
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But what if you suspect pernicious anemia,
order B12, and then continue to treat patient
with folate? It will reverse the anemia but
progressive and irreversible neurologic
damage may result.
In suspect cases, FBC w peripheral
morphology and red cell indices; BF; stool
microscopy; Hb electrophoresis for sickling.
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Anemia is not an indication for termination of
pregnancy or induction of labor. Vaginal delivery
is allowed unless there are contraindications.
Severe anemia where the patient is already in
Congestive HF risks maternal death. Exchange
transfusion with diuretics. Transfusion is always
contraindicated unless indicated.
If patient goes into labor already in heart failure,
allow labor in propped up position with O2 and
assisted 2nd stage of labor using vacuum
extraction.
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Depends on the cause. Management of
obstetric conditions depend on many factors,
including pregnancy term, medical, obstetric
and gyne history, the presenting complaint and
possible complications. The most common
causes of anemia in pregnancy in West Africa are
nutritional as well as parasites. Hemoglobin
counts and blood film are commonly requested.
Remember that one must go beyond Hb to MCV
to accurately ascertain the cause of anemia.
Education at the
clinic/community level.
 Haemantinics (ferrous
sulfate, 200 mg/day,
plus folic acid 500
µg/d.) Given to all
expectant mothers.
 Antimalarials in areas
of high endemicity.
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Mebendazole 100 mg
where hookworm is
present.
 Increased dietary fruit
(Vitamin C utilization of
micronutrients).
 Avoid dietary chelators
like tannins in tea.
 Delay next pregnancy 3
years to replenish
micronutrient stores.
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Refine your clinical skills. Be methodical in
your history taking and examination. Read
between the lines.
Be aware that anemia is usually a symptom
and how it can affect the outcome of the
pregnancy. Have available the RBC indice
reference ranges. Know common dosages of
medications used in anemia treatment.
Be thorough and conscientious.
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Cook, G.C. (ed.) Manson’s Tropical Diseases
(21st). UK: Saunders Publishing, 2003.
Magowan, B. (ed.) Clinical Obstetrics (2nd).
Edinborough: Saunders Publishing, 2009.
McKenzie, S.B. Clinical Laboratory Hematology.
New Jersey: Prentice Hall, 2004.
Parry, E. (ed.) Principles of Medicine in Africa
(3rd). Cambridge: Cambridge U Press, 2004.
Smith, R.P. Netter’s Obstetrics. New Jersey:
Icon Learning, 2002.