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Anaemia in
pregnancy
Hemoglobin concentration of less than 11 g/dL (hematocrit of <33%) in the first
or third trimester or a hemoglobin concentration of less than 10.5 g/dL
(hematocrit< 32%) in the second trimester.
Causes of iron deficiency anemia;
1. Poor nutrition.
2.Repeated and closely spaced pregnancies.
3. Excessive worm load during pregnancy.
4. Bleeding from piles or placenta previa.
During pregnancy, the blood volume increases by approximately 50% and the
red blood cell mass by approximately 33%. This relatively greater increase in
plasma volume results in a lower hematocrit but does not truly represent
anemia. Anemia in pregnancy most commonly results from a nutritional
deficiency in either iron or folate. Iron deficiency is responsible for 95% of the
anemias during pregnancy, due to increased demands for iron.
During the first half of pregnancy, iron requirements may not be increased
significantly, and iron absorbed from food (1mg/d) . However, in the second half
of pregnancy, iron requirements increase due to expansion of red blood cell
mass and rapid growth of the fetus. pregnancy increases a woman's iron
requirements to approximately 3.5 mg/d. This must be met by supplementation
of 40 mg/d of elemental iron (10% of which is absorbed).
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Anemia increases perinatal mortality and morbidity consequent to:
• preterm labor
• Intrauterine growth restriction
• Low iron stores in infant
• Iron deficiency anemia in the infant
• Cognitive and affective dysfunction in the infant
Clinical Findings:
Symptoms and Signs:
The symptoms may be vague and nonspecific, including pallor, easy fatigability,
headache, palpitations, tachycardia, and dyspnea. Angular stomatitis, glossitis,
and koilonychia (spoon nails) may be present in long-standing severe anemia.
Laboratory Findings:
-The red cells are hypochromic and microcytic.
-mean corpuscular volumes of less than 79 fL.
-Serum ferritin concentrations less than 15 g/dL.
-The total iron-binding capacity is elevated in both normal pregnancies and
pregnancies affected by iron deficiency anemia and therefore is of little
diagnostic value by itself.
-Platelet counts are increased, but white cell counts are normal.
-Bone marrow biopsy demonstrates lack of stainable iron in marrow but usually
is unnecessary in uncomplicated iron deficiency anemia.
Differential Diagnosis
1. Anemia due to chronic disease or an inflammatory process (eg,
rheumatoid arthritis) .
2. Anemia due to thalassemia trait can be differentiated from iron deficiency
anemia by normal serum iron levels, the presence of stainable iron in the
marrow, and elevated levels of hemoglobin A
2
.
3. Other less common causes of microcytic, hypochromic anemiae,ganemia
due to lead poisoning.
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Complications
Iron deficiency anemia does not affect the pregnancy unless it is severe, in
which case intrauterine growth retardation and preterm labor may result.
congestive heart failure may develop as a result of marked iron deficiency
anemia.Plummer-Vinson syndrome is a rare condition characterized by
dysphagia and atrophic glossitis
Prevention
During the course of pregnancy and the puerperium, at least 60 mg/d of
elemental iron should be prescribed.
Treatment
1. Oral Iron Therapy
Ferrous sulfate 300 mg (containing 60 mg of elemental iron, of which
approximately 10% is absorbed) should be given 3 times per day. If this agent is
not tolerated, ferrous fumarate or gluconateshould be prescribed.
Therapy should be continued for approximately 3 months after hemoglobin
values return to normal in order to replenish iron stores.Hemoglobin levels
should increase by at least 0.3 g/dL/wk.
Iron is best absorbed in the ferrous or reduced form from an empty stomach.
Administering ascorbic acid at the time of iron supplementation creates a mildly
acidic environment that aids the absorption of iron.
2. Parenteral Iron Therapy
The indication for parenteral iron is intolerance of, or refractoriness to, oral
iron. There are two iron parenteral preparations: iron dextran and ironsorbitol.
They can be given as every other day intramuscular injection and iron dextran
can be given as total dose infusion.
Iron dextran: Each 2mL vial provides 100 mg of elemental iron. After a 0.5-mL
test dose, iron dextran can be administered im or iv .Intramuscular injection
must always be given into the muscle mass of the upper outer quadrant of the
buttock using the Z technique (ie, pulling the skin and superficial musculature to
one side before inserting the needle to prevent leakage of the solution and
subsequent tattooing of the skin).
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Total iron dose can be given: given in 100 ml normal saline slow intravenous
infusion, over 6-8 h. Then Hb measured after 2 weeks.
Risks of parenteral iron administration include anaphylactic reaction, muscle
necrosis, and phlebitis.every 250 mg iron rise the Hb level by one gram.
Also the patient should take vitamins which help to raise the Hb level like; folic
acid, Vit B12, Vit C, Pyridoxin, Riboflavin and Vit A. These are present in eggs,
carrots, green vegetables, fruits and cereals.
3. Blood transfusion is required in patient:
• beyond 36 weeks
• to replenish blood loss due to antepartum or postpartum hemorrhage
• in patient not responding to oral and parenteral iron therapy
Megaloblastic Anemia In Pregnancy
Causes: deficiency of:
1. Folic acid, or
2. Vitamin B12
Folic acid deficiency anemia:
It is due to increased requirement & dietary lack and poor body reserve,use of
antifolate medications.Prevalence: 1.5% of all pregnant, more common in multiple
pregnancies.
Clinical features:
Patient may be asymptomatic, or feeling unwell with loss of appetite. There may
be vomiting, diarrhea, or unexplained fever.There may be pallor, bleeding spot
in the skin, hepatosplenomegaly and polyneuropathy.
Effects on pregnancy:
There is increased incidence of abortion, growth retardation, placental
abruption and preeclampsia.
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Effects on the fetus:
Increased incidence of neural tube defects, abortion, premature babies, small
for dates babies, and folate deficiency in the neonates.
Lab Findings:
• Fall in Hb.
• MCV increased
• MCH increased
• MCHC normal
• macrocytic RBC and hypersegmentaion of neutrophil in peripheral blood film
Treatment of vitamin B-12 deficiency includes 0.1 mg/d for 1 week, followed by
6 weeks of continued therapy to reach a total administration of 2 mg.
Prophylaxis:
500 mcg daily, Pregnant woman should eat more green vegetables. Folate is
destroyed by cooking.
Treatment:
5 mg daily oral folate should be continued for four weeks in puerperium
Sickle cell anaemia
SCD: Autosomally recessive disease with abnormal HBS contain B-globin with
amino acid substitution that result in it is precipitating when it is in reduced
state, RBCs become sickle shaped & occlude small blood vessels.
Management:
• Pre-pregnancy optimization of maternal health.
• High dose folic acid 5 mg \day.
• Low dose aspirin from early pregnancy.
Risk in pregnancy
Increase risk of crises in pregnancy, crises in pregnancy can be precipitated by
hypoxia, stress, infection &hemorrhage.
Increased risk of miscarriage, PE, FGR, PTL, CVT & DVT.
If both partners has sickle cell trait, risk will be 1:4 of having a baby with SCD.
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Management of sickle cell crises in pregnancy:
• Adequate hydration
• Oxygen
• Analgesia
• Screen for infection
• Antibiotic
• Blood transfusion
• Exchange transfusion
• Prophylaxis against thrombosis
• Fetal monitoring
Thalassaemia
• Alpha thalassaemia minor: deletion of one or 2 alpha genes , affected
individual is chronically anaemic , rarely there is obstetrical complication ,
unless there is severe blood loss.
• Beta thalassemia minor :
-mild anaemia in pregnancy.
-low MCV.
-folic acid should be given , iron is given if serum iron is low.
-partner should be screened: if both partner have B thalassemia minor , there is
1:4 chance the baby is affected.
Causes of TCP in pregnancy
• Idiopathic
• Increased consumption
ITP
APS
PE
HELLP
DIC
TTP
Hypersplenism
• Decreased production
Sepsis
HIV
Malignant marrow infiltration
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Thrombocytopenia
• TCP: platelet count ˂ 150 000 mg\dl
• Gestational TCP:-
mild fall in platelet count between 100 000 -150000.
Bleeding occurs when platelet count less than 50 000.
Occur late in pregnancy with no prior history of TCP.
It is Dx by exclusion.
No intervention other than monitoring of platelet count during & after
pregnancy with spontaneous resolution after delivery.
No association with fetalTCP, rarely associated with poor maternal
outcome.
Autoimmune TCP
• Antibodies are produced against platelet causing destruction of platelet in RES.
• Maternal hge occurs when plat count below 50 000 & spontaneous
bleeding occurs when plat count below 20 000.
• Fetal TCP occur in 5-10% of cases which does not correlate with maternal count
Management of ITP
• Serial monitoring of plat count
• Steroid can be given high doses to suppress AB production, take 2-3 wk to act.
• IvIgG : is preferred option when rapid increase in plat count is required near
term.
• Vaginal delivery can be allowed.
• Regional anaesthesia is contraindicated when plat count below 80 000
• FBS & IVD by ventouse is best to be avoided.
• After delivery cord blood sampling should be taken for plat count