Anemia In Pregnancy Flashcards

(26 cards)

1
Q

Anemia

A

 Anemia is a condition in which there is a reduction in Hb concentration, below the reference range according to
the individual’s age, sex, altitude and pregnancy status, resulting in insufficient oxygen carrying capacity to meet
physiologic needs.
 Anemia in Pregnancy is defined as Hb concentration of less than 11g/dl and a hematocrit of < 33%

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2
Q

Grading of pathological anemia based on Hb levels

A

 Mild: Hb is between 8–10 g/dl.
 Moderate: Hb is between 6–8 g/dl.
 Severe: Hb is below 6 g/dl.
 It is also classified according to Haematocrit (PCV) %

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3
Q

Physiological anemia of pregnancy

A

 Haemodilution – Physiological Anaemia due to disproportionate increase in plasma volume (30%-40%) Vs.
Red cell volume increase (25%).
 There is marked extra Fe demand during pregn esp in 2nd half that dietary supplement becomes inadequate.
 Fall in Hb concentration during pregnancy is due to combined effect of hemodilution and negative Fe balance.
 Pregnancy is physiological iron deficiency state with ↓Hb, ↓HCT in 2nd half of pregn associated with low
serum iron, ↑iron binding capacity and increased rate of iron absorption

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4
Q

 Criteria of physiological anemia

A

Occur in 2nd half of pregnancy, fulfilling the following hematological values:
(1) Hb-10 gm%
(2) RBC-3.2 million/mm3
(3) PCV-32%.
(4) Peripheral smear showing normal morphology of the RBC with central pallor

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5
Q

Pathological anemia of pregnancy

A

a) Inadequate erythropoiesis
-Deficiency anemia (isolated or combined) - Deficiency of raw materials necessary for erythropoiesis
Fe deficiency * Folic acid deficiency * Vitamin B12 deficiency * Protein deficiency/erythroid growth factors
-Bone marrow insufficiency/ failure- hypoplasia or aplasia due to radiation, drugs (aspirin, indomethacin),
i. Infiltrative malignancies e.g. Leukemias, lymphomas, multiple myeloma, metastatic carcinomas
ii. Infiltrative infections: TB, Histoplasmosis, CMV
iii. Stem cell defects: Aplastic disorders e.g. pure red cell aplasia, aplastic anemia, Myelofibrosis,
Myelodysplastic syndromes (MDS)
-Chronic renal disease- lead to lack of erythropoietin secreted by the kidney
b) Hemorrhagic anaemia
* Acute: Following bleeding in early months or APH, trauma, surgery etc
* Chronic: Hookworm infestation, bleeding piles, Menorrhagia etc.
c) Haemolytic anaemia
* Hemoglobinopathies- Thalassemias and Sickle cell * other hemoglobinopathies
* Hereditary hemolytic anemias (RBC membrane defects-spherocytosis, elliptocytosis, stomatocytosis)
 Enzymopathies: G6PD deficiency ,Pyruvate kinase deficiency, Pyrimidine 5’ nucleotidase
 Autoimmune haemolytic anaemia (AIHA)- Warm antibodies, cold antibodies
 Microangiopathic: TTP,HUS,DIC
 Anemia of infection - malaria,
 Others - Chronic disease (renal), neoplasm, TB, Splenic sequestration (Hypersplenism)

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6
Q

Types of anaemia, classified by MCV

A

Hypochromic microcytic with a low MCV < 80fL
a) Iron deficiency
b) Thalassemia
c) Sideroblastic anaemia
d) Anaemia of chronic disease (severe cases)
e) Lead poisoning
Normochromic normocytic with a normal MCV of 80-100fL
a) Anaemia of chronic disease (often)
b) Anaemia of renal disease
c) Combined nutritional deficiencies (Fe, folate, Vit B12)
d) Bone marrow failure
e) Hypothyroidism
Macrocytic with a high MCV >100fL
1) Megaloblastic anaemia (folate, or cobalamine deficiency)
2) Non magaloblastic anaemia
a) Alcoholism
b) Liver disease
c) Hypothyroidism
d) Haemolytic anamia (reticulocytosis)
e) Myelodysplasia

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7
Q

Fe deficiency anemia is common in tropics due to…?

A

Before pregnancy:
a. Faulty dietetic habit: carbohydrate rich diet, high phosphate and phytic acid form of insoluble iron phosphate
and phytates in the gut
b. Faulty absorption mechanism: intestinal infestation, ↑gut motility, and hypochlorhydria, associated with
malnutrition hinders absorption.
c. Iron loss:
 More Fe loss through sweat
 Repeated pregnancies at short intervals
 Prolonged period of lactation
 Excessive blood loss during menstruation
 Hookworm infestation
 Chronic malaria and chronic blood loss due to bleeding piles
During pregnancy:
* Its due to:
a. Increased demands of Fe
b. Poor iron intake: due to poor diet, loss of appetite and vomiting
c. Diminished absorption: intake of antacids, H2 blockers and proton pump inhibitors inhibit iron absorption
due to duodenal hypochlorydia
d. Disturbed metabolism: infections even asymptomatic bacteriuria markedly interferes with erythropoiesis
e. Pre-pregnant health status
f. Excess demand: (i) Multiple pregnancy ii) women with rapidly, recurring pregnancy

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8
Q

Erythropoiesis

A
  • Erythropoiesis is confined to bone marrow in adults.
  • RBCs are formed via stages of pronormoblasts → normoblasts → reticulocytes → to mature non-nucleated
    erythrocytes.
  • Average RBCs life span is about 120 days after which they degenerate and hemoglobin is broken down into
    hemosiderin and bile pigment.
  • For erythropoiesis to occur, adequate nutrients must be available: minerals (Fe), vitamins (folate, Vit B12),
    proteins (amino acid for the synthesis of globin moiety) and hormones (Erythropoietin- produced by the kidneys
    (90%) and the liver (10%).
  • Inadequate reserve or increased demand or
    deficient supply of any of the constituents
    interferes with the normal erythropoiesis.
  • Tissue hypoxia stimulates release of Hypoxic
    inducible factor 1(HIF-1) HIF, which promotes
    release of erythropoietin (EPO), Colony
    stimulating factors, transcription factors (GATA1,
    NF-E2 and FOG 1) in the bone marrow, enhancing
    sequential differentiation and maturation of erythroid precursors, burst forming units-erythroid (BFU-E) and
    colony forming units-erythroid (CFU-E) into reticulocytes.
  • Reticulocytes lose their ribosomes after 1-2 days in circulation to become matures RBCs.
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9
Q

Transport Fe in the blood

A

 Normal serum iron level is about 13–32 µmol/L
 Transported in plasma bound to a β-globulin protein synthesized in the liver called transferrin.
 Most of Fe bound to transferrin comes from macrophages in reticuloendothelial system and not from Fe
absorbed by intestine and each transferrin molecule
binds 2 atoms of ferric iron

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10
Q

Iron stores

A

 About 2
/3 of Total body Iron (TBI) - is in Hb (2.5–3 g
in a normal adult man)
 500-1500mg is stored in reticuloendothelial cells,
hepatocytes and skeletal muscle cells-
2
/3 as ferritin
and 1
/3 as haemosiderin
 Small amounts are also found in plasma bound to
transferrin (about 4 mg), with some in myoglobin and
enzymes.
NB: Increase in body iron content (haemochromatosis) are classified into:
1. Hereditary haemochromatosis - where a mutation in the HFE gene causes increased iron absorption
2. Secondary haemochromatosis (transfusion siderosis). Due to Fe
overload in conditions treated by regular BT

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11
Q

Investigations of anemia

A

Objectives are to ascertain: Degree of anemia * Type of anemia * Cause of anemia
Type of anemia
1. FBC; Hb, RBC count, Hct, MCV, PCV and MCH, MCHC (most sensitive index of Fe deficiency anemia).
2. Peripheral blood smear: variation in size (anisocytosis) and shape (poikilocytosis) PBS in Fe deficiency anaemia
- suggest microcytic hypochromic anemia typical in iron deficiency anemia.
- Reticulocyte count may be slightly raised
 Serum bilirubin
 For iron deficiency anemia do, Fe studies;
_ Serum iron is usually below 30 µg/100 mL.
– Total iron binding capacity is elevated to beyond 400 µg/100 mL.
– Transferrin saturation % (i.e. serum iron divided by TIBC) is 10% or less.
– Serum ferritin below 30 µg/L. (reflects amount of stored Fe, normal is 30–300 µg/L). Levels ↑ in inflammatory
/ malignant diseases as it is an acute-phase reactant
 Hb electrophoresis
Cause of anemia
 Stool: For occult blood and ova ( to exclude chronic low GIT bleeding and
helminthic (esp hookworm) infestation, M/C/S
 Sickling test / Hb electrophoresis
 MPS/RDT
 Serum folate
 Coombs test
 Reticulocyte count
 Exclude chronic conditions- TB- CXR, sputum for AFB, M/C/S, Gene expert
 Bone marrow biopsy: not routinely do
a) Trephine- allows an overall view of bone marrow architecture, cellularity & presence/absence of abnormal infiltrate
b) Bone marrow aspiration- microscopic examine for morphology of developing haemopoietic cell
13. Obstetric u/sound- to assess fetal well being, liquor vol,

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12
Q

Complications of anemia in pregnancy

A
  1. Pre-eclampsia- related to malnutrition and hypoproteinemia
  2. Miscarriage
  3. Intercurrent infection- anemia diminish resistance to infection
  4. Heart failure at 30–32 weeks of pregnancy
  5. Preterm labor.
  6. Loss of working hours
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13
Q

Complications of anemia during labor

A
  1. Uterine inertia
  2. Postpartum hemorrhage and pt tolerate badly to bld loss
  3. Cardiac failure - due to accelerated cardiac output
  4. Shock
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14
Q

Comlications of anemia during Puerperium

A

Comlications during Puerperium:
1. Puerperal sepsis
2. Subinvolution
3. Poor lactation
4. Puerperal venous thrombosis
5. Pulmonary embolism.

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15
Q

Effects of anaemia on the baby

A

 Fe transferred to fetus is unaffected in Fe deficiency anemia and so neonate does not suffer from anemia at birth.
1) Miscarriage
2) IUGR/LBW babies
3) IUFD due to severe maternal anoxemia
4) Prematurity
5) Anemia in infancy
6) Increased perinatal loss
7) Neural tube defects (esp folate def)

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16
Q

History taking of anemia

A

 H/O dietary intake,
 Self-medication with NSAIDs drugs (which may give rise to GI bleeding), corticosteroids
 PMHx: Previous gastric surgery (lead to malabsorption of iron and/or vitamin B12), diseases associated with
anaemia e.g. rheumatoid arthritis, chronic illness- RVD, TB, Cancer
 FHx: relevant in haemolytic anaemias and Pernicious anaemia.
 Presence of blood in faeces (may be a sign of haemorrhoids or carcinoma of lower bowel), haematuria,
haemoptysis, Frequant blood donation, blood loss, chronic epistaxis
 Enquiry about duration of periods (normal 3–5/day), occurrence of clots and number of sanitary towels or
tampons used should be made

17
Q

Prophylaxis of anemia

A

Prophylaxis includes:
 Avoidance of frequent child-births- minimum interval betwn pregnancies, is at least 2 yrs with contraceptives
 Supplementary Fe therapy- ferrous sulfate 200mg OD (containing 60mg of elemental Fe) with 1 mg folic acid
 Dietary prescription: Realistic balanced diet, rich in Fe and protein
 Adequate treatment- to eradicate hookworm infestation, dysentery, malaria, bleeding piles, and UTI
 Pre-pregnancy correction of anaemia
 Early detection of falling Hb level- check Hb at ANC booking, at 30th and finally at 36th week
 Intermittent Presumptive treatment- Antimalarials eg Fansidar, Deworming

18
Q

Tx of anemia

A

Curative
 Depends on: Severity, Cause and Gestational age
Severity
 Mild (Hb > 8 – 9.9) - Haematinics – orally (or 1m/1v) - Hb will rise by 0.8 – 1.0g/dl per week.
 Moderate (Hb 6 – 7.9)
1
st and 2nd trimester. Orally/IM or IV
3
rd trimester, term, labour: Transfuse.
 Severe (< 6g/dl) - Transfuse irrespective of gestation age but be careful it may precipitate cardiac failure if the
transfusion is rapid and massive.
 Therefore:
Use packed cells
Give fast acting diuretic eg frusemide before transfusion starts.
Slow transfusion.
Treat the identified cause.
 Malaria.
 Infestations – H/worm
 Stop bleeding
Iron therapy: * Oral therapy * Parenteral therapy
 Establish and treat underlying cause and administer iron to correct anaemia and replace iron stores.
 In Fe def Anaemia, giving Fe will ↑Hb by approx 1.0 g/L/week unless other factors e.g., bleeding are present
 Iron is best absorbed in the ferrous form
 Oral Fe preparations available are ferrous gluconate, ferrous fumarate or ferrous succinate but ferrous sulfate 200
mg which contains 60 mg of elemental iron is widely used
* S/E such as nausea, diarrhoea or constipation, can be reduced by taking tablets with food or using a
preparation with less Fe such as ferrous gluconate 300 mg BD, (has 70mg ferrous iron).
 Give Fe for a long period (atleast 6 months) to correct Hb level and to replenish the iron stores.

19
Q

Failure to respond to oral iron is due to

A

Failure to respond to oral iron may be due to:
a) Lack of compliance d. Multiple deficiencies
b) Continuing haemorrhage e. Incorrect diagnosis, e.g. thalassaemia trait.
c) Malabsorption

20
Q

What to use in pt intolerant to oral iron

A

 Pt intolerant to oral preparation, severe malabsorption & chronic dx (e.g. inflammatory bowel dx) – use
parenteral iron and discontinue oral iron.
a. Low-molecular-weight iron dextran (test dose required)
b. Iron sucrose,
c. Ferric carboxymaltose,
d. Iron isomaltoside 1000

21
Q

 Indications of parenteral iron therapy

A

a. Contraindications of oral therapy as previously mentioned.
b. Patient is not cooperative to take oral iron
c. Cases seen for the first time during the last 8–10 weeks with severe anemia

22
Q

Aministration of iron sucrose

A

 Iron (ferrous) Sucrose: Total iron dose (mg) = 2.3 × W × D + 500
* W = Weight (kg) before pregnancy;
* D = Hb (Target– Actual) g/dL; 500 mg for body store].
* It is given IV, 100 mg (at a time) in 100 mL normal saline over 15 minutes.
Pre-requisites:
(1) Correct diagnosis of true iron deficiency anemia
(2) Adequate supervision
(3) Facilities for management of anaphylactic reaction.
Procedures:
 Admit pt for infusion
 Mix required iron sucrose with 500 mL of 0.9% saline.
 Follow guidance in drug information sheet as regard the total dose and duration of therapy
 Take precautions as for blood transfusion both prior to and during the infusion process
 Set drip rate at 10 drops/min during the 1st 20 min and then increase to 40 drops/min
 Stop drip if any adverse reaction like rigor, chest pain or hypotension calls are observed

23
Q

indication of blood transfusion in anemia

A

 Only indicated :
a) To correct anemia due to blood loss and to combat PPH
b) Severe anemia in later months of pregnancy (> 36 weeks) - to correct anemia, to optimize pt for the strain of
labor and blood loss following delivery.
c) Refractory anemia not responding to either oral or parenteral therapy.
d) Anaemia associated infection

24
Q

Management of anemia during labor

A

First stage:
 Take special precautions when an anemic patient goes into labor as follows:
 Admit in HDU/SOU.
 Nurse pt on comfortable bed and position-
 Give O2 via nasal prongs to increase oxygenation of maternal blood, diminishing the risk of fetal hypoxia.
 Maintain strict asepsis to minimize puerperal infection.
Second stage:
a) Maintain sepsis
b) Shorten duration of 2nd stage with assisted delivery- low forceps or vacuum.
c) Avoid episiotomy if done should be repired promptly
d) Give oxytocin following the delivery of anterior shoulder.
Third stage: One should be.
 Be vigilant
 Active management of of 3rd stage of labour with IV oxytocin is preferred
 Look out for PPH
 Replenish significant blood loss with RCC.
 Blood transfusion under diuretic cover
 Avoid injudicious use of IVF risk of fluid overload
 Avoid circulatory overload postpartumly.

25
 PPH prophylaxis
 IV infusion with oxytocin 40IU in 500mls N/S  Misoprostol 800mcg rectally  Tranexamic 1g TDS IV
26
Tx of anemia in Puerperium
 Predelivery antianemic therapy- Iron and folate supplement x at least 3 months after delivery.  Infections should be treated.  Prophylactic antibiotics to prevent infection.  Warn pt of the danger of recurrence in subsequent pregnancies  Effective contraception for 2 years for iron stores to recover  Carefully watched for puerperal sepsis, failing lactation, sub involution of uterus and thromboembolism