Anemia and pregnancy
Sunil Kumar
 Anemia: Haemoglobin level below 12gm/dl normally
and 10mg/dl at any time during pregnancy or
puerperium
 20% of maternal deaths in 3rd world countries
Introduction
CAUSES IN PREGNANCY
At pregnancy
 demand of iron
 iron intake
 absorption
 Disturbed metabolism
SYMPTOMS
 Exhaustion
 Anorexia
 Indigestion
 Palpitation
 Dyspnoea
 Swelling of legs
SIGNS:
 Pallor with evidence of glossitis and stomatitis
 Edema of legs due to hypoproteinemia or associated
pre-eclampsia
 Systemic murmur in mitral area due to physiological
mitral incompetence
 Crepitations due to pulmonary oedema
CLASSIFICATION
 Physiological anemia of pregnancy
 Pathological
 Deficiency anemia
 Iron deficiency
 Folic acid deficiency
 Vitamin B12 deficiency
 Protein deficiency
CONTD….
 Hemorrhagic
 Acute (in early months/APH)
 Chronic (Hook worm infestation , bleeding
piles)
 Hereditary
 Thalassemia
 Sickle cell
 Hereditary haemolytic anemia
 Bone marrow insufficiency (hypoplasia/
aplasia)
 Anemia of infection (Malaria, T.B.)
 Chronic disease (Renal/neoplasm)
PHYSIOLOGICAL ANEMIA IN
PREGNANCY
Disproportionate increase in plasma volume, RBC
volume, Hb mass
Extra demand of iron especially in 2nd half.
physiological iron deficient state
Hb concentration, HCT value, serum iron,
TIBC
Net Result: Fall in Hb concentration is due to combined
effect of haemodilution and –ve Fe++ balance.
Diagnostic criteria (2nd half of
pregnancy)
 Hb – <10 gm%
 RBC – 3.2 per cubic millimeter (4.2 – 5.4 ×
106 /µl)
 PCV – 32% (37% - 48%)
 Peripheral smear – Normocytic, normochromic
TREATMENT
 If there are signs suggestive of fetal hypoxemia
red cell transfusion
 Resolve by six weeks postpartum since plasma
volume has returned to normal by that time
 Is the most common cause along with acute blood
loss.
 Is due to increase iron demand
 Fe stores being constant or depleted in pregnant
state is the cause.
IRON DEFICIENCY ANEMIA
CRITERIA FOR IRON DEFICIENCY
ANEMIA
 Hb - <10gm%
 RBC - <4 million per cubic mm
 PCV - <30%
 MCHC - <30%
 PBS: microcytic and hypochromic (not seen
in moderate)
 reduced serum ferritin level and increased
TIBC
COMPLICATION OF ANEMIA
During pregnancy:
 Pre-eclampsia
 Intercurrent infection
 Heart failure at 30-32 weeks of pregnancy
 Pre-term labour
During labour:
 Post partum haemorrhage
 Cardiac failure
 Shock
Puerperium:
 Puerperal sepsis
 Sub involution
 Prolactation
 Puerperal venous thrombosis
 Pulmonary embolism
Effects on baby:
 Low birth weight babies
 IUFD due to maternal anoxemia
PROPHYLAXIS
 Avoid frequent child birth
 Supplementary iron therapy
 Dietary prescription
 Treat the underlying cause
 Early detection of Hb level.
CURATIVE
 Hospitalization: If Hb level at or < 9 gm/dl.
 General treatment:
 Diet: protein, iron, vitamins
 Acid pepsin: after meal to improve appetite and
facilitate digestion
 Antibiotics: If septic focus
 Therapy for underlying diseases
 Specific therapy: to restore Hb and iron reserve. Two
types of iron therapy
• Oral
• Parenteral
ORAL THERAPY
 Ferrous gluconate, fumarate, succinate, sulphate
 Ferous sulphate is the widely used
 Regimen:
• 1 tab TDS with or after meal in a day
• Maximum tablet per day is up to 6/day till blood
picture is normal
• Maintenance dose: 1 tablet for 100 days following
delivery
 Points to consider while on therapy:
 Epigastric pain, nausea, vomiting, diarrhea and
constipation
 Absorption reduced by anta-acids, oxalates
&phosphates
 Absorption increased by ascorbate, lactate and
amino acids
 Contraindications:
 Severe oral intolerance
 Severe anemia in advanced pregnancy
PARENTERAL THERAPY
Intravenous:
Drugs:
 Iron Dextran: TDI = 0.3 × W(100-Hb%)mg of elemental
iron
W= wt. in pounds, Hb% = percentage concentration of
Hb
Additional 50% for partial replenishment.
 Iron sucrose: TDI = 2.3 × W × D +500; where W= wt. in
kg before pregnancy, D= Hb(target-actual), 500= 500mg
for body store
PROCEDURES
 Patient is admitted in the morning for infusion
 Required iron is mixed in 500ml of normal saline
 Drips is to be 10 drops/min in 1st 20 mins
 Drips increased to 40 drops/min thereafter
 If rigors, hypo-tension or chest pain seen call it a
INTRAMUSCULAR
THERAPY
 Iron dextran
 Iron sorbitol citric acid complex in dextrin
 50mg elemental iron per ml contained in both
 Total required dose calculated previous formula:
 Oral iron suspended 24 hrs prior to therapy to
avoid reaction
Problems with IM
 Injection is painful
 Staining of the skin
 Fever
 Lymphadenopathy
 Headache
 Nausea
 Vomiting
 Allergic reactions
Blood transfusion
1. If anemia is due to blood loss, combat PPH
2. Severe anemia in later months of pregnancy(beyond
36 weeks to improve anemic state and oxygen
carrying capacity of blood patient goes into labour)
3. Refractory anemia: anemia not responding to either
oral or parenteral therapy inspite of correct typing
Management during labour
 First stage:
 Make the patient lie in bed and make her comfortable
 Arrange for oxygen inhalation
 Strict asepsis
 Second stage
 Asepsis maintained
 Low forceps or vaccum delivery
 IV methergin 0.2mg following delivery of anterior
shoulderMethergin(methylergometrine): Active management of the 3rd stage of labor (as
means to promote separation of the placenta and to reduce blood loss).
 Third stage:
 Should be more attentive.
 Significant amount of blood loss should be replenished
by fresh packed cell transfusion
 Danger of post partum overloading to heart should be
avoided
 Puerperium
 Prophylactic antibiotic
 Continuation of antianemic therapy given before delivery till
patient restores her normal clinical and hematological
states
 Even in normal cases, iron therapy continued for at
least 3 months following delivery
Abnormal precussors (megaloblasts)
Impaired DNA synthesis in RBC in bone marrow
vit B12/ folate/ both deficiency
Megaloblastic anemia
CAUSES OF B12
DEFICIENCY
 Vegetarian diet
 Gastritis
 Gasterectomy
 Ileal bypass
 Chron’s disease
 Drugs: Metformin, PPI
CAUSES OF FOLIC ACID
DEFICIENCY
 Inadequate intake
 Increased demand
 Decreased absorption
 Abnormal demand (infection, hemorrhagic state,
hemolytic state)
 Failure of utilization (anti epileptics, infection)
 Decreased storage (hepatic disorder, vitamin C
deficiency)
 Iron deficiency anemia.
CLINICAL FEATURES
 Insidious onset usually
 First revealed in last trimester or acutely in early
puerperium
 Anorexia or protracted vomiting
 Occasional diarrhea
 Unexplained fever associated
HEMATOLOGICAL FINDINGS of
MbA
1.Hb <10 gm%
2. Peripheral blood smear, 2 or more features seen:
- Neutrophil hypersegmentation (5 or >lobes)
- Macrocytosis and anisocytosis
- Giant polymorphs
- Megaloblasts
- Howell-Jolly bodies
 Buffy coat smear more diagnostic
3. MCV >100micro cube, MCH >33 pg, MCHC-
normal
4. Associated leukopenia and thrombocytopenia
5. Serum iron normal or high, TIBC decreased
6. Serum folate <3mg/ml,(in non-pregnant 2.8-8 ng/ml
normal)
7.Serum vit B12 <90pg/ml (normal- 300pg/ml)
8. BM- megaloblastic erythropoiesis
COMPLICATIONS OF
MEGALOBLASTIC ANEMIA
 Abortion
 Dysmaturity
 Prematuirity
 Abruptio placentae
 Fetal malformation (cleft palate, NTD)
PROPHYLAXIS
 All reproductive age group woman given 400 micro
gm of folic acid
 Additional 4mg given where demand is high (like
in multiple pregnancy, anti-convulsants,
hemoglobinopathies, woman with NTD infants)
MANAGEMENT
 Daily administration of folic acid 4mg orally
 Continued for at least 4 weeks following delivery
APLASTIC ANEMIA
 Rarely seen in pregnancy
 Immunologically mediated or autosomal recessive
inheritance
 Marked decrease in marrow stem cells
COMPLICATIONS
 Hemorrhage
 Infection
Diagnosis:
 Blood: anemia, leukopenia, thrombocytopenia
 Bone marrow: Hypocellular
MANAGEMENT
 Repeated blood transfusion to maintain
HCT>20
 Granulocyte transfusion to combat infection
 Platelet transfusion to control hemorrhage
 Glucocorticoids in some
 In severe cases:
Bone marrow or stem cell transplantation
References
1. Williams Obstetrics, 24th Edition
2. DC Dutta’s Textbook of Obstetrics, 7th Edition
Anemia in pregnancy by Sunil Kumar Daha

Anemia in pregnancy by Sunil Kumar Daha

  • 1.
  • 2.
     Anemia: Haemoglobinlevel below 12gm/dl normally and 10mg/dl at any time during pregnancy or puerperium  20% of maternal deaths in 3rd world countries Introduction
  • 3.
    CAUSES IN PREGNANCY Atpregnancy  demand of iron  iron intake  absorption  Disturbed metabolism
  • 4.
    SYMPTOMS  Exhaustion  Anorexia Indigestion  Palpitation  Dyspnoea  Swelling of legs
  • 5.
    SIGNS:  Pallor withevidence of glossitis and stomatitis  Edema of legs due to hypoproteinemia or associated pre-eclampsia  Systemic murmur in mitral area due to physiological mitral incompetence  Crepitations due to pulmonary oedema
  • 6.
    CLASSIFICATION  Physiological anemiaof pregnancy  Pathological  Deficiency anemia  Iron deficiency  Folic acid deficiency  Vitamin B12 deficiency  Protein deficiency
  • 7.
    CONTD….  Hemorrhagic  Acute(in early months/APH)  Chronic (Hook worm infestation , bleeding piles)  Hereditary  Thalassemia  Sickle cell  Hereditary haemolytic anemia
  • 8.
     Bone marrowinsufficiency (hypoplasia/ aplasia)  Anemia of infection (Malaria, T.B.)  Chronic disease (Renal/neoplasm)
  • 10.
    PHYSIOLOGICAL ANEMIA IN PREGNANCY Disproportionateincrease in plasma volume, RBC volume, Hb mass Extra demand of iron especially in 2nd half. physiological iron deficient state Hb concentration, HCT value, serum iron, TIBC Net Result: Fall in Hb concentration is due to combined effect of haemodilution and –ve Fe++ balance.
  • 12.
    Diagnostic criteria (2ndhalf of pregnancy)  Hb – <10 gm%  RBC – 3.2 per cubic millimeter (4.2 – 5.4 × 106 /µl)  PCV – 32% (37% - 48%)  Peripheral smear – Normocytic, normochromic
  • 13.
    TREATMENT  If thereare signs suggestive of fetal hypoxemia red cell transfusion  Resolve by six weeks postpartum since plasma volume has returned to normal by that time
  • 14.
     Is themost common cause along with acute blood loss.  Is due to increase iron demand  Fe stores being constant or depleted in pregnant state is the cause. IRON DEFICIENCY ANEMIA
  • 15.
    CRITERIA FOR IRONDEFICIENCY ANEMIA  Hb - <10gm%  RBC - <4 million per cubic mm  PCV - <30%  MCHC - <30%  PBS: microcytic and hypochromic (not seen in moderate)  reduced serum ferritin level and increased TIBC
  • 16.
    COMPLICATION OF ANEMIA Duringpregnancy:  Pre-eclampsia  Intercurrent infection  Heart failure at 30-32 weeks of pregnancy  Pre-term labour During labour:  Post partum haemorrhage  Cardiac failure  Shock
  • 17.
    Puerperium:  Puerperal sepsis Sub involution  Prolactation  Puerperal venous thrombosis  Pulmonary embolism Effects on baby:  Low birth weight babies  IUFD due to maternal anoxemia
  • 18.
    PROPHYLAXIS  Avoid frequentchild birth  Supplementary iron therapy  Dietary prescription  Treat the underlying cause  Early detection of Hb level.
  • 19.
    CURATIVE  Hospitalization: IfHb level at or < 9 gm/dl.  General treatment:  Diet: protein, iron, vitamins  Acid pepsin: after meal to improve appetite and facilitate digestion  Antibiotics: If septic focus  Therapy for underlying diseases
  • 20.
     Specific therapy:to restore Hb and iron reserve. Two types of iron therapy • Oral • Parenteral
  • 21.
    ORAL THERAPY  Ferrousgluconate, fumarate, succinate, sulphate  Ferous sulphate is the widely used  Regimen: • 1 tab TDS with or after meal in a day • Maximum tablet per day is up to 6/day till blood picture is normal • Maintenance dose: 1 tablet for 100 days following delivery
  • 22.
     Points toconsider while on therapy:  Epigastric pain, nausea, vomiting, diarrhea and constipation  Absorption reduced by anta-acids, oxalates &phosphates  Absorption increased by ascorbate, lactate and amino acids  Contraindications:  Severe oral intolerance  Severe anemia in advanced pregnancy
  • 23.
    PARENTERAL THERAPY Intravenous: Drugs:  IronDextran: TDI = 0.3 × W(100-Hb%)mg of elemental iron W= wt. in pounds, Hb% = percentage concentration of Hb Additional 50% for partial replenishment.  Iron sucrose: TDI = 2.3 × W × D +500; where W= wt. in kg before pregnancy, D= Hb(target-actual), 500= 500mg for body store
  • 24.
    PROCEDURES  Patient isadmitted in the morning for infusion  Required iron is mixed in 500ml of normal saline  Drips is to be 10 drops/min in 1st 20 mins  Drips increased to 40 drops/min thereafter  If rigors, hypo-tension or chest pain seen call it a
  • 25.
    INTRAMUSCULAR THERAPY  Iron dextran Iron sorbitol citric acid complex in dextrin  50mg elemental iron per ml contained in both  Total required dose calculated previous formula:  Oral iron suspended 24 hrs prior to therapy to avoid reaction
  • 26.
    Problems with IM Injection is painful  Staining of the skin  Fever  Lymphadenopathy  Headache  Nausea  Vomiting  Allergic reactions
  • 27.
    Blood transfusion 1. Ifanemia is due to blood loss, combat PPH 2. Severe anemia in later months of pregnancy(beyond 36 weeks to improve anemic state and oxygen carrying capacity of blood patient goes into labour) 3. Refractory anemia: anemia not responding to either oral or parenteral therapy inspite of correct typing
  • 28.
    Management during labour First stage:  Make the patient lie in bed and make her comfortable  Arrange for oxygen inhalation  Strict asepsis  Second stage  Asepsis maintained  Low forceps or vaccum delivery  IV methergin 0.2mg following delivery of anterior shoulderMethergin(methylergometrine): Active management of the 3rd stage of labor (as means to promote separation of the placenta and to reduce blood loss).
  • 29.
     Third stage: Should be more attentive.  Significant amount of blood loss should be replenished by fresh packed cell transfusion  Danger of post partum overloading to heart should be avoided  Puerperium  Prophylactic antibiotic  Continuation of antianemic therapy given before delivery till patient restores her normal clinical and hematological states  Even in normal cases, iron therapy continued for at least 3 months following delivery
  • 30.
    Abnormal precussors (megaloblasts) ImpairedDNA synthesis in RBC in bone marrow vit B12/ folate/ both deficiency Megaloblastic anemia
  • 31.
    CAUSES OF B12 DEFICIENCY Vegetarian diet  Gastritis  Gasterectomy  Ileal bypass  Chron’s disease  Drugs: Metformin, PPI
  • 32.
    CAUSES OF FOLICACID DEFICIENCY  Inadequate intake  Increased demand  Decreased absorption  Abnormal demand (infection, hemorrhagic state, hemolytic state)  Failure of utilization (anti epileptics, infection)  Decreased storage (hepatic disorder, vitamin C deficiency)  Iron deficiency anemia.
  • 33.
    CLINICAL FEATURES  Insidiousonset usually  First revealed in last trimester or acutely in early puerperium  Anorexia or protracted vomiting  Occasional diarrhea  Unexplained fever associated
  • 34.
    HEMATOLOGICAL FINDINGS of MbA 1.Hb<10 gm% 2. Peripheral blood smear, 2 or more features seen: - Neutrophil hypersegmentation (5 or >lobes) - Macrocytosis and anisocytosis - Giant polymorphs - Megaloblasts - Howell-Jolly bodies  Buffy coat smear more diagnostic 3. MCV >100micro cube, MCH >33 pg, MCHC- normal
  • 35.
    4. Associated leukopeniaand thrombocytopenia 5. Serum iron normal or high, TIBC decreased 6. Serum folate <3mg/ml,(in non-pregnant 2.8-8 ng/ml normal) 7.Serum vit B12 <90pg/ml (normal- 300pg/ml) 8. BM- megaloblastic erythropoiesis
  • 36.
    COMPLICATIONS OF MEGALOBLASTIC ANEMIA Abortion  Dysmaturity  Prematuirity  Abruptio placentae  Fetal malformation (cleft palate, NTD)
  • 37.
    PROPHYLAXIS  All reproductiveage group woman given 400 micro gm of folic acid  Additional 4mg given where demand is high (like in multiple pregnancy, anti-convulsants, hemoglobinopathies, woman with NTD infants)
  • 38.
    MANAGEMENT  Daily administrationof folic acid 4mg orally  Continued for at least 4 weeks following delivery
  • 39.
    APLASTIC ANEMIA  Rarelyseen in pregnancy  Immunologically mediated or autosomal recessive inheritance  Marked decrease in marrow stem cells
  • 40.
    COMPLICATIONS  Hemorrhage  Infection Diagnosis: Blood: anemia, leukopenia, thrombocytopenia  Bone marrow: Hypocellular
  • 41.
    MANAGEMENT  Repeated bloodtransfusion to maintain HCT>20  Granulocyte transfusion to combat infection  Platelet transfusion to control hemorrhage  Glucocorticoids in some  In severe cases: Bone marrow or stem cell transplantation
  • 42.
    References 1. Williams Obstetrics,24th Edition 2. DC Dutta’s Textbook of Obstetrics, 7th Edition