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Obstetrics Simplified - Diaa M. EI-Mowafi

Anaemia in Pregnancy


Normal Blood Standards

Red blood corpuscles (RBCs)

  • Number:
    • In females: 4.5-5 millions/mm3.
  • Haemoglobin (Hb%):
    • In females: 12-14 gm/100 cc (dl) blood. During pregnancy: 10-12 gm/dl i.e. physiological anaemia due to the increase in plasma volume more than RBCs volume.
  • Haematocrit value:
    • It is the volume of packed RBCs in 100 cc of blood.
    • In females: 42%.
  • Reticulocytes:
    • 0-2%. They are cells with remnants of the nucleus. Reticulocytosis indicates over active bone marrow as in haemolytic anaemia.

Leucocytes

  • Total leucocytic count:
    • 4.000-10.000/mm3. It increases during pregnancy to 9.500-10.500/mm3 and up to 16.000/mm3 during labour and the first week of puerperium.
  • Differential leucocytic count:
    • Basophils 0-1%.
    • Eosinophils 3-5%.
    • Monocytes 3-8%.
    • Lymphocytes 20-30%.
    • Neutrophils 60-70%.

Platelets

200.000-400.000/mm3.

Bleeding time

2-4 minutes.

Coagulation time

4-8 minutes.

Definition

Anaemia is a reduction in the number of RBCs and haemoglobin content with a corresponding reduction in the oxygen carrying capacity of the blood.

Iron Deficiency Anaemia

It is the most common type of anaemias (95%).

Daily Requirements

Normal iron requirement is 10 mg/day of which 1mg is absorbed. Requirement increases during pregnancy to 15mg/ day.

Aetiology

  • Inadequate intake of iron.
  • Defective absorption of iron e.g. achlorhydria.
  • Increased demand e.g. menstruation and pregnancy.
  • Chronic blood loss e.g. abnormal uterine bleeding and piles.

Clinical Picture

  • Symptoms: general symptoms of anaemia as;
    • easy fatigability,
    • headache,
    • dyspnoea,
    • palpitation.
  • Signs:
    • Pallor which can be detected in the face, palm of the hand, nail bed and mucus membranes of the mouth and conjunctiva.
    • Angular stomatitis and red glazed tongue.
    • Nails are brittle, striated with loss of their lustre. Spooning of the nails may occur in severe cases.

Investigations

  • RBCs, haemoglobin and haematocrit: below normal.
  • Serum iron concentration: below normal (n=125 m g/dl).
  • Iron binding capacity: below normal (n=400 m g/dl).
  • Transferrin saturation: below normal (n= 30%).
  • Blood film: microcytic hypochromic anaemia.

Treatment

  • Diet: liver, meat, kidney, eggs and green vegetables are rich in iron.
  • Oral iron therapy: ferrous sulphate or ferrous gluconate 300 mg t.d.s. after meals. Side effects: nausea, vomiting and constipation.
  • Parenteral iron therapy:
    • Indications:
      • Malabsorption syndrome.
      • Intolerance to oral iron.
      • Need to rapid response.
    • Preparations:
      • Iron-dextran complex: IV or IM injection.
      • Iron-sorbitol-citrate complex: IM injection only.
    • Side effects:
      • IM injection is irritant, painful, stains the skin and less absorbed so IV injection whether by repeated small doses or infusion in saline solution is preferable.
      • IV therapy may be complicated by flushing, urticaria, arthralgia, fever, lymphadenopathy, phlebitis and anaphylaxis.
  • Packed RBCs: is used if more rapid response is needed e.g. pre-operative.

Prophylactic iron therapy is particularly indicated in high risk group as high parity, multiple pregnancy, and low socio-economic class. In absence of actual anaemia, prophylactic therapy is better deferred till the end of the first trimester as nausea and vomiting are common in this period.

Megaloblastic Anaemia

It is caused by deficiency of folic acid and / or vitamin B12.

Folic Acid Deficiency Anaemia

It is uncommon.

Daily Requirement:

Normal folate requirement is 500 mg /day and a similar amount is needed during pregnancy so that the daily requirement during pregnancy is 1mg.

Aetiology.

  • Inadequate intake.
  • Defective absorption.
  • Increased demand e.g. pregnancy.
  • Drugs: folic acid antagonists as epanutin (anti-epileptic).

Clinical Picture:

  • General symptoms of anaemia (see before).
  • GIT manifestations in the form of:
    • dyspepsia,
    • anorexia,
    • nausea,
    • vomiting,
    • diarrhoea,
    • beefy (red, glassed) tongue,
    • hepatosplenomegaly.

Investigations:

  • Blood film:
    • Macrocytic hyperchromic RBCs.
    • Hypersegmented neutrophilic nuclei (>5 lobes).
  • Serum folate level: is low measured by radioimmunoassay.
  • Bone marrow: abnormal red cell precursors (megaloblasts).

Treatment:

  • Diet rich in folic acid as liver, kidney and meat.
  • Folic acid 5-15 mg /day orally.

Vit. B12 Deficiency Anaemia (Addisonian Pernicious Anaemia)

It is rare.

Daily Requirement: less than 1mg.

Aetiology:

  • Inadequate intake (rare).
  • Deficient intrinsic factor as in atrophic gastritis or gastrectomy.
  • Malabsorption syndrome.
  • Increased demand e.g. pregnancy.

Clinical Picture:

  • General symptoms of anaemia.
  • GIT manifestations: as folic acid deficiency.
  • Nervous manifestations:
    • Subacute combined degeneration.
    • Peripheral neuritis.

Investigations:

As folic acid deficiency + decreased serum vit. B12.

Treatment:

Vit. B12 IM injection.

N.B. Folic acid is never given alone for B12 deficiency anaemia as it will increase the nervous manifestations.

Haemolytic Anaemias

Aetiology

  • Congenital (Intracorpuscular):
    • Spherocytosis.
    • Haemoglobinopathies;
      • Thalassaemia:
        • a - thalassaemia Major.
        • a - thalassaemia Minor.
        • ß - thalassaemia Major.
        • ß - thalassaemia Minor.
      • Sickle cell anaemia.
    • Glucose -6- phosphate dehydrogenase deficiency (G-6-PD).
  • Acquired (Extracorpuscular):
    • Chemicals: e.g. drugs, lead and snake venum.
    • Infections: e.g. malaria and clostridium welchii.
    • Hypersplenism.

Congenital Spherocytosis

An autosomal dominant disorder in which there is deficiency in the lipoprotein of cell membrane leading to increased rigidity of the RBCs and hence its destruction especially in the spleen.

Clinical picture:

  • Features of anaemia (see before).
  • Features of haemolytic jaundice:
    • Lemon yellow skin,
    • ting of jaundice in the sclera,
    • dark stool and normal urine which darkens on standing.
  • Hepatosplenomegaly: are common.

The condition is inherited by 50% of the mother offspring. In the infant, jaundice develops within 48 hours of birth and exchange transfusion may be required.

Thalassaemia

An autosomal inherited disorder resulted from failure of production of either α chain (α- thalassaemia) or β chain (b -thalassaemia) of the haemoglobin molecule and their replacement with other polypeptide chains.

  • α-thalassaemia:
    • α-thalassaemia major (homozygotes):
      • The foetus with this disorder is affected in utero showing polyhydramnios, erythroblastosis, anaemia and hydrops resembling Rh-incompatibility.
      • This foetus does not survive due to inability of oxygen transfer as the α-chain is responsible for O2 carrying capacity.
    • α-thalassaemia minor (heterozygotes):
      • Patient develops mild progressive anaemia during pregnancy.
  • ß-Thalassaemia:
    • ß-thalassaemia major (homozygotes):
      • The disorder starts in childhood leading to death of the patient mostly in the 2 nd or 3rd decade.
    • ß-thalassaemia minor (heterozygotes):
      • As α- thalassaemia minor.

Effect on pregnancy:

  • ß-Thalassaemia major is rarely encountered in pregnant women, but if this happened the prognosis is poor.
  • Anaemia becomes severe in mid-pregnancy and may result in heart failure.

Sickle Cell Anaemia

An autosomal inherited disorder in which glutamic acid in position 6 of the b - chain of the haemoglobin molecule is replaced by valine. This leads to production of HbS. Hb S on exposure to hypoxia forms insoluble aggregations and RBCs become sickle-shaped and are subsequently fragmented.
In addition, these sickle-shaped cells increase the blood viscosity and occlude blood vessels of various organs.
The manifestations appear usually in homozygous not in heterozygous.

Clinical picture:

  • Feature of anaemia and haemolytic jaundice.
  • Multiple infarcts due to obstruction of microcirculation in the spleen, kidney, CNS, retina, bone, lungs and heart.
  • Increased susceptibility to infections especially urinary.
  • Attacks of severe abdominal pain and fever are common due to ischaemia and infarctions.
  • Pre-eclampsia like- syndrome with hypertension, oedema and proteinuria may develop.
  • Increased foetal wastage from abortion, preterm labour and growth retardation associated with placental insufficiency due to maternal placental bed thrombosis.

Management of sickle cell disease during labour:

  • Avoid: hypoxia, dehydration and acidosis.
  • Treat crises by: rehydration, bicarbonate, analgesic, heparin or low molecular weight dextran.
  • Prophylactic antibiotic.

Investigations of Haemolytic Anaemia

  • Serum bilirubin: raised.
  • Urine: increased urobilinogen.
  • Stool: increased stercobilinogen.
  • Blood film: shows normocytic normochromic anaemia and;
    • Small spherical RBCs in case of spherocytosis.
    • Target cells in case of Thalassaemia major.
    • Sickling after inducing hypoxia by addition of Na bisulphite in case of sickle cell anaemia.
  • Electrophoresis: detect type of haemoglobin in haemoglobinopathies.
  • Estimation of glucose-6-phosphate dehydrogenase activity.

Treatment of Haemolytic Anaemia

  • Blood transfusion: in acute attacks.
  • Folic acid and iron therapy: may be indicated.
  • Splenectomy: may be beneficial in spherocytosis and some cases of thalassaemia major, but not to be done during pregnancy.
  • Avoid precipitating factors: as hypoxia in spherocytosis and oxidative agents in G-6-PD deficiency.

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