Anaemia in pregnancy

Anaemia in Pregnancy

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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.



Red blood corpuscles (RBCs):• 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:A. 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.



• Leucocytes: B.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.


Anaemia

• 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.


1.Iron Deficiency Anaemia2.Megaloblastic Anaemia:a. Folic Acid Deficiency Anaemiab. Vit. B12 Deficiency Anaemia (Addisonian

Pernicious Anaemia)3.Haemolytic Anaemias


Iron Deficiency Anaemia



• 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.


Iron Deficiency Anaemia>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.



• Clinical Picture: • 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: Preparations:>Iron-dextran complex: IV or IM injection.> Iron-sorbitol-citrate complex: IM injection only.


Treatment

• 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.


Treatment

• Packed RBCs: is used if more rapid response is needed e.g. pre-operative.


Megaloblastic Anaemia



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

• 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.



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.



• Folic Acid Deficiency Anaemia• Aetiology: * Inadequate intake. * Defective absorption. * Increased demand e.g. pregnancy. * Drugs: folic acid antagonists as epanutin

(anti-epileptic).



• Folic Acid Deficiency Anaemia• Clinical Picture: * General symptoms of anaemia (see before). * GIT manifestations in the form of: > dyspepsia, > anorexia, > nausea, > vomiting, > diarrhoea, > beefy (red, glassed) tongue, > hepatosplenomegaly.



• Folic Acid Deficiency Anaemia• 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).



• Folic Acid Deficiency Anaemia

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.



• Vit. B12 Deficiency Anaemia (Addisonian Pernicious Anaemia)

• 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

• Congenital (Intracorpuscular): A. Spherocytosis. B. Haemoglobinopathies C. Glucose -6- phosphate dehydrogenase deficiency

(G-6-PD).• Acquired (Extracorpuscular): A.Chemicals: e.g. drugs, lead and snake venum. B.Infections: e.g. malaria and clostridium welchii. C.Hypersplenism.


Haemolytic Anaemias

• B. Haemoglobinopathiesa. Thalassaemia: > a - thalassaemia Major. > a - thalassaemia Minor. > ß - thalassaemia Major. > ß - thalassaemia Minor b. Sickle cell anaemia.


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.



>Features of anaemia (see before).>Features of haemolytic jaundice: o Lemon yellow skin, o ting of jaundice in the sclera, o 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 a chain (a- thalassaemia) or ß chain (b -thalassaemia) of the haemoglobin molecule and their replacement with other polypeptide chains.


Thalassaemia

>a- thalassaemia: a- thalassaemia major (homozygotes):a- thalassaemia minor (heterozygotes):>ß-Thalassaemiaß-thalassaemia major (homozygotes): ß-thalassaemia minor (heterozygotes):


Thalassaemia

a- 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 a-chain is responsible for O2 carrying capacity.


Thalassaemia

a- thalassaemia minor (heterozygotes):

Patient develops mild progressive anaemia during pregnancy.


Thalassaemia

ß-thalassaemia major (homozygotes):

The disorder starts in childhood leading to death of the patient mostly in the 2 nd or 3rd decade.


Thalassaemia

ß-thalassaemia minor (heterozygotes):

As a- thalassaemia minor.


Thalassaemia

• 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.


Sickle Cell Anaemia

• 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.


Sickle Cell Anaemia

• Clinical picture:* 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.


Sickle Cell Anaemia

• 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;o Small spherical RBCs in case of spherocytosis.o Target cells in case of Thalassaemia major.o 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.


Treatment of Haemolytic Anaemia

* 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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Anaemia in pregnancy