Download Anaemia in Pregnancy

ANAEMIA IN PREGNANCY
Dr.
Ahmed Jasim
Ass.Prof
MBChB.-DOG-FIBMS
Consultant of gyn.&obst.
OBJECTIVES OF THIS LECTURE
1.
2.
3.
To know the definition, types and the
consequence of anemia.
To know the hematological physiological
changes during pregnancy.
To know the presentation and management of
each type.
NORMAL BLOOD STANDARDS


Red blood corpuscles (RBCs)
Number:


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:



In females: 4.5-5 millions/mm3.
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 Of iron ;
 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
 IM
effects:
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 mcg /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 (antiepileptic).

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 (αthalassaemia) 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
 As
minor (heterozygotes):
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.

THANK
YOU