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ANAEMIA IN
PREGNANCY
DR IBUA
ANAEMIA IN PREGNANCY
 An expectant mother is considered to
have anaemia if her HB level is < 10g/dl.
(WHO: <11g/dl)
 During pregnancy plasma volume
expands by 46-50% whereas red cell
mass increases by 18-25 %. This leads
to haemodilution hence the lower level
taken for HB during pregnancy.
 Normal ranges: Female: 12-16g/dl
 Male: 13-18g/dl
 Anaemia is the most common medical
disorder to occur in pregnant women
particularly in developing countries but
its prevalence varies from region to
region.
 It is a major contributor to
maternal morbidity and mortality and is
also associated with perinatal mortality.
Causes
Are multifactorial and include:
1) Nutritional deficiencies of iron and
folate
- Poor dietary intake
- Poor absorption
- Increased nutrient loss and demand
- Methods of cooking
- Dietary habits
Causes Cont…
- Prohibitive costs
- Some food taboos for pregnant women
NB: Absorption of iron is affected by the
high phytate content in many grains
based diets in the tropics.
2). Malaria infestation
 With its attendant haemolysis increases
folate demand leading to megaboblastic
anaemia.
 Natural acquired immunity is lowered in
pregnancy leading to excessive
destruction of RBCs in some cases.
3). Hookworm infestation:
 Chronic parasite infection affects millions
of women of reproductive age in
developing countries.
 Lives in the duodenum - the site of
optimal iron absorption, therefore
interfering with the latter by their
attachments to the duodenal mucosa
besides sucking blood from the patient
(0.05 – 0.1ml per worm/ day), and leads
to iron deficiency.
4) Other helminthes and parasites e.g
E. histolytica
5) Haemoglobinopathes e.g. sickle cell
disease (SCD), thalasaemia and glucose
6-phosphate dehydrogenase deficiency.
 SCD is the most common inherited
anaemia in the world.
 The anaemia in SCD is related to the
shortened red cell survival (average 17
days) so that these patients suffer from a
chronic haemolytic process reflecting
itself in the form of a crisis in the mother
and IUGR in the foetus. The steady state
HB in SCA is between 6-10%.
6). Chronic diseases e.g. TB, HIV,
Brucellosis, scistosomiasis, UTI, chronic
liver and renal dx, and protein deficiency.
7) Demands of pregnancy parse;
Extra demands to the haemolytic factors
(increased red cell mass plus demands of
the growing foetus = increase in the total
number of rapidly dividing cell leads to
increased requirement of folic acid).
Clinical Features
 Characteristically insidious in onset
 Presentation usually non-specific and depends
on the severity of anaemia, duration of disease
and causative factors.
 Diagnosis depends on history, physical
examination and various lab tests done based
on aetiological factors.
 In the early stages it may only be detected by
routine HB estimation in the ANC.
Symptoms include:
- General weakness, malaise, fatigue,
lethergy or lassitude
- Dizziness
- Dyspnoea on slight excertion
- Breathlessness
- Swelling of legs feet and face (oedema)
Signs include:
 palour (conjunctiva, tongue, palms and nail
beds, sole of the feet etc),
 jaundice (or tingue of),
 Moderate tachycardia at rest,
 Haemic murmur,
 low grade fever without obvios cause is
common plus or minus hepatosplenomegaly in
haemolytic anaemia e.g. of malaria (endemic)
and SCD,
 Orthorpnoea and other signs of cardiac
failure e.g. engorged neck veins in the
semi-upright position, congestion of lung
bases, enlarged tender liver, increased
pulse pressure, and may be present in
very severe cases
 Albuminuria is common
 In the terminal phase acute pulmonary
oedema may supervene and cerebral
anoxia may produce excitement and
mental confusion followed by loss of
consciousness.
Investigations
 H’gram + PBF+ BS for MPs
 Stool: O/C
 Hb electrophoresis/ sickling test
 LFTs for serous proteins as in chronic liver
disease and hypoproteinaemia
 U/Es + Cr + U.A to rule out underlying nephrosis
 CXR- to r/o intercurrent chronic chest infection
Sequale of Anaemia in pregnancy
 CCF= death in pregnancy or soon after
delivery or during labour
 Low resistance = infections e.g.
pneumonias, puerperal sepsis etc
 IUGR
 Late abortions (20 – 28 wks)
 Premature labour
 IUFD/ neonatal death (perinatal death)
due to intrapartum asphyxia
 Infantile anaemia 2-3 months post
delivery due to deficient iron storage in
the last trimester.
Treatment
 Mainly directed at the cause
 Supportive care is similarly important
e.g. administration of haematinics or
blood transfusion or both – depending on
the degree of anaemia and the
gestational age at the time of diagnosis.
General Measures
 Protein intake- Should be adequate – at
least 100grams per /day, 50% of which
should preferably be animal protein
 Chronic diarrhoeas – should be treated
as they interfere with folic acid and B12
absorption
 Hookworm – should be treated with
non-toxic antihelminthics
Specific treatment
1). Oral iron therapy; in Fe def. anaemia of
moderate degree in the first and second
trimester
2). Parenteral iron therapy; in more severe
cases particularly those seen for the first time
near term to achieve quicker response as well
as for those not able to tolerate oral Fe due to
gastric symptoms and also those not
responding due to malabsorption.
3). Suplementary Folic Acid
4). Malaria treatment – when confirmed or
suspected
5). Steroid therapy – in excessive
haemolysis
6). Vit. B12 – for megaloblastic anaemia
unresponsive to folic acid or when B12
def.is confirmed
7).Cardiac failure - treated appropriately with
antifailure regime (digoxine, aminophyline, O2
etc
8). Blood transfusion – for impending CCF,
patient in labour with severe anaemia
- watch for overload
- Packed RBCs is preferred
- Transfuse slowly (not more than 500mls in
at least 6-8 hrs
Mx of labour and the
puerperium in severe anaemia
 Labour and the first 2wks of the
puerperium are the periods of greatest
danger to the anaemic mother.
 Most deaths occur in the first 12hrs after
delivery
 O2 should be delivered in labour by
mask to reduce the risk of foetal
asphyxia
 Aseptic techniques to be employed due
to decreased immunity
 2nd stage should be shortened by
assisted vacuum extraction or low
forceps delivery
 Antibiotic prophylaxis in the puerperium
 Specific treatment for anaemia to
continue for at least 6wks after delivery
(puerperium) to accelerate recovery
 Finally before discharge warn the mother
of possibility of recurrence in subsequent
pregnancies therefore to present as
soon as they become pregnant for
prophylaxis
Prevention
a) Correct faulty dietary habits e.g.
overcooking vegetables and meat
(important sources of folic acid)
b) Increase production and consumption
of foods which contain the raw
materials of erythropoesis.
c) Antimalarial prophylaxis
d) Reduction of hookworm loads
e) Prophylactic medication – haematinics
f) Early detection of anaemia in
pregnancy by screening all pregnant
women (ANP) – first and last visits
 These measures will lead to a
reduction in loss of maternal and
infant lives from anaemia and also
reduce cost of hospitalization and
treatment
Conclusion
 Prevention of anaemia is difficult in
developing countries due to its
multfactorial origin:
- Poor SES
- Poor health facilities
- Socio-cultural factors
- Poor utilization and scarcity of FP and
ANC services
 However prophylactic use of haematinics
and antimalarials has reduced the
severity of anaemia in the tropics.
 THE END

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Anaemia in pregnancy

  • 2. ANAEMIA IN PREGNANCY  An expectant mother is considered to have anaemia if her HB level is < 10g/dl. (WHO: <11g/dl)  During pregnancy plasma volume expands by 46-50% whereas red cell mass increases by 18-25 %. This leads to haemodilution hence the lower level taken for HB during pregnancy.
  • 3.  Normal ranges: Female: 12-16g/dl  Male: 13-18g/dl  Anaemia is the most common medical disorder to occur in pregnant women particularly in developing countries but its prevalence varies from region to region.
  • 4.  It is a major contributor to maternal morbidity and mortality and is also associated with perinatal mortality.
  • 5. Causes Are multifactorial and include: 1) Nutritional deficiencies of iron and folate - Poor dietary intake - Poor absorption - Increased nutrient loss and demand - Methods of cooking - Dietary habits
  • 6. Causes Cont… - Prohibitive costs - Some food taboos for pregnant women NB: Absorption of iron is affected by the high phytate content in many grains based diets in the tropics.
  • 7. 2). Malaria infestation  With its attendant haemolysis increases folate demand leading to megaboblastic anaemia.  Natural acquired immunity is lowered in pregnancy leading to excessive destruction of RBCs in some cases.
  • 8. 3). Hookworm infestation:  Chronic parasite infection affects millions of women of reproductive age in developing countries.  Lives in the duodenum - the site of optimal iron absorption, therefore interfering with the latter by their attachments to the duodenal mucosa besides sucking blood from the patient (0.05 – 0.1ml per worm/ day), and leads to iron deficiency.
  • 9. 4) Other helminthes and parasites e.g E. histolytica 5) Haemoglobinopathes e.g. sickle cell disease (SCD), thalasaemia and glucose 6-phosphate dehydrogenase deficiency.
  • 10.  SCD is the most common inherited anaemia in the world.  The anaemia in SCD is related to the shortened red cell survival (average 17 days) so that these patients suffer from a chronic haemolytic process reflecting itself in the form of a crisis in the mother and IUGR in the foetus. The steady state HB in SCA is between 6-10%.
  • 11. 6). Chronic diseases e.g. TB, HIV, Brucellosis, scistosomiasis, UTI, chronic liver and renal dx, and protein deficiency.
  • 12. 7) Demands of pregnancy parse; Extra demands to the haemolytic factors (increased red cell mass plus demands of the growing foetus = increase in the total number of rapidly dividing cell leads to increased requirement of folic acid).
  • 13. Clinical Features  Characteristically insidious in onset  Presentation usually non-specific and depends on the severity of anaemia, duration of disease and causative factors.  Diagnosis depends on history, physical examination and various lab tests done based on aetiological factors.  In the early stages it may only be detected by routine HB estimation in the ANC.
  • 14. Symptoms include: - General weakness, malaise, fatigue, lethergy or lassitude - Dizziness - Dyspnoea on slight excertion - Breathlessness - Swelling of legs feet and face (oedema)
  • 15. Signs include:  palour (conjunctiva, tongue, palms and nail beds, sole of the feet etc),  jaundice (or tingue of),  Moderate tachycardia at rest,  Haemic murmur,  low grade fever without obvios cause is common plus or minus hepatosplenomegaly in haemolytic anaemia e.g. of malaria (endemic) and SCD,
  • 16.  Orthorpnoea and other signs of cardiac failure e.g. engorged neck veins in the semi-upright position, congestion of lung bases, enlarged tender liver, increased pulse pressure, and may be present in very severe cases  Albuminuria is common
  • 17.  In the terminal phase acute pulmonary oedema may supervene and cerebral anoxia may produce excitement and mental confusion followed by loss of consciousness.
  • 18. Investigations  H’gram + PBF+ BS for MPs  Stool: O/C  Hb electrophoresis/ sickling test  LFTs for serous proteins as in chronic liver disease and hypoproteinaemia  U/Es + Cr + U.A to rule out underlying nephrosis  CXR- to r/o intercurrent chronic chest infection
  • 19. Sequale of Anaemia in pregnancy  CCF= death in pregnancy or soon after delivery or during labour  Low resistance = infections e.g. pneumonias, puerperal sepsis etc  IUGR  Late abortions (20 – 28 wks)  Premature labour
  • 20.  IUFD/ neonatal death (perinatal death) due to intrapartum asphyxia  Infantile anaemia 2-3 months post delivery due to deficient iron storage in the last trimester.
  • 21. Treatment  Mainly directed at the cause  Supportive care is similarly important e.g. administration of haematinics or blood transfusion or both – depending on the degree of anaemia and the gestational age at the time of diagnosis.
  • 22. General Measures  Protein intake- Should be adequate – at least 100grams per /day, 50% of which should preferably be animal protein  Chronic diarrhoeas – should be treated as they interfere with folic acid and B12 absorption  Hookworm – should be treated with non-toxic antihelminthics
  • 23. Specific treatment 1). Oral iron therapy; in Fe def. anaemia of moderate degree in the first and second trimester 2). Parenteral iron therapy; in more severe cases particularly those seen for the first time near term to achieve quicker response as well as for those not able to tolerate oral Fe due to gastric symptoms and also those not responding due to malabsorption.
  • 24. 3). Suplementary Folic Acid 4). Malaria treatment – when confirmed or suspected 5). Steroid therapy – in excessive haemolysis 6). Vit. B12 – for megaloblastic anaemia unresponsive to folic acid or when B12 def.is confirmed
  • 25. 7).Cardiac failure - treated appropriately with antifailure regime (digoxine, aminophyline, O2 etc 8). Blood transfusion – for impending CCF, patient in labour with severe anaemia - watch for overload - Packed RBCs is preferred - Transfuse slowly (not more than 500mls in at least 6-8 hrs
  • 26. Mx of labour and the puerperium in severe anaemia  Labour and the first 2wks of the puerperium are the periods of greatest danger to the anaemic mother.  Most deaths occur in the first 12hrs after delivery  O2 should be delivered in labour by mask to reduce the risk of foetal asphyxia
  • 27.  Aseptic techniques to be employed due to decreased immunity  2nd stage should be shortened by assisted vacuum extraction or low forceps delivery  Antibiotic prophylaxis in the puerperium  Specific treatment for anaemia to continue for at least 6wks after delivery (puerperium) to accelerate recovery
  • 28.  Finally before discharge warn the mother of possibility of recurrence in subsequent pregnancies therefore to present as soon as they become pregnant for prophylaxis
  • 29. Prevention a) Correct faulty dietary habits e.g. overcooking vegetables and meat (important sources of folic acid) b) Increase production and consumption of foods which contain the raw materials of erythropoesis. c) Antimalarial prophylaxis
  • 30. d) Reduction of hookworm loads e) Prophylactic medication – haematinics f) Early detection of anaemia in pregnancy by screening all pregnant women (ANP) – first and last visits
  • 31.  These measures will lead to a reduction in loss of maternal and infant lives from anaemia and also reduce cost of hospitalization and treatment
  • 32. Conclusion  Prevention of anaemia is difficult in developing countries due to its multfactorial origin: - Poor SES - Poor health facilities - Socio-cultural factors - Poor utilization and scarcity of FP and ANC services
  • 33.  However prophylactic use of haematinics and antimalarials has reduced the severity of anaemia in the tropics.