Anemia in pregnancy pdf - د. حيدر

Dr . Hayder Anaemia in pregnancy 14/4/2016

BY:taher ali taher

obestitrics

Objectives :



Recognize the normal physiological changes in pregnancy



describe the scientific bases of pathophysiology of anemia



L ist the risks to the fetus and mother



The student should be able to diagnose anemia and it’s type and
severity effectively and accurately



The student should be able to justify the management of anemia

according to type , severity and gestational age



The student should be able to prevent the development of anemia

specially iron deficiency and folate deficiency



The student should be able to avoid inappropriate treatment that may

compromise patient health

Introduction :

It is the most common medical disorder in pregnancy

Definition :

Anaemia in pregnancy :- is a pathological condition in which the oxygen

–

carrying capacity of the red blood cells is insufficient to meet the body’s needs.
Hb < 11g/100ml

Physiological changes in pregnancy ( normal changes )

 Increase plasma volume by 40 - 50%
 Increase RBC mass by 18

– 25%



→ consequent fall in Hb concentration haemodilution inspite of increase
RBC mass this gives the physiological anaemia in pregnancy 11g/100ml



MCV ↑

 MCHC±


S. Fe , ferritin ↓

 Total iron-

binding capacity ↑



Iron requirement ↑ ( 2.5 mg/day 1

trimester , 6.6mg /day at 3

trimester

) = 1000 mg / total pregnancy



Moderate ↑ Fe absorption

 Increase folate requirements

Incidence :

 30

– 50 % of pregnant women become anaemic during pregnancy

  90% is iron deficiency
  Folate  deficiency 5%
  other  causes are 5%

Dr . Hayder Anaemia in pregnancy 14/4/2016

BY:taher ali taher

Effects of anaemia on pregnancy:

↓ oxygen supply to the fetus

↑ cardiac output of the mother → cardiac failure

Predispose to infection

↑ chance of abortion & PTL 2-3 times

Aggravate complications of bleeding should it occur

↑ chance of fetal hypoxia during labour

Not allow women to start labour with Hb of less than 10g/100ml

Iron deficiency anaemia :

Is the commonest type of anaemia during pregnancy 90% of cases

Iron metabolism :

 Iron in diet 10

– 15 mg/day

  10 -15 % absorbed ( duodenum , upper jejunum )
  Ferrous  is absorbable , ferric less absorbed
  Bound to apoferritin at the bowel mucosa to form ferritin
  Transported as transferrin to b. marrow to form Hb, to all tissues to form

cytochrome oxidase . Muscles myoglobin

   mucosal absorption capacity 1.5 - 4 mg/day
  Requirements more than absorption 6.5 mg/day
  Mobilization of iron stores
  If depleted  cause anaemia
  Stores depleted after few pregnancies

Iron excretion :

o  No mechanism of excretion
o  Loss with menstruation
o  Desquamation of skin hair etc.

Causes of iron deficiency anaemia :

-Decrease intake

-Decrease absorption

-Increase demands repeated pregnancy

Dr . Hayder Anaemia in pregnancy 14/4/2016

BY:taher ali taher

Features of Iron deficiency anemia in pregnancy



Asymptomatic in majority



Fatigue , palpitation, (may regarded as normal symptoms related to preg.)



Pallor not common due to peripheral vasodilatation associated with

pregnancy



So diagnosis depends on Hb level ( booking , 28 wks , 37 wks



If anemic

Investigations:



↓ Hb , MCV, MCHC, RBC count

 Microcytic hypochromic


In severe cases → poikylocytosis, anisocytosis

  S Fe < 50 micro g/100ml
  IBC > 450 micro g / 100ml
  S ferritin < 12 micro g / l

Treatment :

  Depend on gestational age , severity and compliance
  Oral iron (in mild cases , early pregnancy)
  Frerrous sulfate Fe SO4  200

– 350 mg / day

  Max  increase is    0.8 g / week
Advantage of oral
  Cheep, effective and safe
Disadvantage
  Slow
  Side effects GIT,
  Poor compliance


Ferrous fumarate , ferrous gloconate etc. …. Less side effects but less
absorption

 Continue Rx for 3-6 months to correct stores

Dr . Hayder Anaemia in pregnancy 14/4/2016

BY:taher ali taher

Late pregnancy :

  No time for slow correction
  Parentral Rx !!!!!
  Iron sorbitol (( im)) each 250 mg correct 1 g Hb + 500 mg for the stores

correction ((correct 3g/month))

 Iron succarose (( iv )) total dose infusion
 Indications poor compliance, no time for oral correction

After 30 weeks

  No time for parentral Rx
  Blood transfusion needed ( packed RBC transfusion ) each unit 1-2gHb
  Add iron to correct stores
  Add folic acid prophylaxis

Folic acid deficiency anaemia :

  Requirement in non preg . 50 microg/day
  Pregnant 350 microg /day
  Important in nucleic acid synthesis (rapidly divided cells

Etiology :

o  Decrease intake
o    ===== absorption
o  ====== utelization
o

Increase demand ( twins hemolytic anemia…)

Symptoms and signs :

Fatigue , palpitation , very ill , painful tongue , flattened papillae , ulcers
,hepatospleno megaly anorexia , diarrhoea

Investigations :



Low Hb



Low RBC count



MCV Increases



MCH ±



MCHC decrease



WBC == and increase segmentation



Decrease serum folate

Dr . Hayder Anaemia in pregnancy 14/4/2016

BY:taher ali taher

Treatment :

 Folic acid 5 mg /day gives rapid improvement within 2 days see increase

reticulocyte count

 Also give iron because Rx may unmask iron dif.

B 12 deficiency :

  Rare
  More in vegetarians and poor families
  Same as folate even respond  to large dose folate but may cause

neurological lesion in spinal cord

Haemolytic anaemia :

There is reduced life span of RBCs “ normally 120 days“ the RBCs destroyed
and removed from circulation rapidly

Congenital spherocytosis :



Cell membrane defect “ spectrin diffciency “ cause swelling of RBC and
become oval shape instead of biconcave disc

 RBCs become stiff and can not tolerates mechanical stress when pass

through the capillaries

  Excessive  haemolysis in the spleen and liver
  Rapid turnover of bone marrow
  Increase reticulocytes count
  Respond to splenectomy
  Autosomal dominant  (( 50% of newborn will be affected))



Glucose 6 phosphate dehydrogenase deficiency

  More than 400 types
  Most common is an X linked recessive
  Rarely women become affected ( homozygous )
  Deficiency of NADH ( produced by hexose monophosphate  pathway of

glycolysis )

 Oxidative damage of cell membrae


Episodic hemolytic anaemia ( drug, infection , fava beens , etc……)

 Male fetus 100% affected , female 50% carier

Dr . Hayder Anaemia in pregnancy 14/4/2016

BY:taher ali taher

Haemoglobinopathies

Inherited defects in Hb synthesis cause haemolysis

Sickle cell anaemia :

 HbS
 replacement of glutamic acid by valine at position 6 in the

β globin

chain of the Hb

 HbSS ( homozygous sickle ) when deoxigenated , acidosis , or

dehydration it become insoluble crystals → deformity of the RBC which
becomes like a sickle



Repeated sickle → haemolysis



Cells become rigid block capillaries → further sickling

 tissue ischemia and infarcts

Clinical features of sickle cell disease

  Chronic haemolytic  anaemia
  Painful crisis
  Hypersplenism

– autosplenism

  Increase risk of infection
  Avascular bone necrosis
  CVA
  Chest syndrome

Diagnosis of HbSS :

o Sickling test ( incubation with 2% Na metabisulphate)
o

Hb elecrophoresis → HbSS, HbSA

Management during pregnancy :



Crisis more frequent



Higher risk of

  Abortion
  Infection
  IUGR
  Pre eclampsia
  Prematurity
  Thrombo-embolism
  Perinatal mortality
  Maternal  mortality

Dr . Hayder Anaemia in pregnancy 14/4/2016

BY:taher ali taher

management of HbSS

  Joined clinic obst. + haematologist
  Pre-pregnancy  counseling !!!
   stop iron chelation
  Echo
  Folic acid 5mg
  Penicillin prophylaxis
  Regular check for renal , hepatic  functions
  Hb , Hb electrophoresis ± top up transfusion ( HbS < 60%) , exchange

transfusion ???

management of HbSS

  Look for and treat infection aggressively
  Avoid cold exposure , dehydration,
  Crisis and chest syndrome , treated with hydration + O2 + opiate + top up

transfusion

  Thrombo prophylaxis !!
  Fetal monitor by Doppler U/S
  C/S for obstetrical reason , use epidural anasthesia

Management of labor in HbSS :

  Iv fluid to avoid dehydration
  O2
  Analgesia
  Continuous fetal monitoring
  Prophylactic  Antibiotics ??!!
   Prophylactic anticoagulation ! ?

Maternal mortality 2%

Sickle cell trait HbSA :

  Similar but mild
  Fetal outcome like normal
  Maternal complication usually rare
  Avoid acidosis and hypoxia

Dr . Hayder Anaemia in pregnancy 14/4/2016

BY:taher ali taher

Β thalassemia

Deficiency in

β chain synthesis

Hb compose of 4 globin chains

Hb A 2

α + 2β ……….adult Hb

HbF 2

α + 2 γ ………….fetal Hb

HbA2 2

α + 2 Δ

HbH 4

β chains

HbBart 4

Deficiency in

β chain → ↑% of other Hb

↑haemolysis

In homozygous form (severe form ,

β thalassaemia major)

  Hepatosplenomegaly
  Severe anaemia
  Repeated blood transfusion since age of 4-5 months
  Usually  die early !! Hemosiderosis

(

β thalassaemia minor) :

o  Hetrozygous mild form Hb 7-8 g/100ml
o  Microcytic , hypochromic  anaemia , mild haemolysis
o  Avoid iron Rx unless deficiency confirmed
o  May need repeated transfusion during pregnancy
o  Folic acid 5mg/day
o  During labour maintain Hb of 10 g/100ml

α thalassaemia :

  Rare
  Wide range of severity ( controlled by 4 alleles )
  HbH
  HbBarts
  Major cause stillbirth in southeast Asia

…The end…