Anemia in pregnancy

Anaemia in pregnancy

Dr . Hayder Al Shamma’a

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 1st trimester , 6.6mg /day at 3rd 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%

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

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

Causes of iron deficiency anaemia

Decrease intake
Decrease absorption
Increase demands repeated pregnancy


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


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

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

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


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

Sickling test ( incubation with 2% Na metabisulphate)
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

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


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 4γ

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)

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