Anemia in pregnancy What is - PowerPoint Presentation

Slide1

Anemia in pregnancy

Slide2

Slide3

Slide4

What is

Anaemia

?

Anaemia

is defined as reduction in circulating

 

haemoglobin mass below

the

critical

level.

The normal

haemoglobin

(Hb)

is

12-14

gm%.

WHO has

accepted

up to 11 gm% as the

normal

 

haemoglobin level in

pregnancy.

Therefore any haemoglobin

level below

11gm

 

in pregnancy should be considered as

anaemia

Slide5

Total iron requirement is

1000

mg.

Fetus and placenta -- 300

mg

↑ in red cell

mass

– 500

mg

Basal loss –

200

mg

Average

requirement is

4-6mg/day.

2.5 mg/day in early

pregnancy

5.5 mg/day from

20-32

weeks

6-8

mg/day

from 32 weeks

onwards

Slide6

Anaemia is

often

classified as

 

Mild degree

(9-11

gm %)

 

Moderate

(7-9 gms

%)

 

Severe

(4-7

gm

%)

Very

severe

(<4gm

%)

It is also classified

according to

Haematocrit 

(PCV) %.

Slide7

Antenatal

Period

-Poor

weight

gain

-Preterm

labour

Postnatal

Period

-PPH

-Postnatal

sepsis

-Sub

involution

-VTE

Intra

partum Period

-Dysfunctional

Labour

-Hemorrhage-Shock

-Cardiac

Failure

-Anaethesia risk

What are the maternal risk factors ?

Slide8

•

•

•

•

•

Prematurity

Low

birth

weight

 

Poor apgar score

 

Foetal distress

 

Neonatal Anaemia

What are the fetal and neonatal risk factors ?

Slide9

Physiological

 

Nutritional:

Iron

deficiency

Folate

&/or

Vit B12

deficiency

 

Dimorphic

Hemorrhagic: Acute

or

Chronic

Hemoglobinopathies

Hemolytic:

Congenital

or

acquired

Aplastic

anaemia

Slide10

Symptoms

Fatigue

Loss

of

appetite

Digestive

upset

Dyspnoea

Palpitation

Si

g

ns

Pallor

Pale

nails

Koilonychias

Pale

Tongue

Severe Case

-

Oedema

Slide11

CBC

Pheripheral Smear –

Hypochromic

Microcytosis

P

oik

ilocytos

i

s

Anisocytosis

MCV,

MCH,

MCHC

TIBC

Serum

Iron

Serum

Ferritin

Free erythrocyte

protoporphyrin

Bone marrow examination

Urine

examination

Stool

examination

Serum

protein

Slide12

Serum

Folate

RBC

folate

Serum Vit

B12

Serum

Bilirubin

Coombs

test

HB

electrophoresis

Red cell

osmotic fragility

Slide13

Routine

screening for

anaemia

for

adolescent

girls from

school

days

Encouraging

iron rich

foods

Fortification of

widely

consumed

food with

iron

Providing

iron

supplementation

from school

days

Annual screening for those with risk

factors

Slide14

Prophylaxis

of non-pregnant

women

– 60

mg

of elemental iron daily for 3

months.

Iron supplementation during

pregnancy.

Routine

iron

supplementation

is

debatable

in western countries

It has to be given in non-industrialized

countries

W.H.O

RECOMMENDATION:

Universal oral iron supplementation for pregnant women

(60

mg of elemental iron

and 400 µg

of folic acid) for 6

months

in pregnancy and

additional

of 3

months post-partum where the

prevalence is

more than

40%.

Slide15

MOTHER

PREGNANCY-

Cardiac

failure at

30-34 wks of

pregnancy

Increased

susceptibility to

infection

Preterm

labour

Preeclampsia

LABOUR-

Uterine

inertia

Post

partum

haemorrhage

Cardiac

failure

shock

Slide16

Puerperium

Cardiac

failure

Puerperal sepsis

Subinvolution

Failing

lactation

Chronic

ill

health,backache

FETUS&NEONATE

Prematurity

IUGR

Increased perinatal

death

Decreased iron stores in

neonate

Slide17

ORAL IRON

THERAPY

Safe,inexpensive and

effective

way

to administer

iron

National nutritional

anemia

prophylaxis

program

suggest 60 milligrams of elemental

iron and 400

micrograms of folic acid

daily

Slide18

SALT

TABLET

E

L

EME

N

T

AL

IRON

Ferrous

sulfate200mg

60mg[30%]

Ferrous fumarate

200mg

66mg[33%]

Ferrous gluconate

320mg

36mg[12%]

Ferrous succinate

100mg

35mg[35%]

Ferric ammonium citrate

125mg

25mg[17-22%]

Ferrous ascorbate

------100mg

Carbonyl

iron-------

90mg

Sodium feredetate

-------

231mg

Hb preparation

2.1g

[0.33%]

Slide19

SIDE

EFFECTS OF ORAL

IRON

A.

UPPER GI

TRACT

Nausea,gastric

discomfort,loss

of apetite,staining of teeth

A.

LOWER GI TRACT

Constipation,di

arrhoea

,flatul

ance

Slide20

PARENTRAL

IRON

THERAPY

Same efficacy

 

Used if : Side effects . No compliance

Preparation

Iron

sucrose

Iron

sorbital citric

acid complex 

Iron dextran

Slide21

BLOOD

TRANFUSION

Indicated

in

:

S

evere anemia

at

any GA

Ongoing lossNear term

Failure

of response to iron therapy

Hemoglobinopathies as indicated

Slide22

ADVERSE

REACTIONS

Tranfusion

reaction

Infection

Volume

overload

Others

like

hypothermia,citrate toxicity,hyperkalemia,hypocalcemia

and

rarely air

embolism

Slide23

Active

management

of

third

stage

During

puerperium

Adequate

rest

Iron and folate therapy for 3 months

Infection if any should be treated

energeticallyCareful watch

for puerperal sepsis, failing lactation; sub involution of uterus and thromboembolism

Slide24

Thalassemia in pregnancy

Slide25

Thalassemia

Is a blood disorder passed down through families ( inherited ) in which the body makes and abnormal form of hemoglobin .

2 Types :

Alpha

Beta

Slide26

Types

Alpha thalassemia

1 mutated gene : is a carrier , no symptoms , carrier who will pass it on to their children

2 mutated genes will exhibit mild signs and symptoms also called alpha-thalassemia trait

3 mutated genes with have moderate to severe signs and symptoms – HbH Disease

4 mutated genes, Rare but severe, Hemoglobin Barts-affected fetuses are usually stillborn or die shortly after birth. Rarely they can be treated with lifelong transfusions or bone marrow transplant

Beta thalassemia 1 mutated gene (thalassemia minor), mild signs and symptoms2 mutated genes (thalassemia major, Cooley anemia) usually healthy at birth but develop signs and symptoms in the first 2 years of life. A milder form is called thalassemia intermedia .

Slide27

Signs and Symptoms

Severe anemia leading to extramedullary hematopoiesis and its complications including splenomegaly, bone deformities

Fatigue

Growth failure

Jaundice

Aplastic and hemolytic crises

Complications of iron overload from chronic blood transfusions Fetal hydropsSubfertility

Slide28

Alpha thalassemia

 Inherited in a Mendelian recessive manner. They are also associated with deletions of chromosome 16p.

Beta Thalassemia

Caused by mutations in the HBB gene on chromosome 11, inherited in an autosomal recessive fashion.

Slide29

Diagnosis

Clinically

Labs : CBC , electrophoresis , peripheral blood smear .. Etc.

DNA analysis , to investigate deletions and mutations in the alpha- and beta-

globin

-producing genes. This can determine the carrier status.

Not routine .Antenatal by CVS or amniocentesis

Slide30

Treatment

Multiple blood transfusions

Chelation therapy

Bone marrow transplant

Slide31

Additional risks to mother and baby ?

Thalassaemia

is associated with an increased risk to both mother and baby.

Mother : issues surrounding cardiomyopathy due to iron overload and the In addition, with around 9 months of little or no

chelation

, women with

thalassaemia major may develop new endocrinopathies: in particular, diabetes mellitus, hypothyroidism and hypoparathyroidism due to the increasing iron burden.increased risk of fetal growth restriction (FGR).

Slide32

Preconception care

Aggressive chelation in the preconception stage can reduce and

optimise

body iron burden and reduce end-organ damage.

Diabetes mellitus is common in adults with

thalassaemia

. Diabetes is multifactorial, due to insulin resistance, iron-induced islet cell insufficiency, genetic factors and autoimmunity. Similar to women with diabetes without thalassaemia, an HbA1c of less than 6 % is associated with a reduced risk of congenital abnormalities.

Slide33

hypothyroidism is frequently found in patients with

thalassaemia

. Thyroid function should be determined. The woman should be

euthyroid

prepregnancy

. Heart : An echocardiogram and an electrocardiogram (ECG) should be performed as well as T2* cardiac MRI, aim for cardiac T2* > 20 ms wherever possible as this reflects minimal iron in the heart. A T2* < 10 ms is associated with an increased risk of cardiac failure.

Liver and gall bladder (and spleen if present) ultrasound should be used to detect cholelithiasis and evidence of liver cirrhosis due to iron overload or transfusion-related viral hepatitis.Ideally the liver iron should be < 7 mg/g (dry weight) (dw).

Slide34

Osteoporosis is a common finding in adults with

thalassaemia

. The pathology is complex, but thought to be due to a variety of factors including underlying

thalassaemic

bone disease,

chelation

of calcium by chelation drugs, hypogonadism and vitamin D deficiency.

Red cell antibodies : Alloimmunity occurs in 16.5% of individuals with thalassaemia. Red cell antibodies may indicate a risk of haemolytic disease of the fetus and newborn.If antibodies are present there may be challenges in obtaining suitable blood for transfusion.

Slide35

What about medications ?

All bisphosphonates are contraindicated in pregnancy and should ideally be discontinued 3 months prior to conception , and not to be used in the 1

st

trimester owing to lack of safety data.

Folic acid (5 mg) is recommended

preconceptually

to all women to prevent neural tube defects.

Slide36

Genetic counselling

In vitro

fertilisation

/intracytoplasmic sperm injection (IVF/ICSI) with a pre-implantation genetic diagnosis (PGD) should be considered in the presence of

haemoglobinopathies

in both partners so that a homozygous or compound heterozygous pregnancy can be avoided.

When two carriers have children , each child has a 25% ( 1 in 4 ) chance to be affected , a 50% ( 1 in 2 ) chance to be a carrier like each parent , and a 25% ( 1 in 4 ) chance to be unaffected and not to be a carrier .

Slide37

Good practice points

Hepatitis B vaccination is recommended in

HBsAg

negative women who are transfused or may be transfused.

Hepatitis C status should be determined.

All women who have undergone a splenectomy should take penicillin prophylaxis or equivalent.

All women who have undergone a splenectomy should be vaccinated for pneumococcus and Haemophilus influenzae type b if this has not been done before.

Slide38

Antenatal care

Women with

thalassaemia

should be reviewed monthly until 28 weeks of gestation and fortnightly thereafter.

Women with both

thalassaemia

and diabetes should have monthly assessment of serum fructosamine concentrations and review in the specialist diabetic pregnancy clinic. All women with thalassaemia major should undergo specialist cardiac assessment at 28 weeks of gestation and thereafter as appropriate. Thyroid function should be monitored during pregnancy in hypothyroid patients.

Slide39

All women with

thalassaemia

major should be receiving blood transfusions on a regular basis aiming for a

pretransfusion

haemoglobin

of 10 g/dl. Intermedia :If there is worsening maternal anaemia or evidence of FGR, regular transfusions should be considered. If a woman with thalassaemia

intermedia starts transfusion, haemoglobin targets are managed as for thalassaemia major. Generally, in nontransfused patients, if the haemoglobin is above 8 g/dl at 36 weeks of gestation, transfusion can be avoided prior to delivery. Postnatal transfusion can be provided as necessary.

If the haemoglobin is less than 8 g/dl then aim for a top-up transfusion of 2 units at 37–38 weeks of gestation.

Slide40

Is antenatal thromboprophylaxis recommended?

Women with

thalassaemia

major or intermedia have a

prothrombotic

tendency due to the presence of abnormal red cell fragments, especially if they have undergone splenectomy.

Women with thalassaemia who have undergone splenectomy or have a platelet count lower than 600 x 109 /l should commence or continue taking low-dose aspirin (75 mg/day). Women with thalassaemia who have undergone splenectomy and have a platelet count above 600 x 109 /l should be offered low-molecular-weight heparin thromboprophylaxis as well as low-dose aspirin (75 mg/day).

Women with thalassaemia who are not already using prophylactic low-molecular-weight heparin should be advised to use it during antenatal hospital admissions.

Slide41

Management of women with myocardial iron

Those women at highest risk of cardiac

decompensation

should commence low-dose subcutaneous

desferrioxamine

(20 mg/kg/day) on a minimum of 4–5 days a week.

As the cardiac T2* value falls below 20 ms there is an increasing risk of cardiac decompensation. Those women at highest risk are those where the value is below 10 ms. Women with myocardial iron loading and T2* > 20 ms do not require desferrioxamine chelation

during pregnancy unless there is severe hepatic iron overload.cardiac decompensation may present as increasing breathlessness, paroxysmal nocturnal dyspnoea, orthopnoea, syncope, palpitations or peripheral oedema. Presentation in the first trimester is associated with adverse clinical outcome.

Slide42

Management of women with liver iron

Women with severe hepatic iron loading should be carefully reviewed and consideration given to low dose

desferrioxamine

iron

chelation

from 20 weeks.

High concentrations of liver iron (liver iron > 15 mg/g dw as measured by MRI) are associated with an increased risk of myocardial iron and in all women with thalassaemia major the therapeutic aim is to achieve a liver iron concentration below 15 mg/g dw to reduce the risk of myocardial iron overload.

Slide43

Intrapartum care

Timing of delivery should be in line with national guidance.

In the presence of red cell antibodies, blood should be cross-matched for delivery since this may delay the availability of blood. Otherwise a group and save will suffice.

In women with

thalassaemia

major intravenous

desferrioxamine 2 g over 24 hours should be administered for the duration of labour. Continuous intrapartum electronic fetal monitoring should be instituted. Thalassaemia

in itself is not an indication for caesarean section. Active management of the third stage of labour is recommended to minimise blood loss.

Slide44

Postpartum care

Women should receive low-molecular-weight heparin prophylaxis while in hospital.

In addition, low-molecular-weight heparin should be administered for 7 days post discharge following vaginal delivery or for 6 weeks following caesarean section.

Women with

thalassaemia

major who plan to breastfeed should restart

desferrioxamine as soon as the initial 24-hour infusion of intravenous desferrioxamine finishes after delivery. Desferrioxamine is secreted in breast milk but is not orally absorbed and therefore not harmful to the newborn.

Slide45

Sickle cell & thalassemia

Should one parent have sickle cell trait and the other have thalassemia trait, any child they conceive has one chance in four of receiving one gene for sickle cell disease and one gene for b-thalassemia . This condition is called sickle b-thalassemia. The severity varies. Some patients with sickle b-thalassemia have a condition as severe as sickle cell disease itself. Others have few and relatively mild problems. The gene for thalassemia is very common among people of Mediterranean origin. The sickle gene also exists in people of Mediterranean origin, although its frequency is much lower than that for thalassemia.

Slide46

SICKLE CELL

SYNDROME.

Autosomally inherited

. Structural

abnormality.

HbS

-

susceptible to

hypoxia,

when

oxygen

supply

is reduced.

Hb

pre

c

ipi

t

ates &

mak

es the RBCs

rigid & sickle sha

ped.H

eterozygous----Hb

AS. Homozygous-----HbSS.Compound heterozygous---HbSC

etc.

Slide47

Sickle

Cell

Disease

(SCD)

Sickeling

crises frequently

occurs

in

pregnancy, puerperium &in

state

of

hypoxia

Increased incidance of

abortion and still birth

growth restriction, premature birth and intrapartum fetal distress with increased perinatal

mortality.Sickle cell trait:(carrier

state)Does not pose any significanc

ant clinical problems

Slide48

Sickle

Cell

Disease

Structural Hb

variant

Exists in

homo

& heterozygous forms

Under hypoxic

conditions, HbS polymerizes, gels or

crystallizes.

hemolysis of cells, & thrombosis of vessels in various

organs

In long standing cases, multiple organ

damage.

Slide49

SCD

Diagnosis:

Hb. Electrophoresis

Management:

No curative

Tx.

only

symptomatic

Well

hydration,

effective

analgesia, prophylactic

antibiotics, O2

inhalation,

folic

acid, oral

iron supplement

(I/V iron is C/I), blood transfusion

Slide50

Management

During

labour

Comfortable

Position

Adequate analgesia O2

inhalation

Low

threshold of

assisted

delivery

Avoid ergometrine Prophylactic

antibiotics

Continue iron &folate therapy for 3 mo after delivery Appropriate contraceptive advice

Slide51

FOLATE DEFICIENCY

ANAEMIA

At cellular

level

Folic acid reduced

to

Dihydrofolicacid

then

Tetrahydro-folicacid

.

(THF)

c

is required for cell growth & division.

So more active tissue reproduction & growth

more dependant on supply of folic

acid.So bone marrow and epithelial lining are

therefore at particularrisk.

Slide52

FOLATE DEFICIENCY

ANAEMIA

Folic

acid deficiency

more likely

if

. Woman

taking

anticonvulsants.

. Multiple

pregnancy.. Hemolytic anemia; thalasemia

H.spherocytosisMaternal risk:

Megaloblastic anemiaFetal

risk:Pre-conception deficiency cause neural tube defect and cleft palate

etc.

Slide53

FOLATE DEFICIENCY

ANAEMIA

Diagnosis:

Increased

MCV ( >

100

fl)Peripheral smear: - Macrocytosis,

hypochromia Hyp

ersegment

ed neutrophils (

> 5 lobes)Neutropenia

ThrombocytopeniaLow Serum folate

level. Low RBC folate.

Slide54

FOLATE DEFICIENCY

ANAEMIA

Daily

folate

requirement for

:

Non

pregnant

women

-- 50 -100 microgram Pregnant

woman –--------

300-400

microgram

Usually folic acid present

in

diets like fresh

fruits and

vegetables and destroyed by

cooking.Folate

deficiency:0.5-1.0mg folic

acid/day If F/Hx. of neural tube

defect4mg folic acid/day.

Slide55

Vitamins B12

Deficiency

It

is

rare

Occurs

in

patients

with

gastrectomy

, ileitis, illeal

resection, pernicious anaemia,

intestinal

parasites.

Diagnosis:

–

Peripheral smear–Vitamin B12

level < 80 pico g/ml

Treatment of B12

Deficiency:Vit B12 1mg I/M weekly for 6

weeks.

Slide56

Management

of

FDA

Strong

case

for routine

prophylaxis

Prophylaxis with anti

convulsantsContinue routine oral therapy

for hemolytic anaemiaParenteral therapy for

severe deficiency

Slide57

Slide58

Take

Home

Message

Anaemia

although

preventable

is

a

global

problemAnaemia still is the commonest cause of

maternal mortality and morbidity in spite of easy diagnosis and

treatmentAnaemia can be due to a number

of causes, including certain diseases or a shortage of iron, folic acid or

Vitamin B12.The most common cause of

anemia in pregnancy is iron deficiency.

Iron therapy is best given orally