ANAEMIA COMPLICATING PREGNANCY

DR:HUSSEIN H AKL

O&G SPECIALIST

HOSPITAL SEGAMAT

Definition

¨ Anemia - insufficient Hb to carry out O2 requirement

to the tissues.

¨ WHO definition : Hb conc. 11 gm %

¨ CDC definition : Hb conc. < 11gm % in 1st and 3rd trimesters and < 10.5 gm% in 2nd trimester

¨ For developing countries : cut off level suggested is 10 gm %

- WHO technical report Series no. 405, Geneva 1968

Centre for disease control, MMWR 1989;38:400-4

¨ Anemia - insufficient Hb to carry out O2 requirement

to the tissues.

¨ WHO definition : Hb conc. 11 gm %

¨ CDC definition : Hb conc. < 11gm % in 1st and 3rd trimesters and < 10.5 gm% in 2nd trimester

¨ For developing countries : cut off level suggested is 10 gm %

- WHO technical report Series no. 405, Geneva 1968

Centre for disease control, MMWR 1989;38:400-4

ANAEMIA IN PREGNANCY

Definition: By WHO

Hb. < 11 gm /dl

(or haematocrit <32%).

Mild anaemia -------- 9 -10.9 gm /dl

Moderate anaemia--- 7-8.9 gm /dl

Sever anaemia-------- < 7gm /dl

Very sever anaemia-- < 4gm/dl

Degree Hb% Haematocrit (%)

Moderate 7-10.9 24-37%

Severe 4-6.9 13-23%

Very Severe <4 <13%

Degree Hb% Haematocrit (%)

Moderate 7-10.9 24-37%

Severe 4-6.9 13-23%

Very Severe <4 <13%

WHO Classification of Anaemia WHO Classification of Anaemia

Magnitude of ProblemMagnitude of Problem

¨ Globally, is about 30 %

¨ In developing countries & India, incidence is around 40 – 90%.

¨ Responsible for 40% of maternal deaths in third world countries.

¨ Important cause of direct and indirect maternal deaths

- Vitere FE Adv Exp Med Biol 1994;352:127

¨ Globally, is about 30 %

¨ In developing countries & India, incidence is around 40 – 90%.

¨ Responsible for 40% of maternal deaths in third world countries.

¨ Important cause of direct and indirect maternal deaths

- Vitere FE Adv Exp Med Biol 1994;352:127

Infection

Lack of Concentration

Weakness

Irritability

Palpitation

Fatigue

Dizziness

SymptomsSymptoms

Clinical FeaturesClinical Features

Pallor of skin And m/m

Edema

PlatynychiaKoilonychia PlatynychiaKoilonychia

Glossitis

Stomatitis

Tachycardia

Soft ejectionsystolic murmur

Signs

IRON DEFICIENCY ANEMIA

¨ GENERAL ANEMIA’S SYMPTOMS:

•FATIGABILITY

•DIZZENES

•HEADACHE

•SCOTOMAS

•IRRITABILITY

•ROARING

•PALPITATION

•CHD, CHF

pallor

Conjunctival Pallor

Koilonychia

¨  ¨  

CHARACTERISTICS SYMPTOMS

•GLOSSITIS, STOMATITIS• DYSPHAGIA ( Plummer-Vinson syndrome)

•ATROPHIC GASTRITIS

•DRY, PALE SKIN

•SPOON SHAPED NAILS, KOILONYCHIA,

•BLUE SCLERAE

•HAIR LOSS

•PICA (APETITE FOR NON FOOD SUBSTANCES SUCH AS AN ICE, CLAY)

•SPLENOMEGALY (10%)

•INCREASED PLATELET COUNT

Physiological

Pathological

Causes of Anaemia Causes of Anaemia

¨ Nutritional

¨ Haemorrhagic

¨ Haemolytic

¨ Nutritional

¨ Haemorrhagic

¨ Haemolytic

Common Anaemias in pregnancy

Common types:

¨ Nutritional deficiency anaemias

- Iron deficiency

- Folate deficiency

- Vit. B12 deficiency

¨ Haemoglobinopathies:

- Thallassemias

- SCD

Rare types:

- Aplastic

- Autoimmune hemolytic

- Leukemia

- Hodgkin’s disease

- Paroxysmal nocturnal haemoglobinurea

Iron RequirementIron Requirement

Iron Absorption 11 Amount of iron in the

body Amount of iron in the

body

Iron Loss

Skin

Urine

Feces

Menstruation

1-2mg/d1-2mg/d

20-30mg/c20-30mg/c

Physiological changes in pregnancy

• Plasama volume 50% (by 34weeks)

• But RBC mass only 25%

• Results in haemodilution :

• Hb

Haematocrit

RBC count

¨ No change in MCV or MCH

¨ 2-3 fold increase in Fe requierment.

¨ 10-20 Fold increase in folate requirement

Criteria for Physiologic Anemia

¨ Hb: 10gm%

¨ RBC: 3.2 million/mm3

¨ PCV: 30%

¨ Peripheral smear showing normal morphology of RBC with central pallor

Significance of Hypervolemia

1. To meet the demands of the enlarged uterus with its greatly hypertrophied vascular system.

2. To protect the mother, and in turn the fetus, against the deleterious effects of impaired venous return in the supine and erect positions.

3. To safeguard the mother against the adverse effects of blood loss associated with parturition.

¨ Normal hemoglobin by gestational age in pregnant women taking iron supplement

¨ 12 wks 12.2 [11.0-13.4]

¨ 24wks 11.6 [10.6-12.8]

¨ 40 wks 12.6 [11.2-13.6]

Early Pregnancy

2.5 mg / day

32 to 40 weeks

6.8 mg / day

TOTAL800 – 1000

mg

20 to 32 weeks

5.5 mg / day

Iron Requirement During PregnancyIron Requirement During Pregnancy

IRON DEFICIENCY ANAEMIA

¨ Iron required for fetus and placenta ------- 500mg.

¨ Iron required for red cell increment ------- 500mg

¨ Post partum loss --------- 180mg.

¨ Lactation for 6 months - 180mg.

¨ Total requirement -------1360mg

¨ 350mg subtracted (saved as a result of amennorrhoea)

¨ So actual extra demand ----------------------1000mg

¨ Full iron stores --------------------------------1000mg

Hb 13.5 – 14 gm %

R.B.C. 4.5 – 4.7 million/cu mm

Serum Iron 50 – 150 μg / dL

TIBC 300 – 360 μg / dL

Transferrin saturation 25 – 50 %

S. Ferritin level 30 μg / Lit

Red Cell protoporphyrin 30 μg / dL

Erythropoietin 15.20 U / Lit

MCV 76 – 100 fL

MCH 27 – 33 pg

MCHC 33.37 gm / dL

PCV 32 – 40 %

Normal LevelsNormal Levels

ETIOLOGY OF IRON DEFICIENCY ANAEMIA

Depleted iron stores – dietary lack, chronic renal failure, worm infestation, chronic menorrhagia

Chronic infections: ( like malaria)

Repeated pregnancies :

- with interval < 1 year

- blood loss at time of delivery

- multiple pregnancy.

IRON DEFICIENCY ANEMIA¨ ETIOLOGY:

–CHRONIC BLEEDING

•MENORRHAGIA

•PEPTIC ULCER

•STOMACH CANCER

•ULCERATIVE COLITIS

•INTESTINAL CANCER

•HAEMORRHOIDS

–DECREASED IRON INTAKE

–INCREASED IRON REQUIRMENT (JUVENILE AGE, PREGNANCY, LACTATION)

CLINICAL FEATURES

Symptoms usually in severe anaemia

- Fatigue

- Giddiness

- Breathlessness

EFFECTS OF ANAEMA IN PREGNANCY

¨ . Mother :

– High output- due to inadequate tissue oxygenation, increase cardiac failure (more likely if reqirement for excessive blood flow )

– PPH

– Predisposes to infection

– Risk of thrombo-embolism

– Delayed general physical recovery esp after c. section

Fetus: . IUGR

. Preterm birth

. LBW

. Depleted Fe store

. Delayed Cognitive function.

IUGR

IUD ABORTION

CCFCCF

INFECTIONINFECTION

PRETERM LABOUR

PRETERM LABOUR

PIHPIH

Medical DisorderMedical Disorder

Complications - PregnancyComplications - Pregnancy

Instrumental delivery

PPH

FoetalDistressCCF

MATERNALPERINATAL

MorbidityMortality

Complications - LabourComplications - Labour

Laboratory Diagnosis of AnaemiaLaboratory Diagnosis of Anaemia

IDA Thalassemia Chronic Diseases

Serum Iron Decreased Normal / Increased Decreased

TIBC Increased Normal Decreased or N

Transferrin

Saturation

Decreased N or Increased N or Decreased

Serum Ferritin Decreased N or Increased N

Marrow Iron Decreased / absent

N or Increased N

Therapeutic test with oral iron

Rise in Hb No rise in Hb No rise

¨ Serum iron decreased (<12 micro mol / l)

¨ Total iron binding capacity :TIBC in non-pregnant state is 33% saturated with iron .when serum iron level fall ,<15% ofTIBC saturated.by fall in saturation,the TIBC INCREASED.

¨ S. ferritin :In healthy adults ferritin circulate in plasma in range of 15_300 pg/l. in iron deficiency anemia it is the first test to become abnormal.

INVESTIGATIONS

¨ Serum transferrin receptor(TfR) : present on all cells as transmembrane protien that binds transferrin iron and transfer it to cell interior. Increased in iron def. anemia.

¨ Bone marrow examination.

¨ RFTS/LFTS.

¨ Urine for haemturia.

¨ Stool examination for ova ,cyst and occult blood.

BLOOD AND BONE MARROW SMEAR

¨ BLOOD:¨ microcytosis, hipochromia, anisocytosis

poikilocytosis

¨ BONE MARROW¨ high cellularity ¨ mild to moderate erythroid hyperplasia (25-35%;

N 16 – 18%) ¨ polychromatic and pyknotic cytoplasm of

erythroblasts is vacuolated and irregular in outline (micronormoblastic erythropoiesis)

¨ absence of stainable iron

MANAGEMENT

¨ Objectives:

1- To achieve a normal Hb by end of pregnancy

2- To replenish iron stores¨ Two ways to correct anaemia:

I- Iron supplementation . Oral Fe

. Parenteral Fe

II- Blood transfurion ¨

Choice of method: It depends on three main factors:

Severity of the anaemia

Gestational Age.Presence of additional risk factor

National Nutrition Anaemia Prophylaxis Programme (NNAPP 1971 - 72)

National Nutrition Anaemia Prophylaxis Programme (NNAPP 1971 - 72)

Anaemia continues – Major health problem

Nutritional Anaemia :Major Health ProblemsNutritional Anaemia :

Major Health Problems

FS + FA

Pregnancy

Lactating mothers

Family planning acceptors

Children – 1 to 11 years

Reason For Increased Incidence Of Anemia

Reason For Increased Incidence Of Anemia

¨ Poor pre-pregnancy iron balance due to – untreated systemic diseases & menstrual disorders

¨ Improper supplementation of iron in pregnancy ( late registration and poor follow up)

¨ Repeated childbearing

¨ Lack of awareness and illiteracy

¨ Poor pre-pregnancy iron balance due to – untreated systemic diseases & menstrual disorders

¨ Improper supplementation of iron in pregnancy ( late registration and poor follow up)

¨ Repeated childbearing

¨ Lack of awareness and illiteracy

¨ Low socioeconomic status and poor hygiene

¨ Chronic malnutrition

¨ Poor availability of iron due to predominantly veg diet, diet low in calories but rich in phytates. Food and religious taboos

¨ GI infections and infestations (e.g. Kala azar, worm infestations)

¨ Low socioeconomic status and poor hygiene

¨ Chronic malnutrition

¨ Poor availability of iron due to predominantly veg diet, diet low in calories but rich in phytates. Food and religious taboos

¨ GI infections and infestations (e.g. Kala azar, worm infestations)

Reason For Increased Incidence Of Anemia

Reason For Increased Incidence Of Anemia

Management Options Management Options

Pre – pregnancy :

¨ Treat the cause before conception

¨ Pre-pregnancy balanced diet, education

and health support.

¨ Build up iron stores during adolescent

phase

Pre – pregnancy :

¨ Treat the cause before conception

¨ Pre-pregnancy balanced diet, education

and health support.

¨ Build up iron stores during adolescent

phase

Oral Iron

Blood transfusionParenteral

Injectable IronInjectable IronHuman Recombinant

Erythropoietin

Modalities of ManagementModalities of Management

100 mg elemental Iron ------- ↑ 0.18 gm % day100 mg elemental Iron ------- ↑ 0.18 gm % day

Iron stores poor

-ve-ve

Iron absorption

↓ Bioavailability

of Iron

-ve-ve-ve-ve

Phosphate phytate

Worm infestation

Oral IronOral Iron

Oral Iron Therapy Oral Iron Therapy

¨ Ideal dose – 100mg per day (prophylactic)

¨ Ferrous gluconate, ferrous fumarate, ferrous succinate, ferrous sulphate, ferrous ascorbate citrate

¨ Rise in Hb – 0.8 gm / dl / week

¨ Side effects -G I upset most common

¨ Pt. compliance not guaranteed

¨ Ineffective in pts with worm infestations

¨ Inconclusive evidence on benefit of controlled release Iron preparation

¨ Ideal dose – 100mg per day (prophylactic)

¨ Ferrous gluconate, ferrous fumarate, ferrous succinate, ferrous sulphate, ferrous ascorbate citrate

¨ Rise in Hb – 0.8 gm / dl / week

¨ Side effects -G I upset most common

¨ Pt. compliance not guaranteed

¨ Ineffective in pts with worm infestations

¨ Inconclusive evidence on benefit of controlled release Iron preparation

¨ Iron salts are dissociated into bivalent or trivalent iron salts

¨ Diffuses as free iron ions through the upper part of the gastrointestinal mucosa

¨ Taken up by transferrin and incorporated into ferritin.

¨ For binding to ferritin and transferrin ferrous iron has to be converted into ferric iron by oxidation

¨ Highly reactive free radicals are produced during this process

¨ All ionic iron including carbonyl iron are absorbed similarly

¨ Iron salts are dissociated into bivalent or trivalent iron salts

¨ Diffuses as free iron ions through the upper part of the gastrointestinal mucosa

¨ Taken up by transferrin and incorporated into ferritin.

¨ For binding to ferritin and transferrin ferrous iron has to be converted into ferric iron by oxidation

¨ Highly reactive free radicals are produced during this process

¨ All ionic iron including carbonyl iron are absorbed similarly

• Borbolla JR. Cicero RE, Dibilox MM, Sotres RD et al.. Rev Mex Pediatr 2000; 67(2): 63-67

• Heubers KA, Brittenham GM, Csiba E, Finch CA. J Lab Clin Med 1986 ; 108 ; 473-8.

• Borbolla JR. Cicero RE, Dibilox MM, Sotres RD et al.. Rev Mex Pediatr 2000; 67(2): 63-67

• Heubers KA, Brittenham GM, Csiba E, Finch CA. J Lab Clin Med 1986 ; 108 ; 473-8.

Absorption of Ferrous SaltsAbsorption of Ferrous SaltsUncontrolled Passive AbsorptionUncontrolled Passive Absorption

Fe+2Fe+2

Fe+2Fe+2

Dissociation

Passive diffusion

Fe+2

Fe+2

Fe+3

Fe+2

Fe+3

Gut Lumen Mucosal Cell Blood

Ferritin

Iron salts

Fe+3

Free Radical

Fe+2

Fe+2

Fe+2

Fe+2

Fe+2Fe+2

Fe+2

Fe+3

Free Radical

Transferrin

Incorporation into Hb

↑ Hb – 0.21 gm %

Fractionated Irondextran[Iron hydroxide dextran complex]

Les s

Les s

Les

s Les

s

Parenteral TherapyParenteral Therapy

100 mg elemental Iron

Anaphylactic reaction

Anaphylactic reaction

I.M. I.V.

Parenteral Therapy : Traditional IndicationsParenteral Therapy :

Traditional Indications

¨ Intolerance to oral iron

¨ Poor compliance to oral iron

¨ Gastrointestinal disorders

¨ Malabsorption syndromes

¨ Rapid blood loss

¨ Intolerance to oral iron

¨ Poor compliance to oral iron

¨ Gastrointestinal disorders

¨ Malabsorption syndromes

¨ Rapid blood loss

IRON DEFICIENCY ANEMIACURE

¨ PARENTERAL IRON SUBSTITUTION

¨ Bad oral iron tolerance (nausea, diarrhoea)

¨ Negative oral iron absorption test

¨ Necessity of quick management (CHD, CHF)

¨ 50 - 100 mg daily

¨ I.v only in hospital (risk of anaphilactic shock)

¨ I.m in outpatient department

¨ iron to be injected (mg) = (15 - Hb/g%/) x body weight (kg) x 3

¨ TDI(in mg)=2.3xWxD+500

¨ Inability to maintain iron balance (haemodialysis)

¨ Patient donating large amount of blood for auto-transfusion programme

¨ ? Pregnant women with severe IDA, presenting late in pregnancy

¨ Inability to maintain iron balance (haemodialysis)

¨ Patient donating large amount of blood for auto-transfusion programme

¨ ? Pregnant women with severe IDA, presenting late in pregnancy

Parenteral Therapy : Traditional IndicationsParenteral Therapy :

Traditional Indications

The

World Health Organisation states…

‘transfusion should be

prescribed ONLY for

conditions for which there

is NO OTHER TREATMENT’

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 particular risk.

FOLATE DEFICIENCY ANAEMIA

Folic acid deficiency more likely if

. Woman taking anticonvulsants.

. Multiple pregnancy.

. Hemolytic anemia; thalasemia H.spherocytosis

Maternal risk:

Megaloblastic anemia

Fetal risk:

Pre-conception deficiency cause neural tube defect and cleft palate etc.

FOLATE DEFICIENCY ANAEMIA

Diagnosis: Increased MCV ( > 100 fl)

Peripheral smear: - Macrocytosis, hypochromia

- Hypersegmented neutrophils (> 5 lobes) - Neutropenia - Thrombocytopenia

Low Serum folate level. Low RBC folate.

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 defect

- 4mg folic acid/day.

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.

Diagnosis of Folate Deficiency Anemia (FDA)

Diagnosis of Folate Deficiency Anemia (FDA)

Special considerations in diagnosis

• FDA is suspected when the expected response

to adequate iron therapy is not achieved

• Macrocytosis can occur in pregnancy in absence

of FDA

• If FDA + IDA present, it will be masked by IDA

• Definitive diagnosis – Bone marrow aspirate

Special considerations in diagnosis

• FDA is suspected when the expected response

to adequate iron therapy is not achieved

• Macrocytosis can occur in pregnancy in absence

of FDA

• If FDA + IDA present, it will be masked by IDA

• Definitive diagnosis – Bone marrow aspirate

Megaloblastic Anemia- Diagnostic ProblemsMegaloblastic Anemia- Diagnostic Problems

¨ HB estimation

¨ Peripheral smear

¨ MCV estimation

¨ Serum folate

¨ Red cell folate

¨ FIGLU estimations

¨ Marrow aspirate

¨ HB estimation

¨ Peripheral smear

¨ MCV estimation

¨ Serum folate

¨ Red cell folate

¨ FIGLU estimations

¨ Marrow aspirate

Management of FDAManagement of FDA

¨ Strong case for routine prophylaxis

¨ Prophylaxis with anti convulsants

¨ Continue routine oral therapy for

hemolytic anaemia

¨ Parenteral therapy for severe deficiency

¨ Strong case for routine prophylaxis

¨ Prophylaxis with anti convulsants

¨ Continue routine oral therapy for

hemolytic anaemia

¨ Parenteral therapy for severe deficiency

Worm InfestationsWorm Infestations

¨ Common cause of anaemia in developing countries

¨ Most common – hookworm infestation, Round worm, whip worm, etc.

¨ Oral iron therapy becomes ineffective

¨ Treatment by antihelminthics is a must

Treatment

¨ Mebendazole : 100mg twice daily for three days

¨ Pyrantel pamoate : 10mg / kg in single dose.

¨ Albendazole : 400mg once a day for three days

¨ Common cause of anaemia in developing countries

¨ Most common – hookworm infestation, Round worm, whip worm, etc.

¨ Oral iron therapy becomes ineffective

¨ Treatment by antihelminthics is a must

Treatment

¨ Mebendazole : 100mg twice daily for three days

¨ Pyrantel pamoate : 10mg / kg in single dose.

¨ Albendazole : 400mg once a day for three days

Hemoglobinopathies

A collective term for the inherited disorders of Hb synthesis

¨ Disorders of globin synthesis e.g. Thalassemia

¨ Structural Hb variants e.g. Sickle cell anemia, HbC

A collective term for the inherited disorders of Hb synthesis

¨ Disorders of globin synthesis e.g. Thalassemia

¨ Structural Hb variants e.g. Sickle cell anemia, HbC

HAEMOGLOBINOPATHIES.

¨ Normal adult Hb. after age of 6 month,

¨ HbA---97%, HbA2---(1.5-3.5%), HbF2--<1%.

¨ 4 Globin chains associated with haem complex.

¨ Hb. A = 2 alpha +2 beta globin chains.

¨ Hb.A2= 2alpha+2 delta globin chains.

¨ Hb.F = 2 alpha+ 2 gamma globin chains.

¨ Hb. synthesis is controlled by genes.

¨ Alpha chains by 4 gene,2 from each parent.

¨ Beta chains by 2 genes ,1 from each parent.

HAEMOGLOBINOPATHIES

DEFINITION:

¨ Inherited disorders of haemoglobin.

¨ Defect may be in:

- Globin chain synthesis------thalassemia.

- Structure of globin chains-sickle cell disease.

¨ Hb.abnormalities may be:

- Homozygous = inherited from both parents.

(Sufferer of disease)

- Hetrozygous = inherited from one parent.

(Carrier/trait of disease)

THALASSAEMIAS

¨ The synthesis of globin chain is partially or completely suppressed resulting in reduced Hb. content in red cells,which then have shortened life span.

¨ TYPES:

- Alpha thalassaemia.

- Beta thalassaemia:

. Major

. minor

Thalassemia

¨ Genetic disorders; lack or sed synthesis of globin chains

¨ Two types : & thalassemia

¨ chains encoded by 2 pairs of genes on chromosome 16

¨ chains encoded by single pair of genes on chromosome 11

¨ thalassemia more common and presents as either °(major) or + (minor)

¨ Genetic disorders; lack or sed synthesis of globin chains

¨ Two types : & thalassemia

¨ chains encoded by 2 pairs of genes on chromosome 16

¨ chains encoded by single pair of genes on chromosome 11

¨ thalassemia more common and presents as either °(major) or + (minor)

Beta thalassemia minor

¨ Beta Thalassemia trait

¨ Heterozygous inheritance from one parent.

¨ Most frequent encountered variety.

¨ Partial suppression of the Hb. synthesis.

¨ Mild anaemia.

Investigations: Hb----around 10 g/dl.

¨ Red cell indices: low MCV.

low MCH.

normal MCHC.

¨ Diagnostic test: Hb. Electrophoresis.

Beta Thalassemia Minor

¨ Management:

¨ Same as normal woman in pregnancy.

¨ Frequent Hb. Testing.

¨ Iron & folate supplements in usual dose.

¨ Parenteral iron should be avoided. because of iron overload.

¨ If not responded ---I/M folic acid.

¨ blood transfusion close to time of delivery.

Beta Thalassaemia Major

¨ Homozygous inheritance from both parents.

¨ Sever anaemia.

¨ Diagnosed in paediatric era.

¨ T/m: is blood transfusion.

ALPHA THALASSAEMIA:

¨ Both heterozygous & homozygous forms exist.

¨ Alpha thalassaemia trait.

¨ HbH disease.

¨ Alpha thalassaemia major.

Diagnosis of Thalassemia

¨ Hb estimations

¨ Peripheral smear

¨ sed MCV

¨ sed MCH

¨ HbA2 ( 22)

¨ Hb estimations

¨ Peripheral smear

¨ sed MCV

¨ sed MCH

¨ HbA2 ( 22)

Diagnostic Strategy for Thalassemias

Hb Electrophoresis + CBC

Abnormal band

Normal No action

MCV MCH

Quantitative Hb electrophoresis

Raised Hb A2

B Thalassemia

Normal

sed Examine partners blood

? X Thalassemia

DNA analysis for x gene defects

SICKLE CELL SYNDROME.

¨ Autosomally inherited .

¨ Structural abnormality.

¨ HbS - susceptible to hypoxia, when oxygen supply is reduced.

¨ Hb precipitates & makes the RBCs rigid & sickle shaped.

¨ Heterozygous----HbAS.

¨ Homozygous-----HbSS.

¨ Compound heterozygous---HbSC etc.

Sickle Cell Disease (SCD)

¨ Sickeling crises frequently occurs in pregnancy, puerperium &in state of hypoxia like G/A and Hag.

¨ 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 significance clinical problems

Sickle Cell DiseaseSickle 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.

¨ 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.

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

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

Take Home MessageTake Home Message

¨ Anaemia although preventable is a global problem

¨ Anaemia still is the commonest cause of maternal mortality

and morbidity in spite of easy diagnosis and treatment

¨ Anaemia 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

¨ Anaemia although preventable is a global problem

¨ Anaemia still is the commonest cause of maternal mortality

and morbidity in spite of easy diagnosis and treatment

¨ Anaemia 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

¨ The youth need to be educated about diet, sanitation and personal hygiene

¨ Hookworm infestation should be treated

¨ Pregnant women should be given Iron and folate supplements

¨ The youth need to be educated about diet, sanitation and personal hygiene

¨ Hookworm infestation should be treated

¨ Pregnant women should be given Iron and folate supplements

Take Home MessageTake Home Message

Thank YouThank You

Egypt