This document provides an overview of approaches to anemia. It discusses red blood cell development, normal hemoglobin values, types of anemia including their causes, presentations and management. Red blood cell development occurs over 3 stages - yolk sac, liver and bone marrow levels. Physiologic anemia and anemia of prematurity are discussed as well as anemia caused by blood loss, hemolysis and enzymatic deficiencies. Specific types covered include fetal-maternal hemorrhage, ABO hemolytic disease, G6PD deficiency, hereditary spherocytosis, and disorders of hemoglobin such as thalassemia. The document concludes with a brief approach to evaluating and diagnosing different causes of anemia.

1. R E F R E N C E : A V E R Y S O U T H A S I A E D I T I O N
( 7 T H )
P R E S E N T E D B Y : D R . M A H E S H Y A D A V
APPROACH TO ANEMIA

2. OBJECTIVES
 RBC DEVELOPMENT
 FETAL HAEMOGLOBIN AND ADULT HAEMOGLOBIN
 PATHOPHYSIOLOGY
 NORMAL HAEMOGLOBIN VALUES
 ANEMIA OF DIFFERENT TYPES AND PRESENTATION AND
MANAGEMENT
 BRIEF APPROACH TO ANEMIA

3. RBC DEVELOPMENT
 DIVIDED INTO 3 STAGES :
1. Yolk sac level
2. liver level
3. Bone marrow level
YOLK SAC LEVEL
 Primitive hematopoiesis
 Occurs at 16 – 18 days of gestation
 Forms macrophages , nucleated erythrocytes and some
megakaryocytes

5. LIVER LEVEL
 Definitve hematopoiesis
8th week of gestation
Formation of hemapoietic stem cells and various types of leucocytes
(granulocytes , basophils , eosioniphils), lymphocytes ,megakaryocytes,
anucleated erythrocytes .
BONE MARROW LEVEL
At 6th month of gestation

7. ADULT HAEMOGLOBIN
Post natally fetal haemoglobin changed into adult haemoglobin by 6 - 10
months of age ,switch to less sensitive hepatic to more sensitive renal
site for erythropoetin.
Adult haemoglobin have alpha and beta globins .

9. NORMAL HAEMOGLOBIN
 TERM = Hb level 16.9 +/-1.6 gm%
 Pre term =Hb level 15.9 +/- 2.4 gm%
BASED ON HAEMOGLIBIN :
 Cord Hb <13gm% (TERM )
 Cord Hb < 12 gm/% (Pre – term )

10. ANEMIA CAUSES
 PHYSIOLOGIC ANEMIA AND ANEMIA OF PREMATURITY .
 ANEMIA CAUSED BY BLOOD LOSS .
 ANEMIA CAUSED BY HAEMOLYISIS .
 ANEMIA CAUSED BY ENZYMATIC DEFICIENCY AND
ERYTHROCYTE MEMBRANE .

11. PHYSIOLOGIC ANEMIA
 In utero , the fetal aortic oxygen stauration is 45 % ,the EPO levels are
high and the RBC production is rapid . The fetal liver is the major site of
EPO production .
 After birth , the oxygen saturation is 95% and the EPO is undetectable.
RBC production by day <1/10 the level in utero .Reticulocyte are low
and the haemoglobin levels falls .
 At 8 – 12 weeks , haemoglobin levels reach their nadir ,o2 delivery to
the tissues is impaired , renal EPO is stimulated and RBC production
increases .

12. ANEMIA OF PRE-MATURITY
 RBC survival is decreased in comparison with the term infants
 Rapid body growth .
 Haemoglobin nadir in premature babies is lower than in term infants
because EPO is produced by the term infant at a Hb level of 10-11and is
produced by the premature infant at a haemoglobin level of 7-9mg/dl.
 Once nadir is reached ,RBC production is stimulated and iron stores are
rapidly depleted because less iron is stored in the premature infant than
in the term infants .

13. ANEMIA CAUSED BY BLOOD LOSS
 Before Birth – Occult Haemorrhage ,Faetomaternal haemorrhage , TTTB
 Obstetrics Accidents – Malformations of the Placenta and cord .
 Nuchal cord with placental blood trapping
 Internal haemorrhages – Excessive blood sampling .
 OTHERS :-
 Incision of the placentae during Cesarean section
 Placenta Previa
 Abruptio Placentae
 Internal Haemorrhage
 Sub galeal haemorrhage
 Laceration of the liver
 Ruptured Spleen
 Pulmonary Hemorrhage

14. FETO-MATERNAL HEMORRHAGE
 Sudden and unexpected decrease in fetal movement is sign of FMH .
 Manifest as Pallor after birth, sluggish and gasping respiration and signs of
circulatory shock .
 >20 % blood volume is sufficient to produce sign of shock and pallor after
birth within 3 hours of the event .
DIAGNOSIS:-
 Acute haemorrhage and Chronic Haemorrhage appear as Normochromic and
Normocytic and hypchromic , Macrocytic indicating fetal iron deficiency
anemia simultaneously .
 Coombs test – Negative
 No Jaundice
 Demonstration of fetal cells in the maternal blood .

15. TWIN- TO –TWIN TRANSFUSIONS
 CRITERIA:-
1. Monochorionic Twins
2. Polyhydramnios in one twin (Recipient ) and oligohyramnios in other.
3. Markedly Enlarged bladder in one twin (Recipient ) and enlarged
Small Bladder in the other .

17. OBSTETRICS ACCIDENTS
 May create a diagnostics confusion about the cause of shock in early hour of
life or presence of pallor and unexplained anemia and unexplained during the
2nd or 3rd day of life .
Ex: Tight Nuchal cord
 INTERNAL HAEMORRHAGE :-
Traumatic deliveries ( vaccum assisted )
Breech delieveries result in rupture of ADRENALS , KIDNEY , SPLEEN or
RETRO-PERITONEAL AREA.
• DIAGNOSIS:- Appear in 24- 48 hrs of life and suddenly into shock
O/E = Abdomen Distended , Shifting Dullness , Elevation of the Rt.
Hemidiaphragm.
USG IS GOLD STANDARD .

18. ANEMIA CAUSED BY HAEMOLYSIS
 IMMUNE (ALLO-IMMUNE OR AUTO –IMMUNE ).
 NON –IMMUNE (MEMBRANOPATHIES ,ENZYMOPATHIES AND
HAEMOGLOBIN PATHIES ).

19. IMMUNE (ALLO-IMMUNE OR AUTO-IMMUNE)
 Rh. HAEMOLYTIC DISEASE :-
MBG – Rh -ve
BBG - Rh +ve
Rh Antigen is responsible .
Anti – D cause destruction .
• If first baby is Rh +ve , develop Anti-body of IgG in mother .
IgG is responsible for haemolysis .

20. DIAGNOSIS
 SIGNS :-
Jaundice , Pallor , Hepatosplenomegaly .
Petechiae and Purpura can be observed in severe anemia as result of
thrombocytopenia and a disturbance in the Intrinsic System of Coagulation
(vitamin k dependent factor )
• LABORATORY FINDINGS :-
Decrease in Haemoglobin , Hb < 13 in cord blood
Increase in Reti- count , Coombs test is +ve
Increase no of Nucleated Erythrocyte in PS
Polychromasia and Anisocytosis
Spherocytes are not abundant .

21. ABO HAEMOLYTIC DISEASE
 MBG- O +ve ,BBG = A +ve or B+ve
 Maternal Anti –A and Anti – B antibodies on fetal erythrocytes of the corresponding
blood group .
 Anti - A and Anti- B antibodies are seen as IgG , IgM and IgM fractions of plasma .
 IgG is responsible for haemolysis.
 High level of IgG anti- A or anti- B titre +nt .
DIAGNOSIS:-
• Indirect hyperbilirubinemia .
• Jaundice appearing during the first 24 hours life .
• Increased no of spherocyte in the blood .
• Increase Reti-Count
• Presence of IgG , Anti- A , Anti - B in cord plasma or serum .

22. HAEMOLYTIC DISEASE RESULTING FROM MINOR
BLOOD
 Uncommon
 Anti- D , Anti –D or Anti – B not responsible .
 Anti – E , Anti – C and Anti – kell

23. HAEMOLYSIS DISEASE RESULTING FROM
MINOR BLOOD GROUP INCOMPATIBILTY
1. Enzymopathies – G6PD
2. Membrane function –
Herediatery Spherocytosis
Herediatery Elipocytosis
3. Haemoglobin Synthesis.

24. G6PD DEFICIENCY
 Major function of Erythrocyte is the delievery of O2 to the tissues .
CONCEPT :-
• X- linked recessive factor .
CONSTANTAL
LY EXPOSED
TO O2
CELL
ENZYME +nt (Prevent
oxidative damage )
ENZYME –nt (?)

25. HEREDITARY SPHEROCYTOSIS
 Defect in RED CELL CYTO-SKELETON.
 Occur in school going children .
 75% have +ve family history .
CLINICAL PICTURE:
• Anemia , Jaundice And SplenomegalyCLASSIFICA
TION
TRAIT MILD MODERATE SEVERE
Hb N 11-15 8-12 6-8
Retic-Count N 3-6 >6 >10
Bilirubin <17 17-34 >34 >51
Spectric per se 100 80-100 50-80 40-60
Splenectomy Not Required Not necessary Necessary Necessary

26.  DIAGNOSIS:-
1. Splenomegally clinically
2. Red Cell Indices :- Hb , MCV , MCHC , Hyper dense cells , RDW , R.C
3. Blood film :- Abnormal morphology , Microspherocytes
4. Direct Anti globulin test - -ve
5. Evidence of Haemolysis : Bilirubin . Reticulocytosis
OTHER TESTS :-
 Osmotic fragility
 Acidified Glycerol Lysis Test
 Osmotic Gradient Ektacytometry
 Hypertronic Cryohaemolysis test
 Eosin – 5- maleimide bindings

27. DISORDER OF HAEMOGLOBIN
 Fetal haemoglobin.
 Alpha and Gamma thalassemia syndromes .
 Alpha and Gamma chain structural abnormalities .
OTHERS CAUSES:-
 Diamond Black fan syndrome .
 Congenital leukaemia .
 Infections –Rubella and parovirus .
 Osteopetrosis.
 Drug induced suppression of RBC production .

28.  BRIEF APPROACH TO ANEMIA

30.  THANKS