Anemia in tropics

Definition:
Anemia is defined as a condition in which Hb concentration in
peripheral blood is lower than normal for age and sex (less than 13.5 g/dl
in adult male and 11.5 g/dl in adult female)
Aetiology:
Anemias result from 3 basic mechanisms:
1- Blood loss :
a) acute,
b) chornic
Decreased production of red cells
2- Increased destruction of red cells ( haemolysis)

The first principle in the management is the diagnosis and treatment of

the underlying cause.
The transfusion of concentrated R.B.Cs is only required in anaemic
patient in one of the following conditions:

1- A patient in danger of dying with anaemic heart failure

2-A patient about to experience stress e.g. emergency surgery or
obstetric delivery
3- The Anemia is incurable e.g. Thalassaemia or aplastic anemia
I- Heamolytic aneamias
Heamolytic anemias are a group of anamias in which there is an
increase in the R.B.C turn over due to shortening of the R.B.C life span
(N= 90 to 150) average 120 days.
Hemolysis may occur due to : a) Abnormal hemolytic process b)
abnormalities which r usually congenital of R.B.Cs

Classification
I- Hereditary abnormalities in R.B.C.s
 Membrane spherocytosis
 Metabolism G6PDD
 Hemoglibin:
*Abnormal (Hb S, Hb C)
* Decrease synthesis of one chain of Hb
* α Thalassemia
* β Thalassemia
II- Acquired
 Infection e.g. Malaria, Meningococcal sepsis
 Drugs e.g. Sulfonamides, Quinine
 Hypersplenism
Features of hemolytic anemias:
1- Feature of hemolysis
*Jaundice
*Hyperbilirubinaemia
*Increased urine urobilinogen
*Increased fecal stercobilinogen
*Reduced or absent heam- binding protein ( hepatoglobulin)
2- Features of increased RBC production
* Reticulocytosis
* Bone marrow erythroid hyperplasia
Bone marrow depression if hemolysis is more rapid e.g malaria or
parovirus infection is sickle cell disease patients i.e aplastic crisis.
Heamoglobinopathies:
 The inherited disorder of heamglobin synthesis.
 Normal human heamoglobin consists of two peptide chains
associated with one heam molecule.
o Adult Hb ( HbA, αβ)
o Fetal Hb ( HbF, αγ)
o And HbA2 ( αδ)
Molecular basis:
I- inherited defects in the rate of synthesis of one or more of the
globulin chains ( thalassemias)
II- Genetically determined alteration in the sturcutre of globulin
chain ( sickle cell anemia)

At six months of age HbA forms 95%, HbA2 forms 4% amd HbF forms
less than 1%.
Thalassemia:
1- α Thalassemia

2 - β- Thalassemia: classified clinically into

* major, Homozygous
* intermediate,
* minor, Heterozygous
Clinical picture :
 The infant is normal at birth, but the disease is manifest early in life
 There is severe retardation of growth
 Skeletal changes include gross bossing of the skull, over growth of the
maxilla
 Hepatosplenomegaly, hypersplenism leads to worsening of anemia
with greater susceptibility to infection and bleeding tendency,
 Progressive heamosiderosis damages tissues and organs: bronze
discolouration of skin, these may be accompanied by cardiac
arrythmias, endocrinal dysfunction including D.M,
hyperparathyroidism and hypogonadism.
Diagnosis:
1- The Hb is usually 20 to 80 g/L
2- The reticulocytic count is moderately high
3- The bone marrow shows erythroid hyperplasia
4- Hb electrophoresis reveals only HbF and a minor fraction of HbA2
5- Serum iron, saturation of transferring levels are all high
6 - Radiographs of the skull show thinning of the outer table and
specules of bone in the expanded marrow cavity, giving Hair on
end appearance.
Treatment:
1- Blood transfusion to maintain Hb level in a range of 9 – 14g/DL and
so suppressing the patient's own erythropoeisis
Transfusion: Every 6-8 weeks, packed R.B.Cs
2- Administration of iron chelating agents to prevent iron overload
 Iron chelator administration: Desferroxamine (desferal) administered
as a slow subcutaneous infusion using mechanical pump 25-50
mg/Kg during 10-12 hours at night.

3- Splenectomy if hypersplenism occur

4- Folic acid supplement
5- Prophylactic antimalarial in endemic areas
Sickle cell disease:
Pathophysiology:
A point mutation replaces glutamic acid with valine at the position
6 on β globulin. Valine is hydrophilic amino acid, so the solubility of
HbS molecule is much reduced compared to HbA especially in
eoxygenated state.
Sickle cells are fragile and are phagocytosed by the cells of RES so
that there is both intra and extra vascular hemolysis. Sickled cells adhere
to eachother and to the endothelium leading to blockage of small blood
vessels that will eventually end in infarction and death of tissue.
Clinical features :
Anemic crisis:
Catastrophic decline of Hb as a result of:
1- Malaria
2- Acute splenic sequestration.
3- Folate deficiency in untreated African patients have megaloblastic

erythropoiesis from folic acid deficiency when seen first.

Infarctive crisis:
Sickling can lead to infarction in almost any organ or tissue in the
body. The common sites are the bones, chest and abdomen.
 Up to 90% of African children seen with sickle cell anemia between 6
months and years of age have the Hand foot syndrome.
 Sickling of the cerebral vessels
 Acute sever pain in the chest due pulmonary infarction,
 Leg ulceration between the age of 10-20 years
 Retinal vessel obstruction can lead to blindness
 Infarction in the renal pelvis can end in renal failure.
Management of patient in crises
Anemic crisis:
1- Following the treatment with anti malarial, folic acis and antibiotic
if indicated
2- Blood transfusion if necessary
Infarctive crisis:
1- control the pain
2- restoration of hydration and acid-base balance
3- treatment of infection
4- treatment of hypoxia
Malarial Anemia
1- Anemia corresponding to intensity of the parasitemia
2- There is phagocytosis of the parasitized red cell
3- The direct coomb's test ( DCT) is frequently positive so
autoimmune hemolysis may occur
4- Hemolysis of non parasitized cells due to activation of RES
5- Hypersplenism
6- Hemoglobinuria and black water fever, the majority of patients
presenting with heamoglobinuria are G6PDD and have been
treated with oxidant drugs.
Treatment of severe malarial anemia
 Malarial anemia generally responds to antimalarial therapy on
severe case malarial anemia is treated by blood transfusion, but at the cost
of developing AIDs later.
Anemia in Hypersplenism
Splenomegaly is a common clinical feature in tropics especially where
malaria and schistomiasis are endemic in many instances splenomegaly is
accompanied by syndrome of hypersplenism in which the anemia is due
to:
1- increased red cells pooling in the spleen
2- shorten red cell life span
3- Haemodilution from increased plasma volume
The anemia is usually normocytic normochromic, there is
reticulocytiosis and bone marrow shows hyperplasia.