EVALUATION OF ANAEMIA IN GHANAIAN CHILD

EVALUATION OF ANAEMIA IN
THE GHANAIAN CHILD.
GROUP B2.

MEMBERS
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CEPHAS AVOKA
CHRISTIANA BAFFOUR AWUAH
IBIRONKE AZEEZAT
AKUA ADOBEA AYISI
KWAKU AYISI-TETE

Aim & Objectives
Aim:
Increase knowledge of students on evaluation of anemia
Objectives:
1.Understand the various definitions, classifications and aetiology of anaemia
2.Easily identify a child with anaemia

3.To interpret haematological results
4.Successfully treat anaemia

5.Identify with the causes, diagnosis , treatment and prevention OUTLINE
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Definition of Anaemia.
Statistics on Anaemia in Ghana.
RBC and Hb physiology
Pathophysiology
Classification
History, Physical examination and
Investigations
• Treatment, Prevention and complication
• Clinical Cases

DEFINITION OF ANAEMIA
• Reduction in the haemoglobin concentration, haematocrit or number of red blood cells per cubic mm below the mean for age and sex for the normal population (normal range of values for healthy persons)
• Anaemia is not a specific entity but is caused by many underlying pathological conditions.

NORMAL HB VALUES
AGE

MEAN Hb

RANGE

At birth

16.8

13.7-20.1

2 weeks

16.5

13.0-20.0

3 months

12.0

9.5-14.5

6 months-6 yrs 12.0

10.5-14.0

7-12 yrs

13.0

11.0-16.0
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BACKGROUND

• It is known that approximately 78% of Ghanaian children are anaemic (2008 Ghana Demographic
Health Survey (GDHS))
• Accounts for 40% U-5 death ( Dr. Rettig ghanabusinessnews.com 2006 Research by Dr. Osei Akoto et al:
In Ghanaian Children
Sample Size: 148
Anaemia
Stunting
Malnutrition

Moshie Zongo %
66.2
47.0
46.5

Manhyia %
34.5
23.7
24.8

The causes of anaemia were attributed to a combination of malnutrition, helminth infections, infectious disease
(malaria) and hemoglobinopathies.
Nutritional inadequacies also impaired host immunity and further exacerbating infections leading to malaria, anemia and stunting, hence the viscious cycle.
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- Malaria Journal (accessed 26-03-’13)

Blood Formation
1.

Intra-uterine life:
Blood cells are formed in the liver and spleen up to the fifth months.
After 5th month : bone marrow share in the formation of these cells.

2. After birth:
Formation of these cells will be restricted to the bone marrow. Blood Formation
3. Adulthood
The active bone morrow will be:
Restricted to axial skeleton : flat bones, vertebrae, ribs, sternum, ilia .
Some extension to the proximal ends of long bone mainly femur.

4. Extramedullary haemopoiesis: When demand for blood formation is increased: The active red BM extends to other sites – typical in SCD frontal bossing The spleen and liver will regain their ability to produce blood elements when bone morrow is affected by some diseases.

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Erythrocytes (RBCs)
• Biconcave disc shape
• Plasma membrane contains spectrin oGive erythrocytes their flexibility • Anucleate, no centrioles, no organelles o No cell division o No mitochondria means they generate ATP anaerobically

Erythrocyte Function

• Erythrocytes are dedicated to respiratory gas transport
• Hemoglobin reversibly binds with oxygen and most oxygen in the blood is bound to hemoglobin

Regulation and Requirements for Erythropoiesis
• Circulating erythrocytes – the number remains constant and reflects a balance between RBC production and destruction
– Too few red blood cells leads to tissue hypoxia – Too many red blood cells causes undesirable blood viscosity
• Erythropoiesis is hormonally controlled and depends on adequate supplies of iron, amino acids, and B vitamins

Hormonal Control of
Erythropoiesis
• Erythropoietin release by the kidneys is triggered by:
– Hypoxia due to decreased RBCs
– Decreased oxygen availability
– Increased tissue demand for oxygen
• Enhanced erythropoiesis increases the:
– RBC count in circulating blood
– Oxygen carrying ability of the blood

Erythropoietin Mechanism
Start

Normal blood oxygen levels

Increases
O2-carrying
ability of blood

Stimulus: Hypoxia due to decreased RBC count, decreased availability of O2 to blood, or increased tissue demands for O2

Reduces O2 levels in blood

Enhanced erythropoiesis increases RBC count Erythropoietin stimulates red bone marrow

Kidney (and liver to a smaller extent) releases erythropoietin Figure 17.6

Fate and Destruction of
Erythrocytes
• The life span of an erythrocyte is 100–120 days – Travels about 750 miles in that time

• Old erythrocytes become rigid and fragile, and their hemoglobin begins to degenerate
• Dying erythrocytes are engulfed by macrophages • Heme and globin are separated
– Iron is removed from the heme and salvaged for reuse • Stored as hemosiderin or ferritin in tissues

Fate and Destruction of
Erythrocytes
• Heme is degraded to a yellow pigment called bilirubin
– Liver secretes bilirubin into the intestines as bile – Intestines metabolize bilirubin into urobilinogen – Urobilinogen leaves the body in feces, in a pigment called stercobilin

• Globin is metabolized into amino acids which are then released into the circulation Life Cycle of Red Blood Cells

Hemoglobin

• Oxyhemoglobin – hemoglobin bound to oxygen – Oxygen loading takes place in the lungs

• Deoxyhemoglobin – hemoglobin after oxygen diffuses into tissues (reduced Hb)
• Carbaminohemoglobin – hemoglobin bound to carbon dioxide
– Carbon dioxide loading takes place in the tissues Structure of Hemoglobin

Figure 17.4

Rh Incompatibility

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PATHOPHYSIOLOGY
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The clinical feature of the anaemia could be explained by the following factors. • 1-Tissue Hypoxia
Impaired functions of the tissues, the degree of impairment depends an the need of the tissue to O2 so CVS, CNS and skeletal muscles are much affected. • 2- Compensatory mechanisms
Increased Oxygen delivery from HB to the tissue.
Increased erythropoietin production with stimulation of erythropoiesis
Increased plasma volume.
Redistribution of the blood from less to more vital organs.

PATHOPHYSIOLOGY
• 3-Rate of blood loss:
• The rapid the rate of blood loss, the more the severe symptoms will occur. While the slowly falling HB

allows

for

haemodynamic

compensation with less symptom.

The Four Causes of Anemia

• Decreased red blood cell production • Increased red blood cell destruction • Red blood cell loss

Decreased RBC production
• Deficiency of iron, B12, folate
• Marrow is dysfunctional from myelodysplasia, tumor infiltration, aplastic anemia, etc.
• Bone marrow is suppressed by chemotherapy or radiation
• Low levels of erythropoeitin, thyroid hormone, or androgens

Increased RBC destruction
• RBCs live about 100 days
• Acquired: autoimmune hemolytic anemia, TTPHUS, DIC, malaria
• Inherited: spherocytosis, sickle cell, thalassemia RBC Loss
• Bleeding!
• Obvious vs occult
• Iatrogenic: venesection e.g. daily CBC, surgical, hemodialysis • Hemorrhagic disease of the newborn
• Hemophilia

Classification based on
Morphology
Microcytic
Hipochromic

Normocytic

Macrocytic

Iron deficiency
Thalassaemia
Sideroblastic
Chronic disease
Lead poisoning
Severe
malnutrition

Haemolysis
Acute blood loss
20 anemiasinfection, liver, renal disease
Aplastic anemia
Hypersplenism

Normal newborn
Megaloblstic: B12,
Folate deficiency.
Alcohol, liver Dx,
Aplastic anemia
Postsplenectomy
Hypothyroidism

Neonatal Aanemia
• Haemorrhage- acute or chronic
• Haemolysis - usually associated with indirect hyperbilirubinaemia • Failure of Red Cell production- rare, pure red cell aplasia (Diamond-Blackfan anaemia)

Haemorrhage
• Prenatal-fetomaternal, retroplacental, twin-twin transfusion • Intranatal- cord anomalies, placental anomalies
• PostnatalExternal: umbilical, gut, iatrogenic
Internal: intracranial, ruptured spleen or liver

Haemolytic Anaemia
• Congenital erythrocyte defects
-membrane defects, HB defects, enzyme defects
• Acquired erythrocyte defects
Immune-Rh disease, ABO, minor blood grps
Nonimmune-infections, Toxic exposure,etc.

HISTORY
• DEMOGRAPHICSSex – m- G6PD def is more common
Age- the Hb levels varies among ages.

PRESENTING COMPLAINT (basically related to symptoms of anaemia or causes)
• Bleeding, fever, swellings, abdominal distension, irritability, yellowish coloration, FTT, poor feeding, difficulty breathing,lethargy

• HISTORY OF PRESENTING COMPLAINT
Severity, duration, speed of onset.
ODQ
Enquiries to narrow down on early differential diagnoses, Are complications setting in??
SYSTEMIC ENQUIRIES
Complications of anaemia to non-highlighted systems from the HPC.

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PMSHX
Sickle cell disease ? Liver dx? Renal disease?
G6pd def? Any past surgeries-splenectomy? Recurrent infections Febrile illness(malaria)
Frequent and missions and recurrent haemotransfusions
Any malignancy (lymphomas)
Hx of bleeding at circumcision, dactilytis
Chronic illness eg. CKD,CLD

Drug History
Sulphur-containing drugs, anticonvulsants, chloramphenicol, zidovudine. FAMILY HISTORY
SCD, gallstones, cholecystectomy, jaundice, isoimmunization(Rh or
ABO), bleeding disorders (hemophilia)
PREGNANCY AND BIRTH HISTORY
Prematurity, Perinatal risk factors – (maternal illness, drug ingestion, mechanical problems at delivery)
Bleeding from umbilical cord
Birth trauma

• IMMUNIZATION HISTORY
• NUTRITIONAL HISTORY
Malnutrition - malabsorption, environmental , diet
(quality,quantity,frequency), exclusive breastfeeding,
• DEVELOPMENTAL HISTORY
Any indication of impaired cognitive function?
• SOCIAL HISTORY financial situation of family- family size, occupation of parents- this can be linked to diet.
Academic performance in school.
Sanitation ,Insecticide Treated Net use

PHYSICAL EXAMINATION
SKIN
Pallor – severe anaemia
Jaundice – hemolytic anaemia, hepatitis, aplastic anaemia Petechiae /purpura – autoimmune hemolytic anaemia with thrombocytopenia, HUS, bone marrow aplasia
Cavernous hemangioma- microangiopathic hemolytic anaemia HEAD AND NECK
Frontal bossing, Gnathopathy – extramedullary hematopoiesis (thalassemia major, Sickle cell anaemia, cong. Hemolytic anaemia)

PHYSICAL EXAMINATION
• Icteric sclera- hemolysis (congenital, infections, hyper-hemolytic crisis- red cell enzyme def, red cell membrane defects, thalassemias, hemoglobinopathies) • Angular stomatitis- iron deficiency
• Glossitis – vit B12 or Fe deficiency
• Cervical lymphadenopathy- leukemias

• CHEST
• Tachycardia, murmur, gallop rhythm, - congestive heart failure , acute or severe anaemia.

Clinical Signs

PHYSICAL EXAMINATION
• ABDOMEN
• Organomegaly- hepatomegaly, splenomegaly ( infection, blood malignancies, cong. Hemolytic anaemia)
• Abdominal tenderness - sequestration
• EXTREMITIES• Spoon nails – Fe def

INVESTIGATIONS
• FBC, Clotting profile, GXM, BUECr,LFTs,G6PD def, sickling status,mps, • Blood film comment -Target cells,
Spherocytes, Acanthocytes (Spur cells), Echinocytes
(Burr cells), Blister cells, Basophilic stippling,
Howell-Jolly bodies, Heinz bodies, Schistocytes

• Bone marrow aspirate
• Stool R/E
• Urine R/E

• Parameters of FBC include:
1. Hb conc
2. Red Cell count
3. Reticulocyte count
4. Hematocrit or packed cell volume
5. Mean Corpuscular Volume
6. Mean Corposcular Hemoglobin Concentration
7. WBC (total and differential)
8. Platelet count

INVESTIGATIONS
1. Hb concLOW
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Cell numbers(abn production, hemolysis, bleeding)
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Diet- def Fe or folate intake
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intrinsic defect
HIGH
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Chronic lung disease
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Adaptation to high altitudes
2. Hct
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Low- low cell numbers
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High – low blood volume – dehydration (burns or diarrhea ) or polycythemia vera

INVESTIGATIONS
3. MCH
• Low in microcytic anaemia
• High in macrocytic anaemia- folate or vit B12def)
4. MCHC - Average hemoglobin concentrate per given packed cell volume • Low in Fe def, blood loss

5.

RETICULOCYTE COUNT

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Reticulocytes: immature RBCs
Number helps to determine causes of anemia.

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Low reticulocyte means decreased marrow production of RBCs causing anemia

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Elevated reticulocyte means indicates anemia caused by RBC loss

Treatment of Anaemia

Treatment objectives
• Early detection and treatment of life threatening complications
• Treat underlying cause of anaemia

• To restore haemoglobin levels to normal

EMERGENCY TREATMENT
• Stop any bleeding(esp in trauma)
• Check & maintain Airway, Breathing and
Circulation
• If in shock, correct shock with of N/S or R/L
• Give blood if necessary
• Look for and treat the cause of anaemia

TREATMENT OF ANAEMIA
 The treatment depends on the cause of the anaemia.  Counseling on good feeding practices.
 Nutritional deficiency give Iron, folic acid and Bvitamin
 Iron Dose: 1.5-2.0mg/kg elemental iron daily in 3 divided doses. Give 100-200mg elemental iron to older children. Duration: 6-8 weeks after Hb normalizes.  Folic acid- 5mg/day

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TREATMENT cont’d..
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Treat infections like malaria, schistosomiasis

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If the child is ≥2 years & has not had antihelminthics in the previous 6 months
(mebendazole or albendazole for possible hookworm). •

Manage malignancy if it is the cause

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Hydration in Hemolysis, transfuse if severe.

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Autoimmune prednisolone cases.

hemolysis give steroids, e.g. or immunoglobins in refractory

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Transfusion

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Indications for Transfusion
• Hb 6months shld be given Fe supplementation •

Decrease intake of low-Fe containing cow ’ s milk •

Include red meat, beans, dark green leafy vegetables, which are naturally rich in Fe.

should

be

given

Fe-

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PREVENTION OF ANAEMIA

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PREVENTION OF ANAEMIA
• Adequate intake of foods rich in Vit. C which helps in Fe absorption: citrus fruits, vegetables, etc. • Regular deworming of children - every 3months
• Increase awareness of anaemia in the society, and preventive strategies and policies.

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Quiz
• 3 year old boy presented with fatigue and shortness of breath for two weeks duration. He is pale and jaundiced. Results of his initial investigations are as follows; Hb – 6.5 gr/dl, Reticulocute count 6%.

DD
• Hemolytic anemia
– Membrane defects – hereditary
Spherocytosis
– Enzyme defect - G6 PD deficiency
– Extracellular causes – Immune hemolytic anaemia – Thalassaemia – Beta thalasaemia intermedia or E-beta thalasaemia • Blood loss
• Treated for iron deficiency

3 year old boy presented with fatigue and shortness of breath for two weeks duration. He is pale. Results of his initial investigations are as follows; Hb – 5.5 gr/dl, Reticulocute count 0.5 %.
1.What is your DD
2.Tabulate other clinical features that you would like to elicit in order to arrive at a diagnosis and their relevance in a table
3.Tabulate investigations and their relevance

DD for Anaema with low retic count
• Congenital Aplastic anaemia
– Fanconi
– Pure red cell aplasia
• Acquired bone marrow suppression
– Infections – Parvo virus
– Drugs – radiation, chemotheraphy
• Bone marrow infiltration – Leukemia or other infiltrative disease

Clinical feature in history

Relevance

1. Family history of inherited anaemia

Consider Thalassaemia, Hereditary
Spherocytosis,

2. Birth weight maturity, iron supplement Anaemia of prematurity . Iron deficiency anaemia 2. Dark urine

Intra vascular Hemolysis , hematuria

2. History of bleeding rectal , vomiting, hematuria Anaemia due to blood loss

3. Dietetic history

Nutritional anaemia

4. Jaundice

Hemolytic anemia

5. Bruises and echymosis

Evidence of low platelets

6. Recurrent infections

Involvement of white cell line

7. Taking drugs

Bone marrow suppression

8. General ill health, bone pain and fever Leukemia

Clinical feature in examination Relevance

1. Dismorphic features

Fanconi anemia other inherited aplastic anaemia 2. Jaundice

Haemolytic anaemia

3. Hepatomegaly

Hemolytic anaemia, Leukemia

4. Splenomegaly

Hemolytic anaemia, Leukemia
Very large spleen - Hyperspleenism

5. Patichie and echymoses

Low platelets; Bone marrow suppression, leukemia 6. Bone tenderness

Leukemia

7. Emaciated and Chronically ill looking

Anaemia of chronic disease or CRF

8. Acute and critically ill child

DIC, hemolytic disease

• THE END!!!

• THANK YOU!!!

REFERENCES
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Nelson`s textbook of paediatrics, 18th Edition
Illustrated textbook of paediatrics, 4th Edition
Dr. Osei-Akoto, lecture notes http://www.ncbi.nlm.nih.gov/pubmed/11300346 http://www.ghanatoghana.com/78-childrenliving-northern-ghana-anaemic/
• www.slideshare.com