Anemia, Iron deficiency anemia

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Dr. Kalpana MallaMD Pediatrics

Manipal Teaching Hospital

ANEMIA

What is Anemia?

• Reduction of the red blood cell (RBC) volume or hemoglobin concentration below reference level for the age and sex of the individual

• Hb < - 2SD or 95th centile for age and sex

Anemia Basics

All anemias are either due to….

1. Ineffective RBC productionor

2. Accelerated destruction of the RBC

• By RBC morphology and By Etiological factors responsible for anemia

Classification

Microcytic hypochromic anemia

1. Iron deficiency anemia – nutritional, - posthemohragic2. Ineffective Erythropoiesis - hemoglobinopathies, Thalassemia

- Lead poisoning, Sideroblastic anemia - Cu deficiency, Pyridoxine deficiency -Chronic ds - infection, inflammations , renal ds

• Megaloblastic Erythropoiesis a) Nutritional - Folate deficiency, B12 deficiencyb) Toxic – Treatment with antifolate compound – methotrexate,, and drugs that inhibit DNA replication – zidovudine, phenytoinc) Congenital disorders of DNA synthesis like Orotic aciduria etc. d) Malabsorption - liver ds

Macrocytic anemia

Macrocytic anemiaNon - Megaloblastic Erythropoiesis

a) Chronic hemolytic anemia b) Liver dsc) Hypothyroidismd) Diamond blackfan syndrome

1. Impaired cell production (low reticulocyte count) - aplastic anemia - pure red cell aplasia - physiological anemia of infancy - infections - Systemic diseases like endocrinal, renal and hepatic diseases - bone marrow replacement – leukemia, tumors, storage ds, myelofibrosis, osteopetrosis2 Hemolytic anemia ( reticulocyte count high)

Normocytic, Normochromic anemia

DIMORPHIC ANEMIA

• When two causes of anemia act simultaneously, e.g : macrocytic hypochromic due to hookworm infestation leading to deficiency of both iron and vitamin B12 or folic acid

• following a blood transfusion

ETIOLOGICAL CLASSIFICATION OF ANEMIA

• Blood loss Acute

Chronic

• Decreased iron assimilation - Nutritional deficiency - Hypoplastic or aplastic anemia - Bone marrow infiltration like leukemia & other malignancies, - Myelodysplastic syndrome

- Dyserythropoietic anemia

• Increased physiologic requirement - Extracorpscular - - Alloimmune & isoimmune hemolytic anemia - Microangiopathic anemias - Infections - Hypersplenism

ETIOLOGICAL CLASSIFICATION OF ANEMIA

ETIOLOGICAL CLASSIFICATION OF ANEMIA

- Intracorpsular defect

– Red cell membranopathy i.e. congenital spherocytosis,elliptocytosis

– Hemoglobinopathy like HbS, C,D,E etc. Thalassemia syndrome

– RBC enzymopathies like G6PD deficiency, PK deficiency etc.

Follow-up

• Re-check CBC 4-6 weeks (to confirm response)• Continue iron 3-4 months (to replace stores)• If no improvement on adequate iron therapy,

consider evaluating the child for lead poisoning or thalassemia

Differential of Anemia

lead poisoning

chronic d isease

thalssem ia

iron def

Hypochrom ic, m icrocytic

Renal d isease

Transient erythroblastopeniaof childhood

Ca/BM failure

chronic d is

Normochromic,norm ocytic

Drugs (etoh)

Down Syndrome

Liver d isease

B12/fo late def

Macrocytic

Inadequate response (RPI<2)

Im m une Hem olytic anem ia

extrinsic factors(DIC,HUS,TTP)

m em branopathy

enzym opathy

hemoglobinopathy

Adequate response (RPI>3)r/o b lood loss/hem olytic d is

Hgb, indices, retic count and sm ear

IRON DEFICIENCY ANEMIA

• Most common cause of anemia worldwide

• Most important cause of iron deficiency anemia is parasitic infection - hookworms, whipworms and roundworms

IDA

Newborn contains 0.5g of iron, adult contains 5g

A diet containing 8–10mg of iron daily is necessary for optimal nutrition

1mg of iron must be absorbed each day - Absorbed in the proximal small intestine

Absorbed 2-3 times more efficiently from human milk than from cow's milk

GENERAL FEATURES

• Meat• Liver• Kidney• Egg-yolk• Green vegetables• Fruits**** Cow’s milk- poor source of iron

Iron sources:

Distribution of body iron: (adults) - Hemoglobin: 2.3 gm - Storage (ferritin / haemosiderin) : 1.0 gm - Non-available tissue iron: 0.5 gm - Transport iron: 3-4 mg - Total : ~5 gm

Iron metabolism:

Iron absorption: Depends upon – Body stores of iron - Rate of erythropoiesis - Iron needs of the body Increased absorption in presence of: - vitamin C - fruit juices - lactose - amino acids- cystine, lysine , histidine, - gastric Hcl Decreased absorption : - phytates - tannic acid - calcium salts - phosphates

Iron Metabolism:

Figure 16-8: Iron metabolism

Increased physiological demand: - growing children (6-24 months) - adolescence - women during reproductive agesPathological blood loss: -chronic lossInadequate intake of diets rich in iron: -nutritional deficiency -decreased absorption- gastroenterostomy/

tropical sprue/ coeliac disease

Pathogenesis of IDA:

• High Hb conc of the newborn falls during the first 2–3 mo - considerable iron is stored - usually sufficient for blood formation in the first 6–9 mo of life in term

• The most important cause world-wide is infestation with parasitic worms (hookworms- suck 0.03- 0.2 ml of blood per worm /day ),whipworms, roundworms

• Dietary insufficiency• Malabsorption

ETIOLOGY

• Chronic blood loss - occult bleeding : peptic ulcer, Meckel diverticulum, polyp, hemangioma, inflammatory bowel disease, Intravascular hemolysis and hemoglobinuria

• Chronic diarrhea• Milk allergy

ETIOLOGY

• Demograpghic – Eldery, Teenager, Female

• Dieatary – low Iron, low Vit C, excess phytate,tea coffee,

• Social and physical – poverty,alcohol abuse,GIT ds

Risk factors for IDA

- Pallor is the most important sign - Look for pallor : FACE, nails, palms, conj, mucus

membranes- Pagophagia (pica for ice) / pica- Anxiety , Poor appetite- Below 5g/dL: irritability and anorexia are prominent - Tachycardia and systolic murmurs- dyspnea ,

Palpitations

CLINICAL FEATURES

• Hair loss and lightheadedness• Fainting • Sleepiness, Tinnitus• Mouth ulcers, Glossitis ,Angular cheilitis• Constipation• Depression, Twitching muscles, Tingling,

numbness or burning sensations

CLINICAL FEATURES

• Koilonychia (spoon-shaped nails) ,• Platynychia

• Weak,brittle nails• Pruritus• Dysphagia due to formation of esophageal

webs (Plummer-vinson syndrome

CLINICAL FEATURES

Koilonychia - spoon shaped nail

- Neurologic and intellectual function - Affects attention span, alertness, - Verbal learning and memory - Monoamine oxidase (MAO), an iron dependent

enzyme, has a crucial role in neurochemical reactions in the CNS

- breath-holding spells

CLINICAL FEATURES

First: Tissue iron stores represented by bone marrow hemosiderin

disappear Serum ferritin decreases

Next: Serum iron level decreases Serum transferrin,S. iron-binding capacity of the - increases Percent saturation (transferrin saturation) falls below normal Free erythrocyte protoporphyrins (FEP) accumulates

Response to low Hb:

Response to low Hb:

Later: Microcytosis, hypochromia, poikilocytosis, and increased RBC distribution width (RDW)

1.complete blood count (CBC) - High RBC distribution width (RDW) -

reflecting an increased variability in the size of red blood cells (RBCs).

- A low MCV,MCH and MCHC 2. Hemoglobin (Hb)&hematocrit (Hct) value –

low3. Reticulocyte - normal or moderately elevated

Diagnosis - LABORATORY INVESTIGATIONS

3.Peripheral blood smear – microcytic hypochromic anemia, target cells, hypochromic pencil-shaped cells, and occasionally small numbers of nucleated RBC

• Thrombocytosis -activate thrombopoietin receptors in precursor cells which make platelets

Diagnosis - LABORATORY INVESTIGATIONS

4. Diagnostic tests – - Serum ferritin- low- Serum iron - low- Serum transferrin -elevated - Total iron binding capacity (TIBC) - high5.Stool for occult blood6.Stool R/M/E - hookworm and whipworm

LABORATORY INVESTIGATIONS

• Ratio of serum iron to TIBC (called iron saturation or transferrin saturation index - is the most specific indicator of iron deficiency - < 5% - indicates iron deficiency

LABORATORY INVESTIGATIONS

Gold standard• Bone marrow aspiration, with the marrow

stained for iron -Bone marrow is hypercellular, with erythroid hyperplasia

• Leukocytes and megakaryocytes are normal • No stainable iron in marrow reticulum cells

DiagnosisLABORATORY INVESTIGATIONS

• Oral administration - ferrous salts (sulfate, gluconate, fumarate) -4–6mg/kg of elemental iron

• Consumption of milk should be limited • Blood loss from intolerance to cow's

milk proteins is reduced • The amount of iron-rich foods is

increased

TREATMENT

• Incorrect diagnosis (eg, thalassemia) • Patient is not taking the medication • Not absorbed (enteric coated?) malabsorption syndromes gastrectomy/celiac disease• Rapid iron loss?• Anemia of chronic disease-impairs bone

marrow response

Oral iron failure?

• Parenteral iron preparation (iron dextran) : Intolerance to oral iron, severe gastrointestinal complaints

• Packed or sedimented RBCs : with Hb values < 4g/dL• congestive heart failure: fresh-packed RBCs should be

considered

TREATMENT

12–24 hr• Replacement of intracellular iron enzymes; subjective

improvement; decreased irritability; increased Appetite36–48 hr• Initial bone marrow response; erythroid hyperplasia48–72 hr• Reticulocytosis, peaking at 5–7 days4–30 days• Increase in hemoglobin level1–3 mo• Repletion of stores

RESPONSES TO IRON THERAPY

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