History of the patient

For informant, if its older children we can write child and mother
Child has become pale since 1 week - it means the mother has noticed it 1
week ago, it was likely there before also.
Or last 1 week there was a precipitating factor that has worsened the
anemia

Palpitations: tell “acute onset palpitations” instead of “insidious onset

palpitations”
Tell if it’s regular or irregular, association of sweating and urine involvement,
aggravating and relieving factors

Interpretation:
Cardiovascular disease aggravated by anemia.
Or anemia as such a presentation.
Palpitation: indicates a sudden worsening of anemia
Negative history

First neg history:

● R/o underlying cardiac etiology
● R/o causes of blood loss: gi, nose, urine, gum bleeds, skin bleeds
(purplish rashes on skin)
● If there h/o blood transfusion
● H/o fever with chills and rigors or rashes or night sweats
○ Infections can aggravate cardiac conditions
○ Infections can cause anemia (Eg: Malaria: acute onset)
(Tuberculosis: children have low grade fever in evening, can
present with anemia if chronic)
● R/o abdominal pain, abdominal distension, h/o diarrhea, h/o
passage of worms in stools/vomitus
○ Worm colic: Hookworm (specific)
 ○ Abdominal pain: for lead poisoning also
● H/o loss of weight and pain in bones
○ Loss of weight: in TB, malignancy (leukemia)
○ Pain in bones: In leukemia (sternal pain)
● H/o constipation, weight gain, cold intolerance
○ Hypothyroidism is a/w anemia
● H/o exposure to radiation/drug usage causing hemolysis/bone
marrow suppression
○ BM suppression --- anemia
○ Drugs: Chloramphenicol, cytotoxic drugs
○ Antagonize folate synthesis: Phenytoin
○ Primaquine, Quinine --- hemolysis causing anemia
● H/o yellowish discoloration of eyes and skin
○ To r/o ongoing hemolysis
● H/o craving for inedible substances
○ Eg: mud, ice
○ Common in age groups 3-5 years
○ Mud: worm infestation Paint: lead toxicity
○ Pica itself can cause chronic infection causing anemia
○ Substances are non nutritious- can hinder absorption
● Anemia of chronic disease
○ CKD (often children with CKD will have anemia as their only
symptom
■ H/o oliguria, polyuria, nocturia
■ H/o short stature
■ H/o bony deformities
○ TB
○ Hypothyroidism

Interpretation:
Cardiac is ruled out
Anemia
● Rule out blood loss
○ Visible blood loss is absent
 ○ But cannot rule out entirely, because occult blood loss can
still be there
● Increased destruction or less production
○ H/o hemolysis is absent
○ So most likely, anemia is due to less production

Ddx at the end of this history: Nutritional anemia

● Children are fussy eaters
● Their diet may not contain iron rich food
● Common in adolescent age group, any growing period
○ Pregnancy
○ After 6months of age
Second diagnosis: Chronic blood loss related anemia
Third diagnosis: Anemia due to decreased production

Sickle Cell
Anemia
 Vasocs irises

H/o recurrent pallor episodes

● Post viral infections --- episodes of Autoimmune hemolysis
● Hemolytic crisis of sickle cell anemia
● G6PD deficiency is often triggered by drug usage/certain infections

Significance of birth weight, term

● Preterm babies are at risk of developing anemia
○ Iron is supplied in the last trimester
● LBW
○ Decreased iron stores

Preterm presenting as anemia: will present in early infancy and not later.

Anemia presenting as neonatal jaundice: hemolytic anemia

● Rh/ABO incompatibility
● G6PD deficiency
● Cephalhematoma
● Hereditary Spherocytosis
Ask for h/o phototherapy and transfusion therapy

Bioav. Of iron in breast milk is high, (anemia is uncommon <6months)

Continued b feeding w/o complementary feeds: child will develop anemia

Nutritional history: mention if the child is consuming iron rich foods ragi,
maize, green leafy vegetables
Vegetarian diet: deficient in vitamin b12
Specify if the child is consuming cow milk
● CMPA: blood loss through the GI tract

Goat milk
● Vitamin B9 deficient

Development, Immunization, Family history

Mention if in these recent months there is a drop in scholastic performance
, child is irritable, lethargic

Developmental delay with anemia

● Fanconi’s syndrome
● Severe megaloblastic anemia in infancy
● Gaucher disease
● Chronic lead poisoning

Anemias that run in family

● Thalassemia (AR)
● Sickle cell anemia (AR)
● Hereditary spherocytosis (AD)
● G6PD (X-linked)
Don't mention similar illness
Tell h/o bleeding episodes in family, chronic jaundice, gallstones,
transfusions, surgeries in family (splenectomy)

Don’t give h/o habits.

Loss of appetite is present in anemia

Summary:
Take consent from child also

Head to Toe Examination

Chronic anemia: dull, little, lustreless hair, hair loss, brittle
Fronto-parietal-malar bossing: expansion of marrow for hematopoiesis
(hemolytic facies) : characteristic of thalassemia major
● Presents at 6months of age
● Nourishment won’t be good until blood transfusions
Unlikely this child has thalassemia major.

Eye examination in anemia

● Pallor
● Icterus
● Evidence of subconjunctival hemorrhage: bleeding tendency
● Severe iron deficiency can present with bluish sclera
Oral cavity: Hygiene, angular stomatitis, cheilitis.
Tongue appears normal
Teeth in hemolytic facies: malocclusion of teeth, overcrowding of teeth
Skin: hyperpigmentation of knuckles: vitamin b12 deficiency
Generalized hyperpigmentation with anemia: Fanconi’s anemia

Look for leg ulcers/healed scars (sickle cell anemia: RBC clump: block
microcirculation --- recurrent ulcers)
● Presents at 2-4 months of age I
● No h/o crisis Pon na
○ Swelling of fingers
○ Bone pain JRIDIA
acute chest Syndrome
Fanconi’s anemia: age of presentation: 7 years
● Eye: microcornea
● Short stature, microcephaly
● Absent radius
● Generalized hyperpigmentation

Mention: no microcephaly, no knuckle hyperpig, etc

Use the IAP charts after 5 years of age, below 5 years: WHO growth charts

Child with thal major w/o blood transfusion: will have growth retardation
 cannotget above the swelling
Traube
space

II
cannotgetabouttheswelling

Read
A

Anemia with HSM: HSM is d/t extramedullary hematopoiesis (chronic

hemolysis)
● Storage disorders: Gaucher’s disease
Murmur indicating: innocent murmur : flow murmur due to high output state
in anemia (called a hemic murmur)
Points in favor of hemolytic anemia
● No evidence at history level
● Examination
○ Hepatosplenomegaly: Extramedullary hematopoiesis
○ Features of hemolytic facies: ONLY SEEN IN THAL MAJOR not
even intermedia

Why not nutritional anemia

● History is conclusive
● Moderate HSM: NOT seen in simple IDA

Why not bone marrow suppression syndromes

● No symptoms and signs of recurrent episodes of infection and
bleeding
 ● Hypoplastic and aplastic anemias dont present with HSM

Leukemias
● Age is in favor
● Could be leukemia
● Has HSM also

Storage disorders
● Some milder mutation of Gaucher can present later also

Presence of HSM rules out acute/chronic blood loss

Hemolytic anemias
● Age will be much earlier
● Spleen will be much bigger than liver
● Icterus with persistent neonatal jaundice

Sickle Cell anemia

● Splenomegaly rules it out

Thal major
● 6 months of age, should be transfusion dependent

Thal intermedia
● Mild anemia later age (after adolescence, in 2nd decade of life)
● HSM
● No thalassemia facies should be there

Thal minor
● Mild anemia
● No other symptoms

Enzyme deficiencies
● SHould present as acute eps of anemia
● No HSM
AIHA
● Some viral infection should be there
● Acute presentation
● HSM should not be present

So at the end of history and examination, possible ddxes include

● Thal intermedia
● Leukemia
● Gaucher’s disease Testsof Vaso on
crisis i
Confirm diagnosis
● CBC with Hb, TLC, PLC
○ At 7 years of age, normal Hb value: 11-14 g/dL
○ TLC increased: leukemia
● Peripheral smear
○ Morphology of RBCs: microcytic hypochromic
○ Evidence of hemolysis: nucleated RBC<, polychromatophilic
cells, basophilic stippling
○ Leukemia: Immature WBCs (blast cells)
○ Gauchers: characteristic cells:
■ WBC: crumpled tissue paper appearance

Normocytic normochromic anemia:

● Anemia of blood loss (acute/chronic)
● Anemia of chronic disorders (initially NCNC)

Other ddxes of microcytic hypochromic

● IDA
● Late stages of ACD Mx of Ung
● Thalassemia
a
● Sideroblastic anemia

Megaloblastic anemia
● Folate B12 def
Non megaloblastic macrocytic anemia
● Liver disorders
● Hypothyroidism

Confirm leukemia with PS and BM

Thalassemia: Hb electrophoresis:
● In thal intermedia: HbA HbA2 >4.5% HbF upto 50%
● HbA2 is diagnostic
● It is transfusion independent

Hb electrophoresis: parents will be carriers

Some evidence of hemolysis can be seen on their PS.

Thal major
● Absence of HbA
● HbF upto 95%
● HbA2 upto 5% or more

Gaucher’s confirmed with a Bone marrow biopsy.

Bone marrow transplantation:

Definitive therapy
Replaces non functional marrow with a functional marrow

● Autologus transplant
● Allogeneic transplant
● Haploidentical transplant
○ When you use a twin for transplant

Indications for BM transplant

● Leukemia
● Lymphoma
● Sickle cell anemia
 ● Aplastic anemia

Chelating
wise if Hydroxy area
blow to diff history agent
complications
for tx Transfusion
Wethergiven

crisis
Vitals in a
change

Ratty
Anemia
ragtime
Anemia gonlowvolume But Tx Nomad

uncommon
Starting
 from staring
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Thalassemia

9 10.591dL
Ideal Hb for thalassemia

Acute exacerbation of symptoms

hutments cardiac
should NOT be there
there so
If they have neg trans

Sickle Cell Pain legs

Crisis Abd pain

History
Headache
Convulsions

Transfusiondependent
anemia
1 Thalassemiamajor
from
HS Sickle cell
young age 2 Hemolytic
NS in past

Recurrent
3 Inherited BM failure
thn diamond blackton
this
Pertaining to
Nistor 4
Enzymopathry
you ask

Aplastic Anemia is NOT

If
prominent
more prominent
Bleeding