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ANEMIA IN CHILDREN
Presented by: Manisha
Thakur
Child Health Nursing
ANEMIA
• It is greek word
• “Ana” = absent/ decresed
• “emia‟ = blood
DEFINITION
 Anemia is a decrease in Hb concentration or the
number of red blood cells (RBC) as measured
1. gm per cu mm or
2. by volume of packed RBC per 100 ml of blood. This
is clinically obtained by doing a hematocrit (HCT).
 Below average of normal values for age and
sex.
CLASSIFICATION OF ANEMIAS
1. Anemia from inadequate erythropoiesis.
2. Anemia of blood loss (post-hemorrhagic).
3. Anemia due to ↑ destruction (hemolytic).
CLINICAL EVALUATION
Common manifestations:
 Pallor, exercise intolerance, dyspnea,
palpitations, headache, lack of conc., irritability,
syncope, hemic murmurs.
 Less commonly: anorexia, nausea, flatulence,
constipation, mild proteinuria, fever
 Severe cases: ↑ C.O, CHF
LABORATORY INVESTIGATION
 CBC
1. Hct, Hb
2. RBCs count
3. WBCs
4. Platelets
5. Reticulocytes
 Cell morphology •
 Blood Indices: MCV MCH MCHC RDW=11.5-
14.5%
BIOCHEMICAL LABORATORY
INVESTIGATION
A. Iron status
1. Serum iron (N 60-150 µg/dl)
2. TIBC (N 100-400 µg/dl)
3. Serum ferritin (N 10-150 ng/dl)
B. Megaloblastic anemia
1. Serum vit. B12, folate
COMMONEST CAUSE OF
ANEMIA
1. Nutritional Deficiency : Iron Deficiency
2. Acute Hemolytic: G6PDD Chronic
3. Hemolytic: β-Thalassemia
ANEMIA DUE TO DEFICIENCY
OF SPECIFIC NUTRIENTS
IRON DEFICIENCY ANEMIA
 Most common nutritional deficiency in children
and is worldwide.
 Highest :
1. 6 - 24 months
2. Artificially fed infants.
3. Low socioeconomic status.
PREVELANCE OF IDA
• Iron-deficiency anemia remains the most
common nutritional problem from a global
perspective, it is estimated that roughly 2-5% of
the world population are anaemic.
Iron Requirements
 Normal Daily Iron Requirements:
1. 1mg/kg/day elemental iron for infants and
children (max 15 mg/day).
2. 2 mg/kg/day elemental iron for low birth weight
and newborns with very low initial Hb values.
3. 6 mg/kg/day elemental iron is needed for 3 mo.
CAUSES
• An iron poor diet.
• Body not being able to absorb
iron well.
• Blood loss.
• Rapid growth (in first year of
life and in adolescence), when
more iron is needed.
• Young children who drinks a lot
of cow milk rather than eating
foods that supply the body with
more iron.
PATHOPHYSIOLOGY
• ↓ iron stores.
• ↓ iron-storage protein (ferritin)
• ↓ serum iron
• ↑iron binding capacity TIBC.
• Anemia: hypochromia, microcytosis.
• ↓ activity of iron-containing intracellular
enzymes (e.g. CNS -MAO).
CLINICAL MANIFESTATION
GIT: Anorexia, glossitis, Pica (ingestion of wall
plaster, clay), Geophagia (earth), Pagophagia (ice)
CNS: Short attention span, irritability, breath
holding, ↓ alertness, ↓ learning ability and school
performance.
CONT…
• Headache
• Irritability
• Shortness of breath
• Sore tongue
• weakness
• Very pale white eyes,
• Blood in stool
• Brittle nails
• Decreased appetite
• Fatigue
DIAGNOSTIC EVALUATION
• Physical examination
• Lab-investigation:
1. Hematocrit
2. Serum ferritin (the amount of iron stored in
body)
3. Serum iron (iron is in blood)
4. Total iron binding capacity(TBIC) to
measure the ability of a protein called
trasferrin to carry iron in the blood.
MANAGEMENT
1. Iron supplements: ferrous sulphate (P/O) (I/V)
2. The iron is best absorbed on an empty
stomach, some people take with food to avoid
stomach upset.
3. Milk and antacids can interfere with iron
absorption and should not be taken at the same
time as iron supplements.
4. Iron rich foods: raisins, meat(liver), fish, eggs,
legumes, whole grain bread
CONT…
Oral Iron salts:
• Ferrous sulfate drops for infants ( 20% elemental iron).
• Ferrous gluconate drops ( 12 % elemental iron).
• Ferrous fumarate (30% elemental iron) tablets or syrup for
older children.
• Iron better between meals. fibers (e.g. whole bread and
cereals), tannate (like tea), phosphates (in bread, cow's milk
and egg yolk) and phytic acid ↓ absorption of iron.
• Absorption ↑ by vitamin C (e.g. citrous fruits), sugar and
amino acids (meat, poultry, fish).
CONT….
• Parenteral iron therapy: Iron dextran mixture (Imferon)
– 50 mg elemental iron / ml only in intolerance or
malabsorption
– Iron dextran and iron sorbitol both contain 50 mg/mL
recommended dose is 100 mg daily 2 mL on alternate
days until total required dose is administered or
maximum 2 g .
• Packed RBC transfusion: Severely anemic children with
Hb < 4 g/dl
• Treatment of etiology correct diet ,parasite.
FEROSE
It is rapidly absorbed, with a high rate of iron
utilization and produces an effective increase in
Haemoglobin. Due to its favourable nonionic
nature it has the following properties unlike
ionised iron salt preparations: · Ferose does not
give rise to irritation of the intestinal mucosa and
does not stain the teeth. · Ferose has palatable, non
metallic taste (Ferose chewable tablets have
chocolate flavour and are acceptable even by the
most resistant patients of all ages). · Ferose has
excellent tolerance.
MEGALOBLASTIC ANEMIAS
Megaloblastic anemia is a general term used to
describe a group of anemias caused by impaired DNA
synthesis. It is characterized by abnormal findings in
peripheral blood smear (macrovalocytes) and bone
marrow samples (megaloblastic hyperplasia).
Megaloblasts, the hallmark of these anaemias, are
caused by asynchronous maturation between the
nucleus and the cytoplasm due to DNA synthesis
impairment.
DEFINITION
Megaloblastic anemia is a type of anemia
characterized by very large red blood cells. In
addition to the cell being large, inner content of each
cell is not developed fully. The malformation cause
the bone marrow to produce fewer cells and
sometimes cell die earlier. Instead of being round or
disk shaped, the res blood cells can be oval.
The red blood cells are:
 Too large
 Not fully developed
 Abnormally shaped
ETIOLOGY
• Vitamin B₁₂ deficiency or defective metabolism
• Folate deficiency or defective metabolism
• Drug induced ( Purine and Pyramidine analogs)
Others:
Pernicious anaemia(autoimmune)
Surgeries
Nitrous oxide
Lesch-Nyhan syndrome
Sideroblastic anemia
Aplastic anemia
Thiamine responsive megaloblastic anemia
Cont…
1. Inadequate Intake
1. Dietary – Food Fads, veganism, malnutrition
2. Maternal deficiency causing B₁₂ deficiency in
breastmilk.
2. Failure to secrete IF
1. Congenital deficiency of IF
2. IgA deficiency
3. Gastric Atrophy ( Autoimmune )
CONT…
Acquired causes of insufficient folate include:
1. Inadequate dietary intake.
2. Inadequate absorption from proximal small
intestine.
3. Medications associated with folate deficiency:
– Sulfonamides antibiotics
– Antifolate antimetabolite drugs
– Antineoplastic agents: methotrexate
CLINICAL
MANIFESTATION
• Non specific manifestations : weakness,
lethargy, FTT, feeding difficulties.
• Infants may have regression of milestones.
• On examination, most patients have pallor,
sallow yellow complexion.
• Hyperpigmentation of knuckles and nail bed.
• Neurologic symptoms may include paresthesia,
sensory deficits, hypotonia, seizures, and
neuropsychiatric changes.
CONT…
• Difficult walking
• Diarrhea
• Irritability
• Smooth tender tongue
• Weak muscles
Diagnostic evaluation
• Family history collection:
– Congenital absence or deficiency of carrier protein
– Imerslud-grasbeck syndrome: proteinuria, excretion of
cobalamine and intrinsic factor.
• Physical examination:
– Glossitis, stomatitis, hyperpigmentation and weight loss.
– Physical evidence of anemia, thrombocytopenia,
neutropenia
– Lymphadenopathy, hepatomegaly- malignancy
CONT….
– Neurologic status- vibration sensation, tingling.
• Laboratory studies:
– CBC- macrocytic red cell indices and evaluate for
other cytopenias.
– Reticulocyte count
– Serum and RBC folate level
• Bone marrow evaluation: more than one
abnormal cell line in CBC.
• Platelet count.
Management
• Depends on underlying cause:
• Folate deficiency:
• Folate supplements
– Folic acid, 2-5 mg/day P/O or inj. 3-4 wks.
• Eliminate drugs causing folate deficency.
• B12 deficiency:
• Administered orally.
• Can be parentrally if high dose required.
APLASTIC ANEMIA
• It compromises a group of disorders of the hematopoietic
stem cells resulting in the suppression of one or more of
erythroid, myeloid and megakaryotic cell lines.
• It may be inherited or acquired.
Epidemiology
 Annual incidence in Europe and US - 2 cases
per million population, but 4 cases in Bangkok
6 in Thailand and 14 in Japan.
 No racial predisposition exists in the United
States; however, prevalence is increased in the
Far East.
 The male-to-female ratio is approximately 1:1
 Aplastic anemia occurs in all age groups.
 A small peak in incidence in childhood.
Etiopathogenesis
• Hematopoietic stem cell may be deficient due to
:
1. Acquired injury from viruses, toxins, chemicals
2. Abnormal marrow microenvironment
3. Immunological suppression( mediated by Ab or
cytotoxic T cells)
4. Mutation in genes controlling hematopoiesis
Clinical features
• Anemia: pallor and/or signs of
congestive heart failure, such as
shortness of breath.
• Thrombocytopenia: bruising (eg,
ecchymoses, petechiae) on the
skin, gum bleeding, or nosebleeds.
• Neutropenia : fever, cellulitis,
pneumonia, or sepsis
• Jaundice and evidence of clinical
hepatitis in subset of patients
CONT..
• Adenopathy or organomegaly
should suggest an alternative
diagnosis.
• In any case of aplastic anemia, look
for physical stigmata of inherited
marrow failure syndromes such as:
– skin pigmentation
– short stature
– microcephaly
– hypogonadism
– mental retardation
– skeletal anomalies
Investigations
 CBC
 PBS
 Reticulocyte count
 B12/folate.
 Liver function tests
 Virology
 Bone marrow aspirate
CONT…
 Anemia is common, and red cells appear
morphologically normal. The reticulocyte count usually
is less than 1%.
 Thrombocytopenia, with a paucity of platelets in the
blood smear.
 Agranulocytosis (ie. decrease in all granular white
blood cells, including neutrophils, eosinophils, and
basophils) and a decrease in monocytes are observed. A
relative lymphocytosis occurs.
 The degree of cytopenia is useful in assessing the
severity of aplastic anemia.
CONT…..
Other investigations
 Hemoglobin electrophoresis - may show elevated fetal
hemoglobin.
 Biochemical profile, including evaluation of transaminases,
bilirubin, lactic dehydrogenase, Coombs test, and kidney
function, is useful in evaluating etiology and differential
diagnosis.
 Serologic testing for hepatitis EBV, CMV, and HIV
 Autoimmune disease evaluation for evidence of collagen-
vascular disease
 Histocompatibility testing should be conducted early to
establish potential related donors, especially in younger patients.
Diagnosis
• Pancytopenia
• Bone marrow histology and
cytology
- decreased marrow cellularity
(< 25%)
- increased fat cells component
- no extensive fibrosis
- no malignancy or storage
disease
Treatment- AA
 Supportive care
Severe Anemia- packed red
cells
Sever Thrombocytopenia-
Platelets Transfusion
Infection- Antibiotics
Definitive therapy
 Hematopoietic stem cell
transplant (HSCT)
Sickle cell anemia
 Is an inherited form of
anemia — a condition in
which there aren't enough
healthy red blood cells to
carry adequate oxygen
throughout your body.
 Normally, your red blood
cells are flexible and
round, moving easily
through your blood
vessels.
Cont…
 In sickle cell anemia, the red blood cells
become rigid and sticky and are shaped like
sickles or crescent moons.
 These irregularly shaped cells can get stuck in
small blood vessels, which can slow or block
blood flow and oxygen to parts of the body.
DEFINITION OF SCA
 Sickle Cell disease: is a genetic disorder that
affects erythrocytes (RBC) causing them to
become sickle or crescent shaped.
 The effects of this condition due to an
abnormality of the hemoglobin molecules found
in erythrocytes.
HISTORY
 In 1904, Walter Clement Noel traveled from Grenada
to the United States to start studying at the Chicago
College of Dental Surgery.
 A few months later he was admitted to the Presbyterian
Hospital in Chicago when he developed severe
respiratory distress and a leg ulcer, both of which we
now know are symptoms of sickle cell.
 Dr. Earnest E. Irons, the intern who was on duty that
day, performed a routine blood test and a urine analysis
for Noel and was the first to observed these “pear
shaped, elongated” sickled blood cells.
Report of blood test on Walter Clement Noel dated 31
December 1904
CONT…
 It was not until 1910 that Dr James
Herrick, the supervisor of Dr Irons,
published his article describing these
“peculiar elongated and sickle shaped
red blood corpuscles in a case of severe
anemia.”
 This was the first documented and
recorded case of Sickle cell in Western
medicine.
 Dr Noel returned to Grenada in 1907
and ran his dental practice in St.
Georges, the capital city, until he died
at the age of 32 from the acute chest
syndrome.
CHARACTERISTICS OF
BLOOD
HEMOGLOBIN
 The oxygen-carrying pigment and predominant
protein in the red blood cells.
 Hemoglobin forms an unstable, reversible bond
with oxygen.
 Oxyhemoglobin: Oxygenated ( bright red).
 Deoxyhemoglobin: Reduced ( purple-blue).
CONT..
 Each hemoglobin molecule
is made up of four heme
groups surrounding a
globin group.
 Heme contains iron and
gives a red color to the
molecule.
 Globin consists of two
linked pairs of polypeptide
chains.
Genetics of SCD
 The change in cell structure arises from a change in the
structure of hemoglobin.
 A single change in an amino acid causes hemoglobin to
aggregate.
CONT…
INHERITANCE OF SCD
 If one parent has sickle cell trait
(HbAS) and the other does not
carry the sickle hemoglobin at all
(HbAA) then none of the
children will have sickle cell
anemia.
 There is a one in two (50%)
chance that any given child will
get one copy of the HbAS gene
and therefore have the sickle cell
trait.
 It is equally likely that any given
child will get two HbAA genes
and be completely unaffected.
CONT…
 If both parents have sickle cell
trait (HbAS) there is a one in
four (25%) chance that any
given child could be born with
sickle cell anemia
 There is also a one in four
chance that any given child
could be completely unaffected.
 There is a one in two (50%)
chance that any given child will
get the sickle cell trait.
CONT..
 If one parent has sickle cell trait (HbAS) and
the other has sickle cell anemia (HbSS) there is
a one in two (50%) chance that any given child
will get sickle cell trait and a one in two (50%)
chance that any given child will get sickle cell
anemia.
 No children will be completely unaffected.
CONT…
 If one parent has sickle cell anemia (HbSS) and the
other is completely unaffected (HbAA) then all the
children will have sickle cell trait.
 None will have sickle cell anemia.
 The parent who has sickle cell anemia (HbSS) can
only pass the sickle hemoglobin gene to each of their
children.
Mechanism
 When sickle hemoglobin (HbS) gives up its oxygen to the tissues,
HbS sticks together
Forms long rods form inside RBC
RBC become rigid, inflexible, and sickle-shaped
Unable to squeeze through small blood vessels, instead blocks
small blood vessels
Less oxygen to tissues of body
 RBCs containing HbS have a shorter lifespan
 Normally 20 days
Chronic state of anemia
SYMPTOMS
• They vary from person to person
and change over time, include:
• Anemia
– Sickle cells break apart easily and
die, leaving you without enough red
blood cells. But sickle cells usually
die in 10 to 20 days, leaving a
shortage of red blood cells (anemia).
Without enough red blood cells, your
body can't get the oxygen it needs to
feel energized, causing fatigue.
Cont….
Episodes of pain.
 Periodic episodes of pain, called crises, are a
major symptom of sickle cell anemia.
 Pain develops when sickle-shaped red blood
cells block blood flow through tiny blood
vessels to your chest, abdomen and joints. Pain
can also occur in your bones.
 The pain varies in intensity and can last for a
few hours to a few weeks. Some people have
only a few pain episodes. Others have a dozen
or more crises a year. If a crisis is severe
enough, you might need to be hospitalized.
Some adolescents and adults with sickle cell
anemia also have chronic pain, which can
result from bone and joint damage, ulcers and
other causes.
Cont…
 Painful swelling of hands and feet.
The swelling is caused by sickle-
shaped red blood cells blocking blood
flow to the hands and feet.
 Frequent infections.
Sickle cells can damage an organ that
fights infection (spleen), leaving you
more vulnerable to infections. Doctors
commonly give infants and children
with sickle cell anemia vaccinations
and antibiotics to prevent potentially
life-threatening infections, such as
pneumonia.
Cont…
 Delayed growth.
 Red blood cells provide your body
with the oxygen and nutrients you
need for growth. A shortage of
healthy red blood cells can slow
growth in infants and children and
delay puberty in teenagers.
 Vision problems.
 Tiny blood vessels that supply your
eyes may become plugged with sickle
cells. This can damage the retina —
the portion of the eye that processes
visual images, leading to vision
problems.
Cont…
 Jaundice
 Syncope
 Dactylitis
 Weakness and pallor
 Neurological symptoms
Diagnositic test
1. Peripheral smear
2. Sickling test
3. Hb-electrophorosis
4. PCR
SICKLING TEST
Sickling test is a simple blood test
used to determine if you have
sickle cell disease or sickle cell
trait. People with this disease have
red blood cells that are shaped
abnormally. Instead of looking like
doughnuts like normal red blood
cells, they’re shaped like a crescent
moon. The disease is named for the
C-shaped farm tool known as a
sickle.
CONT..
 If the screening test is negative, there is no
sickle cell gene present.
 If the screening test is positive, further tests will
be done to determine whether one or two sickle
cell genes are present.
 Check for a low red blood cell count (anemia)
will be done.
TREATMENT
 There is no single best treatment for all people
with Sickle cell disease.
 Treatment options are different for each person
depending on the symptoms.
 Treatments can include receiving blood
transfusions, maintaining a high fluid intake
(drinking 8 to 10 glasses of water each day),
receiving IV (intravenous) therapy (fluids given
into a vein) and medications to help with pain.
CONT….
 Treatment is usually aimed at avoiding crises,
relieving symptoms and preventing
complications. Babies and children age 2 and
younger with sickle cell anemia should make
frequent visits to a doctor.
 Children older than 2 and adults with sickle cell
anemia should see a doctor at least once a year,
according to the Centers for Disease Control
and Prevention
Main treatment methods
• There is no known cure for
sickle cell anemia.
• The four main treatment
options are:
1. Blood Transfusions
2. Drug Treatment
3. Blood and Marrow Stem Cell
Transplantation
4. Gene Therapy
MEDICATIONS
Antibiotics
 Children with sickle cell anemia
may begin taking the antibiotic
penicillin when they're about 2
months old and continue taking
it until they're at least 5 years
old.
 Doing so helps prevent
infections, such as pneumonia,
which can be lifethreatening to
an infant or child with sickle cell
anemia.
CONT…
• Pain-relieving
To relieve pain during a sickle
cell crisis.
• Hydroxyurea (Droxia, Hydrea).
When taken daily, hydroxyurea
reduces the frequency of
painful crises and might reduce
the need for blood transfusions
and hospitalizations.
CONT…
• Assessing stroke risk
• Using a special ultrasound machine (transcranial),
doctors can learn which children have a higher risk of
stroke. This painless test, which uses sound waves to
measure blood flow, can be used on children as young
as 2 years. Regular blood transfusions can decrease
stroke risk. Vaccinations to prevent infections
Childhood vaccinations are important for preventing
disease in all children.
• Vaccinations
• such as the pneumococcal vaccine and the annual flu
shot, are also important for adults with sickle cell
anemia.
• Blood transfusions
• Increase the number of normal
red blood cells in circulation,
helping to relieve anemia. In
children with sickle cell anemia
at high risk of stroke, regular
blood transfusions can decrease
the risk. Transfusions can also
be used to treat other
complications of sickle cell
anemia, or they can be given to
prevent complications.
CONT..
• Nitric oxide.
• People with sickle cell anemia
have low levels of nitric oxide
in their blood.
• Nitric oxide is a gas that helps
keep blood vessels open and
reduces the stickiness of red
blood cells. Treatment with
inhaled nitric oxide might
prevent sickle cells from
clumping together.
• Studies on nitric oxide have
shown little benefit so far.
CONT…
• Bone Marrow Transplant
• A bone marrow transplant involves
replacing bone marrow affected by
sickle cell anemia with healthy
bone marrow from a donor. The
procedure usually uses a matched
donor, such as a sibling, who
doesn't have sickle cell anemia.
For many, donors aren't available.
But stem cells from umbilical cord
blood might be an option.
Prevention
1. Genetic screening
2. Testing for sickle cells in
babies.
a) Chronic vill sampling
b) Amniotic fluid sampling
c) Fetal blood samplin
3. Daily penicillin for newborn
babies with the disease.
“Your little effort can give others second
chance to live life.”

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ANEMIA IN PEDIATRICS: IRON DEFICIENCY ANEMIA, MEGALOBLASTIC ANEMIA, APLASTIC ANEMIA, SICKLE CELL ANEMIA

  • 1. ANEMIA IN CHILDREN Presented by: Manisha Thakur Child Health Nursing
  • 2. ANEMIA • It is greek word • “Ana” = absent/ decresed • “emia‟ = blood
  • 3. DEFINITION  Anemia is a decrease in Hb concentration or the number of red blood cells (RBC) as measured 1. gm per cu mm or 2. by volume of packed RBC per 100 ml of blood. This is clinically obtained by doing a hematocrit (HCT).  Below average of normal values for age and sex.
  • 4.
  • 5. CLASSIFICATION OF ANEMIAS 1. Anemia from inadequate erythropoiesis. 2. Anemia of blood loss (post-hemorrhagic). 3. Anemia due to ↑ destruction (hemolytic).
  • 6. CLINICAL EVALUATION Common manifestations:  Pallor, exercise intolerance, dyspnea, palpitations, headache, lack of conc., irritability, syncope, hemic murmurs.  Less commonly: anorexia, nausea, flatulence, constipation, mild proteinuria, fever  Severe cases: ↑ C.O, CHF
  • 7. LABORATORY INVESTIGATION  CBC 1. Hct, Hb 2. RBCs count 3. WBCs 4. Platelets 5. Reticulocytes  Cell morphology •  Blood Indices: MCV MCH MCHC RDW=11.5- 14.5%
  • 8. BIOCHEMICAL LABORATORY INVESTIGATION A. Iron status 1. Serum iron (N 60-150 µg/dl) 2. TIBC (N 100-400 µg/dl) 3. Serum ferritin (N 10-150 ng/dl) B. Megaloblastic anemia 1. Serum vit. B12, folate
  • 9. COMMONEST CAUSE OF ANEMIA 1. Nutritional Deficiency : Iron Deficiency 2. Acute Hemolytic: G6PDD Chronic 3. Hemolytic: β-Thalassemia
  • 10. ANEMIA DUE TO DEFICIENCY OF SPECIFIC NUTRIENTS IRON DEFICIENCY ANEMIA  Most common nutritional deficiency in children and is worldwide.  Highest : 1. 6 - 24 months 2. Artificially fed infants. 3. Low socioeconomic status.
  • 11. PREVELANCE OF IDA • Iron-deficiency anemia remains the most common nutritional problem from a global perspective, it is estimated that roughly 2-5% of the world population are anaemic.
  • 12. Iron Requirements  Normal Daily Iron Requirements: 1. 1mg/kg/day elemental iron for infants and children (max 15 mg/day). 2. 2 mg/kg/day elemental iron for low birth weight and newborns with very low initial Hb values. 3. 6 mg/kg/day elemental iron is needed for 3 mo.
  • 13. CAUSES • An iron poor diet. • Body not being able to absorb iron well. • Blood loss. • Rapid growth (in first year of life and in adolescence), when more iron is needed. • Young children who drinks a lot of cow milk rather than eating foods that supply the body with more iron.
  • 14. PATHOPHYSIOLOGY • ↓ iron stores. • ↓ iron-storage protein (ferritin) • ↓ serum iron • ↑iron binding capacity TIBC. • Anemia: hypochromia, microcytosis. • ↓ activity of iron-containing intracellular enzymes (e.g. CNS -MAO).
  • 15.
  • 16. CLINICAL MANIFESTATION GIT: Anorexia, glossitis, Pica (ingestion of wall plaster, clay), Geophagia (earth), Pagophagia (ice) CNS: Short attention span, irritability, breath holding, ↓ alertness, ↓ learning ability and school performance.
  • 17. CONT… • Headache • Irritability • Shortness of breath • Sore tongue • weakness • Very pale white eyes, • Blood in stool • Brittle nails • Decreased appetite • Fatigue
  • 18. DIAGNOSTIC EVALUATION • Physical examination • Lab-investigation: 1. Hematocrit 2. Serum ferritin (the amount of iron stored in body) 3. Serum iron (iron is in blood) 4. Total iron binding capacity(TBIC) to measure the ability of a protein called trasferrin to carry iron in the blood.
  • 19. MANAGEMENT 1. Iron supplements: ferrous sulphate (P/O) (I/V) 2. The iron is best absorbed on an empty stomach, some people take with food to avoid stomach upset. 3. Milk and antacids can interfere with iron absorption and should not be taken at the same time as iron supplements. 4. Iron rich foods: raisins, meat(liver), fish, eggs, legumes, whole grain bread
  • 20. CONT… Oral Iron salts: • Ferrous sulfate drops for infants ( 20% elemental iron). • Ferrous gluconate drops ( 12 % elemental iron). • Ferrous fumarate (30% elemental iron) tablets or syrup for older children. • Iron better between meals. fibers (e.g. whole bread and cereals), tannate (like tea), phosphates (in bread, cow's milk and egg yolk) and phytic acid ↓ absorption of iron. • Absorption ↑ by vitamin C (e.g. citrous fruits), sugar and amino acids (meat, poultry, fish).
  • 21. CONT…. • Parenteral iron therapy: Iron dextran mixture (Imferon) – 50 mg elemental iron / ml only in intolerance or malabsorption – Iron dextran and iron sorbitol both contain 50 mg/mL recommended dose is 100 mg daily 2 mL on alternate days until total required dose is administered or maximum 2 g . • Packed RBC transfusion: Severely anemic children with Hb < 4 g/dl • Treatment of etiology correct diet ,parasite.
  • 22. FEROSE It is rapidly absorbed, with a high rate of iron utilization and produces an effective increase in Haemoglobin. Due to its favourable nonionic nature it has the following properties unlike ionised iron salt preparations: · Ferose does not give rise to irritation of the intestinal mucosa and does not stain the teeth. · Ferose has palatable, non metallic taste (Ferose chewable tablets have chocolate flavour and are acceptable even by the most resistant patients of all ages). · Ferose has excellent tolerance.
  • 23. MEGALOBLASTIC ANEMIAS Megaloblastic anemia is a general term used to describe a group of anemias caused by impaired DNA synthesis. It is characterized by abnormal findings in peripheral blood smear (macrovalocytes) and bone marrow samples (megaloblastic hyperplasia). Megaloblasts, the hallmark of these anaemias, are caused by asynchronous maturation between the nucleus and the cytoplasm due to DNA synthesis impairment.
  • 24. DEFINITION Megaloblastic anemia is a type of anemia characterized by very large red blood cells. In addition to the cell being large, inner content of each cell is not developed fully. The malformation cause the bone marrow to produce fewer cells and sometimes cell die earlier. Instead of being round or disk shaped, the res blood cells can be oval. The red blood cells are:  Too large  Not fully developed  Abnormally shaped
  • 25. ETIOLOGY • Vitamin B₁₂ deficiency or defective metabolism • Folate deficiency or defective metabolism • Drug induced ( Purine and Pyramidine analogs) Others: Pernicious anaemia(autoimmune) Surgeries Nitrous oxide Lesch-Nyhan syndrome Sideroblastic anemia Aplastic anemia Thiamine responsive megaloblastic anemia
  • 26.
  • 27. Cont… 1. Inadequate Intake 1. Dietary – Food Fads, veganism, malnutrition 2. Maternal deficiency causing B₁₂ deficiency in breastmilk. 2. Failure to secrete IF 1. Congenital deficiency of IF 2. IgA deficiency 3. Gastric Atrophy ( Autoimmune )
  • 28. CONT… Acquired causes of insufficient folate include: 1. Inadequate dietary intake. 2. Inadequate absorption from proximal small intestine. 3. Medications associated with folate deficiency: – Sulfonamides antibiotics – Antifolate antimetabolite drugs – Antineoplastic agents: methotrexate
  • 29. CLINICAL MANIFESTATION • Non specific manifestations : weakness, lethargy, FTT, feeding difficulties. • Infants may have regression of milestones. • On examination, most patients have pallor, sallow yellow complexion. • Hyperpigmentation of knuckles and nail bed. • Neurologic symptoms may include paresthesia, sensory deficits, hypotonia, seizures, and neuropsychiatric changes.
  • 30. CONT… • Difficult walking • Diarrhea • Irritability • Smooth tender tongue • Weak muscles
  • 31. Diagnostic evaluation • Family history collection: – Congenital absence or deficiency of carrier protein – Imerslud-grasbeck syndrome: proteinuria, excretion of cobalamine and intrinsic factor. • Physical examination: – Glossitis, stomatitis, hyperpigmentation and weight loss. – Physical evidence of anemia, thrombocytopenia, neutropenia – Lymphadenopathy, hepatomegaly- malignancy
  • 32. CONT…. – Neurologic status- vibration sensation, tingling. • Laboratory studies: – CBC- macrocytic red cell indices and evaluate for other cytopenias. – Reticulocyte count – Serum and RBC folate level • Bone marrow evaluation: more than one abnormal cell line in CBC. • Platelet count.
  • 33. Management • Depends on underlying cause: • Folate deficiency: • Folate supplements – Folic acid, 2-5 mg/day P/O or inj. 3-4 wks. • Eliminate drugs causing folate deficency. • B12 deficiency: • Administered orally. • Can be parentrally if high dose required.
  • 34. APLASTIC ANEMIA • It compromises a group of disorders of the hematopoietic stem cells resulting in the suppression of one or more of erythroid, myeloid and megakaryotic cell lines. • It may be inherited or acquired.
  • 35. Epidemiology  Annual incidence in Europe and US - 2 cases per million population, but 4 cases in Bangkok 6 in Thailand and 14 in Japan.  No racial predisposition exists in the United States; however, prevalence is increased in the Far East.  The male-to-female ratio is approximately 1:1  Aplastic anemia occurs in all age groups.  A small peak in incidence in childhood.
  • 36. Etiopathogenesis • Hematopoietic stem cell may be deficient due to : 1. Acquired injury from viruses, toxins, chemicals 2. Abnormal marrow microenvironment 3. Immunological suppression( mediated by Ab or cytotoxic T cells) 4. Mutation in genes controlling hematopoiesis
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  • 39. Clinical features • Anemia: pallor and/or signs of congestive heart failure, such as shortness of breath. • Thrombocytopenia: bruising (eg, ecchymoses, petechiae) on the skin, gum bleeding, or nosebleeds. • Neutropenia : fever, cellulitis, pneumonia, or sepsis • Jaundice and evidence of clinical hepatitis in subset of patients
  • 40. CONT.. • Adenopathy or organomegaly should suggest an alternative diagnosis. • In any case of aplastic anemia, look for physical stigmata of inherited marrow failure syndromes such as: – skin pigmentation – short stature – microcephaly – hypogonadism – mental retardation – skeletal anomalies
  • 41. Investigations  CBC  PBS  Reticulocyte count  B12/folate.  Liver function tests  Virology  Bone marrow aspirate
  • 42. CONT…  Anemia is common, and red cells appear morphologically normal. The reticulocyte count usually is less than 1%.  Thrombocytopenia, with a paucity of platelets in the blood smear.  Agranulocytosis (ie. decrease in all granular white blood cells, including neutrophils, eosinophils, and basophils) and a decrease in monocytes are observed. A relative lymphocytosis occurs.  The degree of cytopenia is useful in assessing the severity of aplastic anemia.
  • 44. Other investigations  Hemoglobin electrophoresis - may show elevated fetal hemoglobin.  Biochemical profile, including evaluation of transaminases, bilirubin, lactic dehydrogenase, Coombs test, and kidney function, is useful in evaluating etiology and differential diagnosis.  Serologic testing for hepatitis EBV, CMV, and HIV  Autoimmune disease evaluation for evidence of collagen- vascular disease  Histocompatibility testing should be conducted early to establish potential related donors, especially in younger patients.
  • 45. Diagnosis • Pancytopenia • Bone marrow histology and cytology - decreased marrow cellularity (< 25%) - increased fat cells component - no extensive fibrosis - no malignancy or storage disease
  • 46. Treatment- AA  Supportive care Severe Anemia- packed red cells Sever Thrombocytopenia- Platelets Transfusion Infection- Antibiotics Definitive therapy  Hematopoietic stem cell transplant (HSCT)
  • 47.
  • 48. Sickle cell anemia  Is an inherited form of anemia — a condition in which there aren't enough healthy red blood cells to carry adequate oxygen throughout your body.  Normally, your red blood cells are flexible and round, moving easily through your blood vessels.
  • 49. Cont…  In sickle cell anemia, the red blood cells become rigid and sticky and are shaped like sickles or crescent moons.  These irregularly shaped cells can get stuck in small blood vessels, which can slow or block blood flow and oxygen to parts of the body.
  • 50. DEFINITION OF SCA  Sickle Cell disease: is a genetic disorder that affects erythrocytes (RBC) causing them to become sickle or crescent shaped.  The effects of this condition due to an abnormality of the hemoglobin molecules found in erythrocytes.
  • 51. HISTORY  In 1904, Walter Clement Noel traveled from Grenada to the United States to start studying at the Chicago College of Dental Surgery.  A few months later he was admitted to the Presbyterian Hospital in Chicago when he developed severe respiratory distress and a leg ulcer, both of which we now know are symptoms of sickle cell.  Dr. Earnest E. Irons, the intern who was on duty that day, performed a routine blood test and a urine analysis for Noel and was the first to observed these “pear shaped, elongated” sickled blood cells.
  • 52. Report of blood test on Walter Clement Noel dated 31 December 1904
  • 53. CONT…  It was not until 1910 that Dr James Herrick, the supervisor of Dr Irons, published his article describing these “peculiar elongated and sickle shaped red blood corpuscles in a case of severe anemia.”  This was the first documented and recorded case of Sickle cell in Western medicine.  Dr Noel returned to Grenada in 1907 and ran his dental practice in St. Georges, the capital city, until he died at the age of 32 from the acute chest syndrome.
  • 55. HEMOGLOBIN  The oxygen-carrying pigment and predominant protein in the red blood cells.  Hemoglobin forms an unstable, reversible bond with oxygen.  Oxyhemoglobin: Oxygenated ( bright red).  Deoxyhemoglobin: Reduced ( purple-blue).
  • 56. CONT..  Each hemoglobin molecule is made up of four heme groups surrounding a globin group.  Heme contains iron and gives a red color to the molecule.  Globin consists of two linked pairs of polypeptide chains.
  • 57. Genetics of SCD  The change in cell structure arises from a change in the structure of hemoglobin.  A single change in an amino acid causes hemoglobin to aggregate.
  • 59. INHERITANCE OF SCD  If one parent has sickle cell trait (HbAS) and the other does not carry the sickle hemoglobin at all (HbAA) then none of the children will have sickle cell anemia.  There is a one in two (50%) chance that any given child will get one copy of the HbAS gene and therefore have the sickle cell trait.  It is equally likely that any given child will get two HbAA genes and be completely unaffected.
  • 60. CONT…  If both parents have sickle cell trait (HbAS) there is a one in four (25%) chance that any given child could be born with sickle cell anemia  There is also a one in four chance that any given child could be completely unaffected.  There is a one in two (50%) chance that any given child will get the sickle cell trait.
  • 61. CONT..  If one parent has sickle cell trait (HbAS) and the other has sickle cell anemia (HbSS) there is a one in two (50%) chance that any given child will get sickle cell trait and a one in two (50%) chance that any given child will get sickle cell anemia.  No children will be completely unaffected.
  • 62. CONT…  If one parent has sickle cell anemia (HbSS) and the other is completely unaffected (HbAA) then all the children will have sickle cell trait.  None will have sickle cell anemia.  The parent who has sickle cell anemia (HbSS) can only pass the sickle hemoglobin gene to each of their children.
  • 63.
  • 64. Mechanism  When sickle hemoglobin (HbS) gives up its oxygen to the tissues, HbS sticks together Forms long rods form inside RBC RBC become rigid, inflexible, and sickle-shaped Unable to squeeze through small blood vessels, instead blocks small blood vessels Less oxygen to tissues of body  RBCs containing HbS have a shorter lifespan  Normally 20 days Chronic state of anemia
  • 65.
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  • 67.
  • 68. SYMPTOMS • They vary from person to person and change over time, include: • Anemia – Sickle cells break apart easily and die, leaving you without enough red blood cells. But sickle cells usually die in 10 to 20 days, leaving a shortage of red blood cells (anemia). Without enough red blood cells, your body can't get the oxygen it needs to feel energized, causing fatigue.
  • 69. Cont…. Episodes of pain.  Periodic episodes of pain, called crises, are a major symptom of sickle cell anemia.  Pain develops when sickle-shaped red blood cells block blood flow through tiny blood vessels to your chest, abdomen and joints. Pain can also occur in your bones.  The pain varies in intensity and can last for a few hours to a few weeks. Some people have only a few pain episodes. Others have a dozen or more crises a year. If a crisis is severe enough, you might need to be hospitalized. Some adolescents and adults with sickle cell anemia also have chronic pain, which can result from bone and joint damage, ulcers and other causes.
  • 70. Cont…  Painful swelling of hands and feet. The swelling is caused by sickle- shaped red blood cells blocking blood flow to the hands and feet.  Frequent infections. Sickle cells can damage an organ that fights infection (spleen), leaving you more vulnerable to infections. Doctors commonly give infants and children with sickle cell anemia vaccinations and antibiotics to prevent potentially life-threatening infections, such as pneumonia.
  • 71. Cont…  Delayed growth.  Red blood cells provide your body with the oxygen and nutrients you need for growth. A shortage of healthy red blood cells can slow growth in infants and children and delay puberty in teenagers.  Vision problems.  Tiny blood vessels that supply your eyes may become plugged with sickle cells. This can damage the retina — the portion of the eye that processes visual images, leading to vision problems.
  • 72. Cont…  Jaundice  Syncope  Dactylitis  Weakness and pallor  Neurological symptoms
  • 73. Diagnositic test 1. Peripheral smear 2. Sickling test 3. Hb-electrophorosis 4. PCR
  • 74. SICKLING TEST Sickling test is a simple blood test used to determine if you have sickle cell disease or sickle cell trait. People with this disease have red blood cells that are shaped abnormally. Instead of looking like doughnuts like normal red blood cells, they’re shaped like a crescent moon. The disease is named for the C-shaped farm tool known as a sickle.
  • 75. CONT..  If the screening test is negative, there is no sickle cell gene present.  If the screening test is positive, further tests will be done to determine whether one or two sickle cell genes are present.  Check for a low red blood cell count (anemia) will be done.
  • 76. TREATMENT  There is no single best treatment for all people with Sickle cell disease.  Treatment options are different for each person depending on the symptoms.  Treatments can include receiving blood transfusions, maintaining a high fluid intake (drinking 8 to 10 glasses of water each day), receiving IV (intravenous) therapy (fluids given into a vein) and medications to help with pain.
  • 77. CONT….  Treatment is usually aimed at avoiding crises, relieving symptoms and preventing complications. Babies and children age 2 and younger with sickle cell anemia should make frequent visits to a doctor.  Children older than 2 and adults with sickle cell anemia should see a doctor at least once a year, according to the Centers for Disease Control and Prevention
  • 78. Main treatment methods • There is no known cure for sickle cell anemia. • The four main treatment options are: 1. Blood Transfusions 2. Drug Treatment 3. Blood and Marrow Stem Cell Transplantation 4. Gene Therapy
  • 79. MEDICATIONS Antibiotics  Children with sickle cell anemia may begin taking the antibiotic penicillin when they're about 2 months old and continue taking it until they're at least 5 years old.  Doing so helps prevent infections, such as pneumonia, which can be lifethreatening to an infant or child with sickle cell anemia.
  • 80. CONT… • Pain-relieving To relieve pain during a sickle cell crisis. • Hydroxyurea (Droxia, Hydrea). When taken daily, hydroxyurea reduces the frequency of painful crises and might reduce the need for blood transfusions and hospitalizations.
  • 81. CONT… • Assessing stroke risk • Using a special ultrasound machine (transcranial), doctors can learn which children have a higher risk of stroke. This painless test, which uses sound waves to measure blood flow, can be used on children as young as 2 years. Regular blood transfusions can decrease stroke risk. Vaccinations to prevent infections Childhood vaccinations are important for preventing disease in all children. • Vaccinations • such as the pneumococcal vaccine and the annual flu shot, are also important for adults with sickle cell anemia.
  • 82. • Blood transfusions • Increase the number of normal red blood cells in circulation, helping to relieve anemia. In children with sickle cell anemia at high risk of stroke, regular blood transfusions can decrease the risk. Transfusions can also be used to treat other complications of sickle cell anemia, or they can be given to prevent complications.
  • 83. CONT.. • Nitric oxide. • People with sickle cell anemia have low levels of nitric oxide in their blood. • Nitric oxide is a gas that helps keep blood vessels open and reduces the stickiness of red blood cells. Treatment with inhaled nitric oxide might prevent sickle cells from clumping together. • Studies on nitric oxide have shown little benefit so far.
  • 84. CONT… • Bone Marrow Transplant • A bone marrow transplant involves replacing bone marrow affected by sickle cell anemia with healthy bone marrow from a donor. The procedure usually uses a matched donor, such as a sibling, who doesn't have sickle cell anemia. For many, donors aren't available. But stem cells from umbilical cord blood might be an option.
  • 85. Prevention 1. Genetic screening 2. Testing for sickle cells in babies. a) Chronic vill sampling b) Amniotic fluid sampling c) Fetal blood samplin 3. Daily penicillin for newborn babies with the disease.
  • 86. “Your little effort can give others second chance to live life.”