The clinical value of blood. .

Allowance for doctors'

(Institute of Pediatric Hematology, the drafters of the A.G
.Rumyantsev, E.B .Vladimirskaya), Moscow, 1999

Automatical Units Normal Short Form

Counting Measure- Level
ment

HGB- G/Liter 120-160 Hb

Hemoglobin
RBC - 12 3,9-5,9 Er
erythrocyte 10 /L

HCT -
Hematocryte % 36,0-48,0 Ht
 3
MCV- average 1 micron = 80 - 95
volume of 1 - femtoliter
erythrocyte (fl)
MCH the average Pikogram Colour Index
content of Hb in 1 =1012 27,0-31,02 (0,85-1,0)
erythrocyte pikograms
MCHC average G/dl
concentration of Hb g %, 32,0-36,0
in erythrocyte less g/l

RDW width of the

distribution curve of % 11,5-14,5 anisocytosis
erythrocyte by
volume
 RETICULOCYTE

Normal values:
The relative number of reticulocyte
0,5-1,2%
The absolute number of reticulocyte
30-70 x 10 * 9 / L
In cord blood of newborns 20-60%.
nemia pathologic state,accompanied
by decrease in the level of hemoglobin
and the quantity of erythrocytes per unit
of volume of the blood.
Erythrocytes - less informative index of
anemia than the level of hemoglobin
therefore, in the general practice the
basic criterion of severity is precisely
Hb:
Light degree of anemia - Hb 110-90 g /
l,
The average degree of severity - Hb 90-
70 g / l,
Severe anemia - Hb below 70 g / liter
 In terms of number of
reticulocyte, anemia are divided
into:
Regenerative- reticulocyte from 1.5 to
5% (or 15 to 50 ppm)

Hyper-regenerative - reticulocyte more

than 5% (or more than 50 ppm)

Aregenerative- Low reticulocyte (less than

0.5%), not according to the severity of
anemia or lack of reticulocyte.
 Classification of Anemia
I. Anemias resulting from acute blood loss
II. Anemias resulting from a deficit of erythropoesis

1) At the expense of maturation (mainly microcyte):

violation of absorption and utilization of iron (iron)

violation of transportation of iron (atransferrinemia)

violation of recycling iron (thalassemia, sideroblastic

anemia )

violation of reutilization of iron (anemia of chronic

disease);
 Anemia (continued)
2) At the expense of differentiation
(essentially normal):

aplastic anemia (congenital and acquired)

3) At the expense of proliferation (mainly

macrocytes)

B12-DEFICIENCY anemia

Folic-DEFICIENCY anemia.
 Anemia (continued)
Anemias resulting from increased destruction
of erythroid series cells - haemolytic:

1) caused by internal defects of erythrocytes

membranopathy, enzimopathy,
haemoglobinopathies;

2) the external (extracllular) effects:

autoimmune, traumatic, etc.

Classification D. Nathan, F. Oski, 2003, (book Anemias in

children, NA Finogenova et al, 2004.):
 IRON DEFICIENCY ANEMIA
(IDA)
ID recorded 20% of the world's
population.

83-90% of all anemia constitute IDA.

In children the first 2 years of life the

frequency of iron deficiency was 73%.

The second peak IDA development -

adolescence.
 CAUSES FOR DEVELOPMENT
of IDA
Alimentary iron deficiency as a consequence of an unbalanced
diet;

Increasing demand for iron and the reduction of the deposit

(or the frequency of multiple pregnancies, prematurity,
lactation periods of rapid growth, sports)

Chronic blood loss (nasal bleeding, diaphragmatic hernia, and

bleeding from GIT and diverticulitis, menorrhagia, renal
hemorrhage, idiopathic lung hemosiderosis)

Reduction of iron absorption (malabsorption, chronic

inflammatory diseases GIT, gastrectomy).
The total content of iron in the body -
about 4.2 g.
From them:
- 75-80% belongs to the hemoglobin

- 20 - 25% reserve

- 5-10% part of the myoglobin

-1% is part of the enzyme for the tissue

respiration
 Anemic Syndrome
- Decrease amount of Hemoglobin
Complaints: General weakness, reduction in the
appetite, physical and mental fatigue, shortness
of breath, vertigo, noise in the ears, flashing
flies before the eyes, unconscious states, in
heavy cases leads to coma.
Symptoms: the pallor of the skin and mucosa,
tachycardia, hypotonia, the expansion of the
boundaries of heart, muting tones and systolic
murmur.
Laboratory signs: a decrease in the level Hb and a
drop in hematocrit (lower than 35% in children,
37% in girls and 42% in youths)
 Sideropenic Syndrome (Deficit of Iron)

dystrophic changes in the skin and its appendages

(shedding of hair, the brittleness of nails), the
atrophy of the mucous membranes of nose,
esophagus and stomach, gingivitis, glossitis,
angular stomatitis);
the distortion of taste and sense of smell
muscular pain (deficit of myoglobin)
muscular hypotonia
alteration in the nervous system: slowing down of
conditioned reflexes, decrease attentiveness,
worsening of memory, delay of intellectual
development.
 Laboratory Signs of Iron Deficit Anemia
A decrease MCV - less than 75
Reduction in the colored index - less than 0,85
Increase RDW
A decrease MCHC - less than 30.
Morphology of the erythrocytes - hypochromic,
anisocytosis and poikilocytosis
Biochemical - decrease level of serum ferritin
Decrease level of serum iron
Increase Total Iron Binding Capacity (TIBC)
Increase level of serum transferrin
 Developmental Stages of Iron Deficiency
Anemia (WHO, 1977)
Pre-latent (exhaustion of tissue reserve of iron;
index of the blood within the standard; there are
no clinical manifestations)
Latent (deficit of iron in the tissue and the
decrease of its reservoir transport; index of the
blood within the standard; clinical picture is
caused by the sideropenic syndrome)
Iron Deficiency Anemia (deviation from the
standard index of the blood in dependence on the
degree of severity; the clinical manifestations in
the form of sideropenic syndrome and general
anemic symptoms)
 Differential Diagnosis of Iron Deficiency
Anemia
it is carried out with other forms of the hypochromic
anemias:
Thalassemia - there are no signs of deficit of iron, the
presence of pathologic hemoglobin with the
electrophoresis.
Sideroblastic Anemia - examination of the puncture
specimen of bone marrow.
Chronic poisoning by lead - specific starts in the
erythrocytes.
Against the background chronic infectious and
inflammatory diseases - hypochromic normocytic (thinner
frequent microcytic) anemia, normal or increased level of
ferritin in combination with the lowered content of serum
iron and transferrin.
 Ferritin
water-soluble complex of iron
hydroxide with the protein apoferritin.
It is located in cells of the liver, spleen,
bone marrow, in the reticulocytes.
Ferritin is the basic protein in human
which deposits iron and concentration
of ferritin in the serum reflects the
reserve of iron in the organism.
 Serum Transferrin
(Beta-globulin).
Main function - transport of absorbed iron in the depot (liver,
spleen), into the medullary erythroid predecessors and into
the reticulocytes.
Basic place of synthesis - liver.
An increase in the content of transferrin with lowering in the
level of iron of serum is characteristic for the iron-deficiency
state.
A decrease in the level of transferrin can be with the damage
of the liver (different genesis) and with the loss of protein (for
example, in nephrotic syndrome).
The level of transferrin is increased in the last term of
pregnancy.
 Transferrin
LIMITATION
The concentration of TF is subjected to the daily
variations
Acute inflammation contributes to lowering the
TF level
CLINICAL SIGNIFICANCE
Basic clinical index for the differentiation between
the iron-deficiency ([TF]) and hemolytic anemia
([TF])
More precise index than total iron binding
capacity
After the liberation of iron from the complex, TF
ion of Fe3+ must be restored into Fe2+
 Treatment of Iron Deficiency Anemia
Diet: meat, liver, yeast, fish
Oral preparations: recovery rate Hb does
not differ from parenteral introduction, side
effects are less, excessive introduction does
not lead to hemosiderosis.
- Dosage : 1 hour prior to the meal
in the evening time (absorption increase in
the second-half of a day)
During first 3 days - half dose of the selected
preparation.

Possibilities : dark colour of stool and transitory

dyspeptic disorders (nausea, diarrhea or watery
stool)

Check analysis of the blood: in 7-10 days

reticulocyte reaction; 4 weeks - increase Hb and
Ht

During the normalization of the indices of the blood

reduce the dose of preparation
 Parenteral Introduction of Iron
in exceptional cases
in severe iron deficiency anemia
rendering to special aid
intolerance of oral preparations (after repeated
replacement and reduction in the dose)
diseases of gastro-intestinal tract
syndrome of the disrupted intestinal absorbtion
after the extensive resection of the small intestine
continuous blood loss
not compensated by oral method
 Complications of Parenteral
Introduction
Local reactions (pains, phlebitis)
General reactions (anaphylaxis, fever, head
and articulate pains, vomiting, rash,
bronchospasm).
Preparations:
Venofer - for the intravenous introduction,
Maltofer, Ferrum-Lek - intramuscular
 Overdose of Iron

In the first 6-8 hours - epigastral pains, nausea,

vomiting (including with the blood), diarrhea,
pallor, sleepiness, acrocyanosis)

For 12-24 hours - metabolic acidosis,

leukocytosis, there can be spasms, coma, after 2-4
days - necroses of the liver and kidneys.

Treatment: emetic means, stomach lavage, the

method of milk with the egg white, Deferoksamin,
Desferal, symptomatic therapy.
 Iron Overload Syndrome
! Human does not have special mechanism of the excretion
of iron! Its excessive introduction leads to hemosiderosis.
Clinical manifestations: Gradual increase of the dimensions
of the liver, spleen, cardiopathy, suprarenal insufficiency,
diabetes mellitus, eunuchoidism.

Laboratory signs:

Increase in serum iron (more than 30 mmol/liter),

percentage of saturation transferrin by iron it is more than
45%, ferritin of serum it is more than 1000 ng/ml; Test
with desferalom; + the specific signs of the defect of
internal organs (ECG, level biochemical index of functions
of the liver, the level of hormones and others)
Anemia due to the
disturbance of the
proliferation

B12 and Folate

Deficiency Anemia
Megaloblastic
 Causes of B12 Deficiency Anemia
Deficiency of the internal factor of Kastla
Atrophy of the mucous membrane of stomach
as the most frequent reason, gastrectomy
Inflammatory or autoimmune diseases of
small intestine, the removal of its specific
sections
Helminthic invasion (tapeworms),insufficiency
of the vitamin B12 in the food (it is contained
in the meat, bean).
 Causes of Folic Acid Deficiency
Alimentary
Increase in need (prematurity birth, rapid
growth rate, pregnancy)
Feeding by the goat milk
Disease of the small intestine
Comsumtion of folate antagonist with
metatreksat
Anti-convulsant (diphenine),oral contraceptives
Chronic hemolysis
 Clinical
Anaemic syndrome
Skin is pale with the lemon shade

Slight jaundice of the scleras

Disturbance of the proliferation of the

epithelium of gastro-intestinal tract: dry-
red tongue, loss of appetite, achylia,
diarrhea, erosive and ulcerous changes
in the mucous membranes
Only for B12-Deficiency Anemia

Damage of CNS - funicular myelosis

(degeneration and the sclerosis of the
posterior and lateral horn of spinal cord),
paresthesia, paralyses with the disorder of
the function of pelvic organs.
 Diagnosis of B12 and Folate
Deficiency Anemia
General Analysis of Blood:
reduction in the quantity of erythrocytes and
hemoglobin hyperchromatic (macrocytic)
anisocytosis of the erythrocytes

hyper-segmentation of the neutrophils

Jolly body and Cabbots rings as the

microscopical picture of the erythrocytes
 Continuation
Reduced reticulocyte in blood count
Normoblasts in the smear of the blood

Leucopenia, thrombocytopenia

Bone marrow:
Irritation in erythroid growth,
megaloblasts, the disintegration of
erithrokaryocytes.
 Biochemical Analysis of Blood
an increase in unconjugated bilirubin
an increase in serum iron

12 decrease or

Folate status (Folic acid in the blood)

decrease
 Criteria of Effective Treatment
Subjective improvement during the first days of
treatment;
Reticulocytosis, maximally expressed (to 20%)
on 5-7th day of treatment;
Increase in hemoglobin and number of
erythrocytes, beginning from the 2nd week of
treatment;
The normalization of the blood index, number
of leukocytes and thrombocytes in 3-4 weeks of
treatment.