Dr. Sachin Verma is a young, diligent and dynamic physician. He did his graduation from IGMC Shimla and MD in Internal Medicine from GSVM Medical College Kanpur. Then he did his Fellowship in Intensive Care Medicine (FICM) from Apollo Hospital Delhi. He has done fellowship in infectious diseases by Infectious Disease Society of America (IDSA). He has also done FCCS course and is certified Advance Cardiac Life support (ACLS) and Basic Life Support (BLS) provider by American Heart Association. He has also done a course in Cardiology by American College of Cardiology and a course in Diabetology by International Diabetes Centre. He specializes in the management of Infections, Multiorgan Dysfunctions and Critically ill patients and has many publications and presentations in various national conferences under his belt. He is currently working in NABH Approved Ivy super-specialty Hospital Mohali as Consultant Intensivists and Physician.

1. Dr. Sachin Verma MD, FICM, FCCS, ICFC
Fellowship in Intensive Care Medicine
Infection Control Fellows Course
Consultant Internal Medicine and Critical Care
Web:- http://www.medicinedoctorinchandigarh.com
Mob:- +91-7508677495

2. • Bone marrow
– Pluripotent stem cells
– Chemical regulation
• Cytokines
• Erythroid specific growth factor
• Erythropoietin (EPO)
– Life span
• Reticulocyte- 4 days
• RBC –120 days

3. Anemia-values of hemoglobin, hematocrit or RBC
counts which are below the values expected for
age and sex matched normal subjects.
HGB<13 g/dL (men) <12 (women)
HCT<41% (men) <36 (women)

4. HISTORY
- family history
- ethnicity geographical distribution
-Is the patient bleeding?
Actively? In past?
-Is there evidence for increased RBC
destruction?-jaundice, gall stone etc
-Is the bone marrow suppressed?
-Is the patient nutritionally deficient? Pica?
-medication review, toxin exposure
-history of chronic diseases,fever ,weight
loss etc.

5. REVIW OF SYMPTOMS
Decreased oxygen delivery to tissues
-Exertional dyspnea
-Dyspnea at rest
-Fatigue
Signs and symptoms of hyperdynamic state
-Bounding pulses
-Palpitations
Life threatening: heart failure, angina,
myocardial infarction
Hypovolemia
-Fatiguablitiy, postural dizziness,
lethargy,hypotension, shock and death

6. PHYSICAL EXAM
•Stable or Unstable?
-ABCs
-Vitals
•Pallor
•Jaundice
-hemolysis
•Lymphadenopathy
•Hepatosplenomegally
•Bony Pain
•Petechiae
•Rectal-? Occult blood

7. Functional Classification :
Hypoproliferative
Ineffective erythropoesis
Increased Destruction/hemolytic or blood loss
Classification by Morphology:
Normocytic
Microcytic
Macrocytic

8.  I.Complete blood count (CBC)
 A. Red blood cell count
1. Hemoglobin
 2. Hematocrit
 3. Reticulocyte count
 B. Red blood cell indices
 1. Mean cell volume (MCV)
 2. Mean cell hemoglobin (MCH)
 3. Mean cell hemoglobin concentration (MCHC)
 4. Red cell distribution width (RDW)
 C. White blood cell count
 1. Cell differential
 2. Nuclear segmentation of neutrophils
 D. Platelet count
 E. Cell morphology
1. Cell size
 2. Hemoglobin content
 3. Anisocytosis
 4. Poikilocytosis
 5. Polychromasia

9.  II. Iron supply studies
 A. Serum iron
 B. Total iron-binding capacity
 C. Serum ferritin
 III. Marrow examination
 A. Aspirate
 1. M/E ratioa
 2. Cell morphology
 3. Iron stain
 B. Biopsy
 1. Cellularity
 2. Morphology

10. An accurate reticulocyte count is key to the initial classification
of anemia. Normally, reticulocytes are red cells that have been
recently released from the bone marrow. They are identified
by staining with a supravital dye that precipitates the
ribosomal RNA (Fig. 58-12). These precipitates appear as blue
or black punctate spots. This residual RNA is metabolized over
the first 24–36 h of the reticulocyte's lifespan in circulation.
Normally, the reticulocyte count ranges from 1–2% and reflects
the daily replacement of 0.8–1.0% of the circulating red cell
population. A reticulocyte count provides a reliable measure
of red cell production.
In order to use the reticulocyte count to estimate marrow
response, two corrections are necessary

11. The first correction adjusts the reticulocyte count based on the reduced number
of circulating red cells. With anemia, the percentage of reticulocytes may be
increased while the absolute number is unchanged.
For this second correction, the peripheral blood smear is
examined to see if there are polychromatophilic macrocytes
present. These cells, representing prematurely released
reticulocytes, are referred to as "shift" cells. The correction is
necessary because these prematurely released cells survive as
reticulocytes in circulation for >1 day, thereby providing a
falsely high estimate of daily red cell production. If
polychromasia is increased, the reticulocyte count, already
corrected for anemia, should be divided again by a factor of 2
to account for the prolonged reticulocyte maturation time

12. Correction #1 for anemia:
This correction produces the corrected reticulocyte count
In a person whose reticulocyte count is 9%, hemoglobin 7.5 g/dL, hematocrit 23%, the
absolute reticulocyte count = 9 x (7.5/15) [or x (23/45)]= 4.5%
Correction #2 for longer life of prematurely released reticulocytes in the blood:
This correction produces the reticulocyte production index will
In a person whose reticulocyte count is 9%, hemoglobin 7.5 gm/dL, hematocrit 23%, the
reticulocyte production index will be 4.5/2(maturation time correction)

14. MCV
Microcytic Normocytic Macrocytic
(MCV<80) (80<MCV<100)(MCV>100)

15.  -The presence of anemia with an inappropriately low
reticulocyte production index, macro- or microcytosis
on smear, and abnormal red cell
 -divided into two categories: nuclear maturation
defects, associated with macrocytosis and abnormal
marrow development, and cytoplasmic maturation
defects, associated with microcytosis and hypochromia
usually from defects in hemoglobin synthesis.
 -The inappropriately low reticulocyte production index
is a reflection of the ineffective erythropoiesis that
results from the destruction within the marrow of
developing erythroblasts.
 -Bone marrow examination shows erythroid
hyperplasiaoglobin synthesis

16. Anemia of Chronic Disease
Iron Deficiency
Lead PoisoningThalassemia
Sideroblastic

17. Gold Standard?
Bone marrow aspirate
Lab studies?
Ferretin
Serum iron
Total Iron Binding Capacity
Fe Saturation

18. Ferritin Serum TIBC RDW
Fe
Fe defic decreas decreas increase (>15)
AOCD N/incre decreas decreas N
Sideroblasti N/incre N/incre N N
c
Thalassemia N/incre N/incre N N/

19. Normal serum iron:50-150ug/dl
Normal serum ferritin:100ug/L
(male)and 30ug/L (female)
Normal TIBC :300-360ug/dl
Normal percentage saturation(serum
iron/TIBCx100):25-50%
MCV(hamatocritx10)/ (red cell countx10 ):82-98
MCH(hemoglobinx10/(red cell countx10 ):27-33
MCHC (MCH/MCV) :31-34

20.  General examination : Jaundice, pallor
 Other physical findings : Spleen may be enlarged;
bossing of skull in severe congenital cases
 Hemoglobin :From normal to severely reduced
MCV, MCH : Usually increased
 Reticulocytes : Increased
 Bilirubin : Increased (mostly unconjugated)
 LDH : Increased (up to 10X normal with
intravascular hemolysis)
 Haptoglobin : Reduced to absent

21. Intracorpuscular Defects
Hereditary:
Hemoglobinopathies
Enzymopathies
Membrane-cytoskeletal defects
Acquired :
Paroxysmal nocturnal hemoglobinuria (PNH)

22.  Extracorpuscular Factors
 Familial hemolytic uremic syndrome (HUS)
 Mechanical destruction (microangiopathic)
 Toxic agents
 Drugs
 Infectious
 Autoimmune

23.  Mismatched blood transfusion
 PNH
 Septicemia
 Microangiopathic
 March hemoglobinuria
 In all these cases hemoglobinuria is the unique
feature

24.  -comprises 75% of all anemias
 -reflects absolute or relative marrow failure in which
the erythroid marrow has not proliferated
appropriately for the degree of anemia.
 -can result from marrow damage, iron deficiency, or
inadequate EPO stimulation.
 -loewEPO production may reflect impaired renal
function, suppression of EPO production by
inflammatory cytokines such as interleukin 1, or
reduced tissue needs for O2 from metabolic disease
such as hypothyroidism

25.  Pancytopenia with Hypocellular Bone
Marrow
 Acquired aplastic anemia
 Constitutional aplastic anemia (Fanconi's
anemia, dyskeratosis congenita)
 Some myelodysplasia
 Rare aleukemic leukemia (AML)
 Some acute lymphoid leukemia
 Some lymphomas of bone marrow

26.  Pancytopenia with Cellular Bone Marrow
 Primary bone marrow diseases
 Myelodysplasia
 Paroxysmal nocturnal hemoglobinuria
 Myelofibrosis
 Some aleukemic leukemia
 Myelophthisis
 Bone marrow lymphoma
 Hairy cell leukemia
 Secondary to systemic diseases
 Systemic lupus erythematosus
 Hypersplenism
 B12, folate deficiency
 Overwhelming infection
 Alcohol
 Brucellosis
 Sarcoidosis
 Tuberculosis
 Leishmaniasis