Approach to a patient of anemia1 copy


Published on

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.

  • Be the first to comment

No Downloads
Total views
On SlideShare
From Embeds
Number of Embeds
Embeds 0
No embeds

No notes for slide

Approach to a patient of anemia1 copy

  1. 1. Dr. Sachin Verma MD, FICM, FCCS, ICFC Fellowship in Intensive Care Medicine Infection Control Fellows Course Consultant Internal Medicine and Critical CareWeb:- Mob:- +91-7508677495
  2. 2. • Bone marrow – Pluripotent stem cells – Chemical regulation • Cytokines • Erythroid specific growth factor • Erythropoietin (EPO) – Life span • Reticulocyte- 4 days • RBC –120 days
  3. 3. Anemia-values of hemoglobin, hematocrit or RBCcounts which are below the values expected forage and sex matched normal subjects. HGB<13 g/dL (men) <12 (women) HCT<41% (men) <36 (women)
  4. 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. 5. REVIW OF SYMPTOMSDecreased 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 infarctionHypovolemia -Fatiguablitiy, postural dizziness, lethargy,hypotension, shock and death
  6. 6. PHYSICAL EXAM •Stable or Unstable? -ABCs -Vitals •Pallor •Jaundice -hemolysis •Lymphadenopathy •Hepatosplenomegally •Bony Pain •Petechiae •Rectal-? Occult blood
  7. 7. Functional Classification : Hypoproliferative Ineffective erythropoesis Increased Destruction/hemolytic or blood lossClassification by Morphology: Normocytic Microcytic Macrocytic
  8. 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. 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. 10. An accurate reticulocyte count is key to the initial classificationof anemia. Normally, reticulocytes are red cells that have beenrecently released from the bone marrow. They are identifiedby staining with a supravital dye that precipitates theribosomal RNA (Fig. 58-12). These precipitates appear as blueor black punctate spots. This residual RNA is metabolized overthe first 24–36 h of the reticulocytes lifespan in circulation.Normally, the reticulocyte count ranges from 1–2% and reflectsthe daily replacement of 0.8–1.0% of the circulating red cellpopulation. A reticulocyte count provides a reliable measureof red cell production.In order to use the reticulocyte count to estimate marrowresponse, two corrections are necessary
  11. 11. The first correction adjusts the reticulocyte count based on the reduced numberof circulating red cells. With anemia, the percentage of reticulocytes may beincreased 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. 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%, theabsolute 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%, thereticulocyte production index will be 4.5/2(maturation time correction)
  13. 13. MCVMicrocytic Normocytic Macrocytic(MCV<80) (80<MCV<100)(MCV>100)
  14. 14.  -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
  15. 15. Anemia of Chronic DiseaseIron DeficiencyLead PoisoningThalassemiaSideroblastic
  16. 16. Gold Standard? Bone marrow aspirateLab studies? Ferretin Serum iron Total Iron Binding Capacity Fe Saturation
  17. 17. Ferritin Serum TIBC RDW Fe Fe defic decreas decreas increase (>15) AOCD N/incre decreas decreas NSideroblasti N/incre N/incre N N cThalassemia N/incre N/incre N N/
  18. 18. Normal serum iron:50-150ug/dl Normal serum ferritin:100ug/L(male)and 30ug/L (female) Normal TIBC :300-360ug/dlNormal percentage saturation(serumiron/TIBCx100):25-50%MCV(hamatocritx10)/ (red cell countx10 ):82-98 MCH(hemoglobinx10/(red cell countx10 ):27-33MCHC (MCH/MCV) :31-34
  19. 19.  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
  20. 20. Intracorpuscular DefectsHereditary: Hemoglobinopathies  Enzymopathies    Membrane-cytoskeletal defects   Acquired :Paroxysmal nocturnal hemoglobinuria (PNH)
  21. 21.  Extracorpuscular Factors Familial hemolytic uremic syndrome (HUS)   Mechanical destruction (microangiopathic)     Toxic agents   Drugs     Infectious     Autoimmune
  22. 22.  Mismatched blood transfusion PNH Septicemia Microangiopathic March hemoglobinuria In all these cases hemoglobinuria is the unique feature
  23. 23.  -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
  24. 24.  Pancytopenia with Hypocellular Bone Marrow  Acquired aplastic anemia Constitutional aplastic anemia (Fanconis anemia, dyskeratosis congenita) Some myelodysplasia Rare aleukemic leukemia (AML) Some acute lymphoid leukemia Some lymphomas of bone marrow
  25. 25.  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