ANEMIA

DIAGNOSIS AND MANAGEMENT

WHAT IS ANEMIA?

• Defined as the decrease below the normal limit(below the normal limit the
reference level for the age and sex of the individual)of the hemoglobin
concentration , erythrocyte count or hematocrit(ratio of packed red cells to
total blood volume)
• It can also be defined as a reduction of the total circulating red blood cell
mass, below normal limits
• Functionally it is the decrease of oxygen carrying capacity of blood which
leads to tissue hypoxia.
INDICES TO NOTE

• Mean Corpuscular Volume

82-98 fl
• Mean Corpuscular Hemoglobin
27-32pg
• Mean Corpuscular Hemoglobin Concentration
31-35g/dL
• Red cell Distribution Width
11.5-14.5%
Normal Hb levels:
Males- 14 to 18g/dL
Females- 12 to 16g/dL
CLASSIFICATION: MORPHOLOGICAL

• Size:
Normocytic
Microcytic(<80 fl)
Macrocytic(>100fl)
• Degree of Haemoglobinization
Normochromic
Hypochromic(<30g/dL)
CLASSIFICATION: ETIOLOGY

• Blood Loss:
Trauma
Gastrointestinal lesions
• Impaired Red Blood Cell Production:
Nutritional Decencies-Iron, Vit B 12, Vit B9
Genetic defects-Thalasemia
Immune mediated
• Increased Red blood Cell Production(Hemolytic Anemias):
Enzyme deficiencies-G6PD
RBC membrane disorders-Spherocytosis
Trauma
Toxic Injury-Snake bite
 COMMON PRESENTING COMPLAINTS THAT
ACCOMPANY ANEMIA:
• General Signs and Symptoms:
Fatigue, malaise, and lassitude are seen in patients with moderate to severe anemia
Weight loss is seen in malignancies, HIV and tuberculosis which can also cause
anemia
• Nervous System Complaints:
Headache is seen in severe anemia
Paresthesia may occur because of peripheral
neuropathy in pernicious anemia
Confusion may occur with severe anemia
• Eyes
Conjunctival Pallor
• Ear
Vertigo, tinnitus, and “roaring” in the ears may occur
with marked anemia
• Nose
In some cases of severe Anemia ; epistaxis can be seen
• Oral Cavity
Pale and bald tongue in anemia, red beefy tongue in Vit B12 deficiency.
• Chest and Heart
Exertional dyspnea and palpitations are seen in
anemia.
Congestive heart failure can occur in severe anemia
• Gastrointestinal System
Dysphagia may occur due to iron deficiency
(Plummer-Vinson disease).
Abdominal pain may occur in abdominal crises of
sickle cell disease
• Skin and Nails
-Pallor is seen in anemia.
-Platynychia (flat nails) and koilonychia (spoon shaped
nails) are seen in iron deficiency anemia.
-Jaundice may be present in pernicious anemia or
hemolytic anemia
IRON DEFICIENCY
• Symptoms
-Insidious onset of fatigue and exertional dyspnea.
-Palpitations, tinnitus and headache due to hyperdynamic circulation.
-Dysphagia which is more for solids than for liquids due to formation of mucosal webs at the
pharyngoesophageal junction (Plummer-Vinson syndrome).
-Amenorrhea or menorrhagia, excess hair loss and Pica due to iron deficiency.-
-Geophagia is common in children and pregnant women. Pagophagia (excessive eating of
ice) may be seen, especially in women. All forms of pica are relieved by iron therapy even
before the anemia is corrected.
-Iron deficiency also causes functional impairment of various tissues such as the
myocardium, peripheral nerves, jejunum, cerebral cortex, kidneys and liver.
• Signs
-Glossitis and angular stomatitis may be present.
-Papillary atrophy of the tongue makes it appear
smooth and pale (bald tongue).
-Flattening and concavity of the nails are called
platynychia and koilonychia respectively
-Mild hepatosplenomegaly may be present
• Investigations:
• -Complete blood picture—RBC count, hemoglobin, hematocrit, MCV, MCH
and MCHC are all decreased in iron deficiency anemia.
• -Peripheral blood smear—it shows microcytic hypochromic RBCs. There
may be other morphological abnormalities such as poikilocytosis and
presence of target cells
• -Serum iron is decreased, TIBC is increased, transferrin saturation is low, and
serum ferritin is less than 10 μg/L.
• -Bone marrow shows micro normoblasts. Iron stores are absent or markedly
reduced.
 TREATMENT:
• Main form of Treatment is Iron therapy it can be either oral or parenteral
-Oral forms-ferrous fumarate, ferrous sulfate and ferrous gluconate
-Hemoglobin level will normalize in about 6–8 weeks of iron therapy. However, iron therapy has
to be continued for a total of 6 months to ensure repletion of the body iron stores.
-Adverse effects of oral iron include nausea, vomiting, epigastric discomfort, constipation or
diarrhea
• Parenteral Iron Therapy
Indications: It is indicated in patients who cannot tolerate oral iron and in pregnant
women who present with severe anemia very late in pregnancy. Patients with
gastrointestinal diseases such as peptic ulcer and ulcerative colitis are likely to be
aggravated by oral iron and need parenteral iron.

Side effects:
Local reactions include pain, muscle necrosis, and phlebitis in adjacent vessels.
Other systemic effects include fever, urticaria, joint pains, nausea, vomiting,
diarrhea, abdominal pain, backache, body ache, chest pain, angioneurotic edema,
and hypotension
 MACROCYTIC ANEMIA/PERNICIOUS ANEMIA
• Symptoms:
-Easy fatigability, weakness, dyspnea, and effort intolerance
-Hyperdynamic circulation due to anemia may lead to palpitations, tinnitus and
headache.
-Vit B12 deficiency causes atrophic glossitis and neurologic symptoms
-Vit B12 deficiency causes symmetrical peripheral neuropathy. In severe
deficiency, subacute combined degeneration
-Other neurologic symptoms of Vit B12 deficiency include memory loss,
irritability, and dementia.
INVESTIGATIONS
• Complete blood count
-Hemoglobin level is low.
- Mean corpuscular volume (MCV) is over 100 fl (normal 80–95).
- Mean corpuscular hemoglobin (MCH) and mean corpuscular hemoglobin
concentration (MCHC) are usually normal.
• Peripheral blood smear
- Shows oval macrocytes, few myelocytes and occasional normoblasts. There is
anisocytosis and poikilocytosis
-Hyper segmented neutrophils are common.
• Vit B12 and folic acid levels
• Shcilling test can be done to diagnose the cause of Vit B12 deficiency
• Upper GI scopy is useful in cases of pernicious anemia.

• Treatment:
Packed red cell transfusion is given. Before transfusion it is necessary
to collect samples for B12 and folic acid estimation.
Vit B12 replacement:
Vit B12 should be replaced by parenteral route since malabsorption is the cause most of the time.
1000 μg should be given intramuscularly per week for 4 weeks, followed by 1000 μg every month for
the rest of the patient’s life.
Any underlying cause of Vit B12 deficiency should be treated (e.g. antibiotics for intestinal bacterial
overgrowth, deworming for tapeworm infestation
PERNICIOUS ANEMIA:

• Additional Investigations:
-Histamine or pentagastrin test: Acid secretion does not increase even after
injection of histamine or pentagastrin.
-Barium meal examination: Shows atrophic mucosal pattern of stomach.
FOLIC ACID DEFICIENCY

• Clinical Features
-Macrocytic anemia.
-Folate deficiency does not cause neurologic symptoms (unlike Vit B12
deficiency). Only depression, irritability, poor judgment, forgetfulness and
sleep deprivation have been seen in some patients.
-Glossitis is less common than in vitamin B12 deficiency.
-Anorexia and occasional diarrhea may be present.
• Investigations
- Low serum folate levels (normal–6 to 20 ng/mL;
-values ≤4 ng/mL are diagnostic of folate deficiency).
- Peripheral blood smear shows macrocytes.
-Bone marrow shows megaloblastic picture.
-Elevated serum homocystiene levels and normal methylmalonic acid levels.
Management:
• Correct the underlying cause.
• Oral folic acid supplementation (5–15 mg/day) should be given in deficiency
states.
• It should be given prophylactically (350 μg/day) to all pregnant women,
premature babies, patients receiving dialysis, and in severe and chronic hemolytic
states.
• Patients receiving folic acid antagonists such as methotrexate should be given
folinic acid daily orally (15 mg).
• In the presence of Vit B12 deficiency, folate therapy can aggravate neurological
symptoms. Hence, care should be taken to replace Vit B12 before folate therapy.
BLOOD LOSS ANEMIA

Treatment
• In acute blood loss, volume replacement either by blood transfusion, or IV
fluids is very important.
• In chronic blood loss anemia, if the patient is severely anemic, packed RBC
should be transfused.
• Underlying cause of blood loss should be treated in both acute and chronic
blood loss.
HEMOLYTIC ANEMIAS.

Physical Findings
• Anemia.
• Mild jaundice.
• Splenomegaly.
• Hemolytic facies due to marrow hyperplasia in skull bones and other bones.
• Ankle ulcers (seen in sickle cell anemia).
• Signs of any underlying disease responsible for hemolysis.
INVESTIGATIONS

Evidence of Increased RBC Destruction:

- Indirect hyperbilirubinemia, usually less than 5 mg/dl.
• Increased urobilinogen excretion in urine.
• Decreased plasma haptoglbin and hemopexin.
• Increased plasma lactate dehydrogenase (LDH).
• Shortened RBC survival as demonstrated by chromium-51 labeled RBCs
• Evidence of Increased RBC Production:
- Increased reticulocyte count (reticulocytosis).
- Finding premature RBCs in peripheral smear (macrocytes, polychromasia,
nucleated RBCs).
- Erythroid hyperplasia of bone marrow
Additional Findings in Intravascular Hemolysis
Hemoglobinuria.
Hemosiderinuria.
TESTS

• Peripheral blood smear examination.

• Coomb’s test (to detect antibodies causing hemolysis).
• Hemoglobin electrophoresis (for thalassemias).
• Osmotic fragility, sucrose lysis and hams test (for membrane defects).
• Measurement of enzyme activity (G6PD, pyruvate kinase).
• Other tests are done depending on the suspected
• underlying cause.
TREATMENT
• Supportive Therapy
- Blood transfusion for severe anemia
-Replacement of vitamins due to increased erythropoiesis (iron, folic acid)
- Treatment of infections
- Treatment of ankle ulcers
- Splenectomy in selected cases
Specific Therapy
- This depends on the underlying cause—steroids for immune hemolytic anemia, splenectomy
in sickle cell anemia and hereditary spherocytosis, withdrawal of offending drug, etc.
APLASTIC ANEMIA

Clinical Features
• The onset is insidious and symptoms and signs are due to anemia, leukopenia and
thrombocytopenia (pancytopenia).
• Anemia causes easy fatigability, exertional dyspnea and pallor.
• Leukopenia causes recurrent infections (pneumonia, urinary tract infections, fungal infections,
septicemia).
• Thrombocytopenia causes bleeding manifestations (mucosal hemorrhages, menorrhagia, and
petechiae).
• Splenomegaly and lymphadenopathy are not a feature of aplastic anemia
Investigations
• Hemoglobin is low.
• There is pancytopenia.
• Reticulocyte count is low in relation to the degree of anemia.
• ESR is elevated.
• Peripheral blood smear shows pancytopenia and normochromic-normocytic RBCs. No
abnormal cells are seen in peripheral blood.
• Direct and indirect Coombs’ tests
• Bone marrow examination shows profoundly hypocellular
• marrow with a decrease in all cell elements
THERAPY:

• Antifibrinolytic agents (tranexamic acid or epsilonamino caproic acid)

• Blood and platelet transfusions should be used sparingly in patients who are
candidates for hematopoietic stem cell transplantation to avoid sensitization
• Bone marrow transplantation
• Immunosuppressive regimens are recommended for those above 45 years.
They are not curative, but improve survival
THANKYOU