DR. HARIKRISHNAN.R.

MBBS,
MD(MEDICINE)
PGD HSc.DIABETOLOGY ( AU)
C .DIAB ( DR.MOHAN’S CENTRE– WHO
AFFILIATED)
PHYSICIAN- DIABETOLOGIST
ASSOCIATE PROFESSOR
INTERNAL MEDICINE & HAEMATOLOGY
MEDICAL COLLEGE TRIVANDRUM
 Anemia is defined as an absolute reduction in
the quantity of the oxygen-carrying pigment
hemoglobin (Hb) in the circulating blood.
 Reduction in HB for the age & gender of the
individual.
Criteria for Diagnosis of Anemia

Hb.( g/dl) Hct (%)

Children < 11.0 33

Male < 13.0 40

Female ( 15-50 ) < 12.0 36

Female ( > 50 ) < 13.0 40

Pregnant women < 11.0 33

 Anemia is broadly subcategorized into acute
and chronic.

 Anemia usually is grouped into 3 etiologic

categories:
 1)decreased red blood cell (RBC) production,
 2)increased RBC destruction, and
 3)blood loss.
 Anemia is a manifestation of an underlying
disease process and is not a diagnosis in
itself.
 A wide array of diseases, including
inflammations, infections, and malignancies,
may at some point be associated with
anemia.
 A disease may lead to anemia through a
combination of mechanisms.
 For example, a GI malignancy may cause
anemia through blood loss, as well as lead to
anemia of chronic disease.
 1)Microcytic hypochromic anemia
 Chief causes of this condition include iron
deficiency, thalassemia, sideroblastic anemia
and lead poisoning.
 Anemia of chronic disease commonly is
manifested by normocytic normochromic
indices; however, microcytic hypochromic
indices also can be associated with anemia of
chronic disease.
 Many RBCs
smaller than
nucleus of normal
lymphocytes,
increased central
pallor.
 Iron deficiency,
thalassemias,
anemia of chronic
disease.
 2)Macrocytic anemia
Main causes of macrocytic anemia include
 Vitamin B-12 deficiency
 Folate deficiency
 Liver disease
 Hypothyroidism
 Alcoholism, drugs
 BMFS
 Most RBCs larger
than nucleus of
normal
lymphocytes,
increased MCV.
 Folate or Vitamin
B12 deficiencies,
alcoholism, and
liver disease.
 Vitamin B 12 Folate Deficiency
Deficiency
MCV > 100 > 100
Smear Macrocytosis with Macrocytosis with
hypersegmented hypersegmented
neutrophils neutrophils

Pernicious anemia Yes NO

Homocystine Elevated Elevated

Methylmalonic Acid Elevated NORMAL

 3)Normocytic anemia
 Normocytic anemia is further divided into 2
broad categories:
 a) Anemia with primary bone marrow
involvement and
 b) Anemia secondary to underlying chronic
disease.
 Anemias with primary bone marrow
involvement further includes aplastic
anemia and myelophthisic anemia.
 The etiology of myelophthisic anemia
involves interruption of normal
hematopoiesis due to the accumulation of
malignant or reactive cells or cell products.
 It is characterized by the appearance of
immature myeloid cells and nucleated RBCs in
the peripheral blood. (LEBP)
 The 3 major classes of disorders that can
produce myelophthisic anemia are
 (1)Intrinsic bone marrow malignancies (eg,
leukemia, lymphoma, myeloma),
 (2) metastatic tumors (eg, neuroblastoma,
melanoma) & cancers that are more prone to
bone marrow metastasis (eg, prostate, breast,
lung, stomach, renal carcinomas), and
 (3)granulomatous disease (eg, tuberculosis,
sarcoidosis).
 Most cases of anemia in the world are
secondary to an underlying disease.
 The marrow does not respond appropriately
to microcytic anemia, leading to decreased
production of RBCs.
 This type of anemia includes that associated
with liver cirrhosis, uremia, chronic
inflammations and infections, and
hypoendocrine conditions (eg, thyroid,
adrenal, pituitary disorders).
 This type of anemia includes sickle cell
anemia, thrombotic thrombocytopenic
purpura (TTP), hemolytic uremic syndrome,
aortic valve prosthesis, disseminated
intravascular coagulation (DIC), cold
agglutinin disease, and paroxysmal cold
hemoglobinuria (PCH).
 The incidence of anemia mirrors the
incidence of the underlying cause.
 Some published studies report the incidence
of anemia to be 2-15% in the general
population globally but this is higher in India.
 Anemia is far more common in
underdeveloped countries.
 The true incidence of anemia is difficult to
define because of multiple factors (eg, patient
population, geographic location, normal
range reference, ability to adequately screen
for the disease).
 African Americans have a higher incidence of
sickle cell anemia and glucose-6-phosphate
dehydrogenase (G-6-PD) deficiency.
 Mediterranean populations show a higher
incidence of beta thalassemia.
 Sex distribution varies based on the
underlying cause.
 Overall, females have approximately twice the
incidence of males of anemia.
 Anemia is prevalent in all age groups.
 Some younger patients may have a better
ability to compensate for anemia, which may
delay initial diagnosis.
 A comprehensive history and physical
examination are vital in determining the
cause of anemia.
 For example, a family history of a dominant
inheritance pattern would suggest
spherocytosis.
 In addition, knowing what medications the
patient is taking is vital, as many drugs and
toxins can cause anemia (eg, alcohol,
isoniazid, lead).
 The spectrum of symptoms manifested by
anemia is dependent on many factors,
including underlying medical condition,
medications, rate of onset, and the
individual's ability to compensate for the
deficit.
 The hallmark of chronic anemia is the ability
of patients to sustain a relatively normal level
of function at significantly lower than normal
Hgb levels.
 Primary symptoms result from tissue hypoxia
and might include the following:
 Fatigue, weakness, irritability
 Headache
 Dizziness, especially postural
 Vertigo
 Tinnitus
 Syncope
 Dyspnea, especially with increased physical
activity (exercise intolerance)
 Chest pain, palpitations
 Difficulty sleeping or concentrating
 Thirst
 Anorexia
 Decreased urine output/bowel irregularity
 Decreased libido or impotence
 Physical findings mirror the underlying
disease process and the duration from the
onset.
 Patients with chronic anemia usually do not
manifest typical physical findings associated
with acute anemia.
 The usefulness of skin pallor as a sign is
limited by the color of the skin, the HB
concentration, and the fluctuation of blood
flow to the skin.
 The colour of the palmar creases is a better
indicator. If they are as pale as the
surrounding skin, Hb is usually less than 7
g/dL.
 Patients also may exhibit purpura, petechiae,
and jaundice.
 Ocular findings may include the following:
 Pale conjunctiva
 Retinal hemorrhages
 Cardiovascular findings may include the
following:
 Tachycardia
 Orthostatic hypotension

 Pulmonary findings may include the

following:
 Tachypnea
 Rales
 Abdominal findings may include the following:
 Hepatomegaly and/or splenomegaly
 Ascites
 Masses
 Positive result on Hemoccult test
 Neurologic findings may include the following:
 Peripheral neuritis/neuropathy
 Pyramidal signs
 Mental status changes
 The following laboratory measurements are
critical in the workup of anemia:
 Measurement of red blood cell (RBC) indices
 Examination of peripheral blood smear
 Bone marrow examination (not necessary in
all patients)
 Additional laboratory tests that allow
differentiation of anemias based on RBC
index information include the following:
 Serum ferritin
 Serum iron concentration
 Total iron-binding capacity (TIBC)
 Transferrin saturation
 Serum vitamin B-12
 Serum folate
 Serum bilirubin
 Liver function tests (LFTs)
 Thyroid panel
 Hb electrophoresis
 Heavy metal studies
 The ultimate diagnosis of chronic anemia is
based on results of blood studies.
 In the initial emergency department
evaluation, a prudent choice of labs includes
the following:
 Complete blood count (CBC) with leukocyte
differential and peripheral smear
 RBC indices
 Reticulocyte count
 Bilirubin
 RBC
 WBC
 PLATELETS
 MOST NUMEROUS
 7.2 – 8.0 MICROMETRE
 TISSUE RESPIRATION
 LACK NUCLEI/MITOCHONDRION
 CONTAIN HB – IRON CONTAINING PROTEIN,
ACTS IN O2/CO2 TRANSPORT
 LIFESPAN 120 DAYS
 Normal range 4.2-
6.0 million per mm3
in adults.
 Biconcave shape.
 Diameter 7
microns.
 Cells for transport
of O2 and CO2.
 Life span 120
days.
 SERVE IMMUNE FUNCTION
 VARIOUS TYPES
 SPECIFIC FUNCTION AND DIFFERENT
MORPHOLOGY
 NUCLEATED
 5 TYPES
 Normal range 4 -
11 thousand per
mm3 in adults.
 Five types.
 Size 8-20 microns.
 Involved in
fighting infection,
combatting
allergic reactions,
and immune
responses.
 DISCOID
 2-4 MICROM
 3 TYPES OF GRANULES
 ALPHA- FIBRINOGEN, VWF
 DELTA- ADP, SEROTONIN
 LYSOSOMES- ACID HYDROLASES
 3-10 days
 Smallest cells in
the blood.
 Normal range
150,000-400,000.
 Active role in
coagulation and
hemostasis.
Morphology Lab tests Diagnosis
Hypochromic, microcytic Low Fe, high TIBC, low Iron deficiency
ferritin
Hypochromic, microcytic High Hb A2 or high Hb F Beta-
thalassemia
Macrocytic Low B12 or low folate B12 or folate
deficiency
Macrocytic, Normal B12,folate, low WBC, Myelodysplasia
other cell lines abnormal low plt
Normocytic, Low Fe, low TIBC, abnormal Anemia of
normochromic LFT, abnormal RFT high chronic
ESR, normal or high ferritin inflammation
Morphology Lab tests Diagnosis
Nucleated RBC, Other cell lines, Myelofibrosis,
Teardrops marrow aspirate and Marrow infiltration
biopsy
Schistocytes Coombs test, Microangiopathic
PTT, INR, fibrinogen hemolytic anemia, ie.
DIC
Spherocytes Coombs test Immune hemolysis,
Osmotic fragility Hereditary
spherocytosis
Sickle cells Sickling test Sickle cell syndromes

Target cells Abnormal Hb HbC, D, thalassemia

electrophoresis
 MCV

MCV < 80 MCV 80-100 MCV >100

microcytic anemia normocytic anemia macrocytic anemia
 MCV

MCV < 80 MCV 80-100 MCV >100

microcytic anemia normocytic anemia macrocytic anemia

iron deficiency
chronic disease
hemoglobinopathy
sideroblastic anemia
 MCV

MCV < 80 MCV 80-100 MCV >100

microcytic anemia normocytic anemia macrocytic anemia

megaloblastic anemias, alcholism,

drugs, liver disease, primary marrow disorder,
hypothyroidism
 MCV

MCV < 80 MCV 80-100 MCV >100

microcytic anemia normocytic anemia macrocytic anemia

reticulocyte count

increased normal or decreased

evidence of hemolysis
renal, endocrine or chronic disease?
(morphology, biochemistry, Coombs test)

yes no yes no

anemia of chronic
immune non immune recent bleed primary marrow problem
inflammation
 Based on the RBC indices, further blood work
may be initiated in the ED.
 Iron studies may be performed. These can
include ferritin, TIBC, total iron, and
transferrin percent saturation.
 Typically, iron studies are helpful in the
diagnosis of microcytic and normocytic
anemias.
 Serum vitamin B-12, folate levels, and the red
cell folate level are useful in evaluating
macrocytic anemias.
 Order concurrent liver and thyroid function
studies for patients with macrocytic anemia.
 Hb electrophoresis may delineate sickle cell
anemia and thalassemias.
 Osmotic fragility and sickling tests
 Ham’s test, sucrose lysis test with CD 55, 59
detection by flow cytometry.
 ADAMTS mutation analysis
 Heavy metal studies (eg, serum lead level)
may be considered when a high level of
suspicion is present, historically and
clinically, for heavy metal poisoning.
 No specific imaging tests exist for chronic
anemia; however, several imaging modalities
can be used in examining the underlying
etiology (eg, computed tomography [CT]
scanning for abdominal mass, chest
radiography for
histoplasmosis/coccidioidomycosis).
 Bone marrow examination may be diagnostic
in cases in which workup is otherwise
nonspecific.
 This is not a procedure performed in the
acute setting.
 Hematocrit
 Hematocrit also is known as the packed cell
volume (PCV) and indicates the percentage of
RBCs in a volume of whole blood.
 Increased values occur with severe
dehydration, erythrocytosis, polycythemia,
severe burns, and shock, and in people living
in high altitudes, males, and infants.
 Decreased values occur with anemia and the
many differential diagnoses that encompass
anemia (eg, hyperthyroidism, leukemia, liver
disease, hemolytic reactions).
 Other causes of decreased hematocrit values
include female sex, advanced age, and
pregnancy.
 Hematocrit value is not reliable immediately
after blood loss or blood transfusions.
 Hb concentration is expressed in grams per
100 mL of blood.
 Each gram of Hb has a carrying capacity of
1.34 mL of oxygen.
 Increased Hb values can indicate severe
dehydration, erythrocytosis, polycythemia,
severe burns, shock, chronic obstructive
pulmonary disease (COPD), or congestive
heart failure (CHF).
 Increased values also occur in people living in
high altitudes, people consuming drugs such
as gentamicin or methyldopa, and infants.
 Decreased values indicate anemia and the
many differential diagnoses that encompass
anemia (eg, hyperthyroidism, leukemia, liver
disease, hemolytic reactions).
 Overhydration
 Pregnancy
 Drugs (eg, acetaminophen, antineoplastic
agents, chloramphenicol, hydralazine,
monamine oxidase inhibitors [MAOIs],
nitrites, penicillin, tetracycline, sulfonamide)
 Mean corpuscular volume (MCV) is the
hematocrit divided by the RBC count.
 It is a measurement of the volume occupied
by a single RBC and is an indicator of
individual cell size.
 Increased values indicate differentials that
encompass macrocytic anemia (eg, vitamin B-
12 or folate deficiency, liver disease,
alcoholism).
 Decreased values indicate microcytic anemia
(ie, iron deficiency, thalassemia, anemia of
chronic blood loss).
This is the most important of the RBC
indices.
A normal value can appear when a wide
variety of cell sizes is present (ie, macrocyte,
microcyte). ( N : 80- 100)
 Mean corpuscular Hb concentration (MCHC) is
the Hb divided by the hematocrit.
 It represents the average concentration of Hb
in the red blood cells.
 MCHC
 The value is expressed as a percentage.
 Increased values point to spherocytosis (eg,
congenital hemolytic anemia, AIHA)
 Decreased values indicate iron deficiency,
thalassemia, or macrocytic anemia.( N : 32-
36)
 Mean corpuscular Hb (MCH) is the Hb divided
by the RBC count.
 It represents the average weight of Hgb in the
RBCs and serves to confirm the accuracy of
MCV value.
 Increased values occur in macrocytic anemia,
newborns, and infants.
 Decreased values indicate microcytic anemia.
.( N : 28 -32)
 The first question a clinician must address is
whether the anemia is due to a decreased
production of RBCs or to increased
destruction or loss of RBCs.
 The reticulocyte count is the most valuable
test in answering this question.
 A reticulocyte is a nonnucleated, immature
RBC formed in the bone marrow.
 Normal : 0.2 – 2.0 %

 Corrected Reticulocyte count

= RC * Pts HCT/45
 The Reticulocyte PROLIFERATION Index (RPI)
is defined as the corrected reticulocyte count
divided by maturation time
 Good marrow response is defined as an RPI
value of 2-6.
 Reticulocyte index (RPI) =
Corrected Reticulocyte Count/Maturation time
 Maturation time
 1 for HCT 45%
 1.5 for 35%
 2 for 25%
 2.5 for 15%.
 reticulocyte count

low or normal high

bone marrow problem evidence of renal failure, blood loss or hemolysis

endocrine failure,
or chronic inflammation?

MCV anemia of chronic inflamation

microcytic normocytic macrocytic

 Increased values indicate accelerated
erythropoiesis.
 Treatment of anemia, after splenectomy, 3-4
days following hemorrhage, in sickle cell
disease ,hemolytic anemia, during pregnancy,
or in infants.
 Immature RBCs.
 Contain residual
ribosomal RNA.
 Reticulin stains
blue using a
supravital stain
(new methylene
blue).
 Counted and
expressed as % of
total red cells.
 Decreased values indicate decreased RBC
production by the bone marrow and can be a
result of aplastic anemia, chronic infection, or
radiation therapy.
 A persistent reticulocyte deficiency(
reticulocytopenia) is a poor prognostic sign.
 Outpatient depts/EDs rarely treat anemia
beyond the emergent needs.
 Discharging the patient on iron, vitamin B-
12, or folate may mask other problems and
cloud the correct diagnosis.
 Unless cardiopulmonary or cerebrovascular
disease is present, transfusion is rarely
needed in patients who have chronic anemia
with an Hgb greater than 7 g/dL.
 Most patients presenting with chronic anemia are
not in distress.
 Prehospital care most often is initiated for
patients in extremis. Attention to ABCs is most
appropriate. All such patients should have
intravenous (IV) placement, fluid resuscitation,
and airway management as necessary.
 The initial status and appearance of the patient
may hold useful information and should be
elicited from prehospital personnel.
 Patients with chronic anemia usually do not
require intervention in the ED.
 Ultimate treatment requires investigation into the
etiology of the anemia and correction of the
underlying cause.
 Records of previous hospitalizations or ED visits
are invaluable in many aspects of patient
management.
 Such patients frequently have undergone
previous workup, and previous Hb or hematocrit
trends indicate the time course of the illness.
 Patients with chronic anemia requiring
admission include the following:
 Patients presenting with hypovolemia, active
bleeding, angina, tachypnea, altered mental
status, transient ischemic attack (TIA), or
exacerbation of congestive heart failure
(CHF) .
 Patients who demonstrate a considerable
drop in Hb and hematocrit values when
compared with previous values or who have
new-onset or worsening pancytopenia.
 Patients with an initial Hb of less than 10
g/dL or a hematocrit of less than 30%
 Patients who may not comply with follow-up
or those in whom the clinician anticipates the
need for an extensive workup
 Patients can be admitted to a general ward
bed, a monitored bed, or an intensive care
unit (ICU) bed, depending on their condition.
 One conspicuous exception in the treatment
of chronic anemia is the use of transfusion
therapy. Unless cardiopulmonary or
cerebrovascular disease is present,
transfusion is rarely needed in patients who
have chronic anemia with an Hb greater than
7 g/dL.
 Multiple situations that may require
transfusion include angina, chronic heart
failure, transient ischemic attack (TIA), and
signs of tissue hypoxia.
 It is important to weigh the risks and benefits of
blood transfusion.
 Many adverse reactions are associated with
transfusion therapy.
 Most frequently encountered is a febrile
nonhemolytic reaction. Patients who have had
previous transfusion or patients who are
pregnant are at greatest risk. Treatment is
supportive with antipyretics.
 The clinician should maintain a high level of
suspicion for a hemolytic reaction, because fever
may the first symptom.
 Many patients fear infection.
 Hepatitis C occurs in 1 of 1.03,000
transfusions
 Hepatitis B occurs in 1 of 2,00,000
transfusions,
 HIV occurs in 1 of 4,90,000 transfusions.
 The graft versus host reaction is rare but is
especially dangerous in patients who are
immunocompromised. It carries a mortality
rate of greater than 90%.
 Pathogenesis in this reaction involves donor T
lymphocytes attacking host human leukocyte
antigens (HLA).
 High fever, erythematous rash, diarrhea, and
abnormal LFTs associated with recent or
concurrent transfusion may herald the severe
reaction.
 Symptoms may not appear until 8 days after
transfusion, and death occurs in 3-4 weeks.
 Using irradiated blood can decrease the
incidence of graft versus host reaction and
should be considered in all patients deemed
immunocompromised, as well as in fetuses
receiving intrauterine transfusions, patients
receiving units from a blood relative, and
patients transplanted with marrow.
 Care should be taken when transfusing patients
with CHF.
 Preferably, transfusion should occur over 3-4
hours in the sitting position.
 Patients with chronic anemia most often are
treated in the outpatient setting.
 Clear instructions must be given to the
patient regarding proper follow-up.
 Consideration of the patient’s financial
situation and ability to comply with follow-up
care is imperative.
 The key to minimizing complications from
chronic anemia is ongoing reassessment and
patient compliance with proposed medical
therapy.
 Mineral supplements are used to provide
adequate iron for hemoglobin synthesis and
to replenish body stores of iron.
 Iron is administered prophylactically during
pregnancy because of the anticipated
requirements of the fetus and the losses that
occur during delivery.
 Ferrous sulfate is the mainstay treatment for
treating patients with iron deficiency anemia.
 It should be continued for about 2 months
after correction of the anemia and its
etiologic cause in order to replenish body
stores of iron.
 Ferrous sulfate is the most common and
cheapest form of iron used.
 Tablets contain 50-60 mg of iron salt.
 Other ferrous salts( Fumarate, Bisglycinate)
are used and may cause less intestinal
discomfort because they contain a smaller
dose of iron (25-50 mg).
 Oral solutions of ferrous iron salts are
available for use in pediatric populations.
 Carbonyl iron is used as a substitute for
ferrous sulfate.
 It has a slower release of iron and is more
expensive than ferrous sulfate.
 The slower release affords the agent greater
safety if ingested by children.
 On a milligram-for-milligram basis, it is 70%
as efficacious as ferrous sulfate.
 Claims are made that there is less
gastrointestinal (GI) toxicity, prompting use
when ferrous salts are producing intestinal
symptoms and in patients with peptic ulcers
and gastritis.
 Incorrect diagnosis (eg, thalassemia)
 Anemia of chronic disease
 Patient is not taking the medication
 Not absorbed (enteric coated?)
 Rapid iron loss
 Beneficial No benefit Investigational

Anemia of renal failure, with
or without erythropoietin
therapy, Patients with
ongoing blood loss,
Jehovah's Witness patients
with iron deficiency, blood
loss or both
Autologous blood donation
in patients with or without
iron deficiency
Blood loss, iron deficiency,
and erythropoietin therapy,
Anemia of chronic disease
and erythropoietin therapy,
Perisurgical anemia, with or
without erythropoietin

Absolute iron deficiency is defined as ferritin <200 µg/L with or without iron
saturation <20%, or relative iron deficiency (ferritin <400 µg/L in dialysis
patients receiving erythropoietin therapy or the presence of >10%
hypochromic erythrocytes, reticulocytes, or both.
 Dextran-iron replenishes depleted iron stores
in the bone marrow, where it is incorporated
into hemoglobin.
 Parenteral use of iron-carbohydrate
complexes will cause severe anaphylactic
reactions, and its use should be restricted to
patients with an established diagnosis of iron
deficiency anemia whose anemia is
not/cannot be corrected with oral therapy.
 Hemoglobin iron deficit (mg) = weight (kg) x
(14 – Hb of patient) x (2.145)
 For intravenous (IV) use, this agent may be
diluted in 0.9% sterile saline.
 Do not add to solutions containing
medications or parenteral nutrition solutions.
 Iron sucrose is used to treat iron deficiency
(in conjunction with erythropoietin) due to
CKD patients on chronic hemodialysis.
 Iron deficiency in this setting is caused by
blood loss during the dialysis procedure,
increased erythropoiesis, and insufficient
absorption of iron from the GI tract.
 Iron sucrose has shown a lower incidence of
anaphylaxis than other parenteral iron
products.
 Features Iron Dextran Iron Sucrose Sodium Ferric
Gluconate
Nature Dextran complex Sucrose Iron bound with 1
covering iron covering iron gluconate + 4
core oxide core sucrose
Mol. Wt 96-265 kd 34 – 60 kd 289 – 440 kd

Direct Iron No No No
Transfer
Half life 40-60 hours 6 hrs 1 hrs

Renal Excret. Negligible <5% Nil

Brands Imferon Orofer Ferrlecit(NA in

India)
 Vitamins are used to meet necessary dietary
requirements and are used in metabolic
pathways, as well as in DNA and protein
synthesis.
 Cyanocobalamin (vitamin B-12) and folic acid
are used to treat megaloblastic and
macrocytic anemias secondary to deficiency.
 Both vitamin B-12 and folic acid are required
for the synthesis of purine nucleotides and
the metabolism of some amino acids.
 Each is essential for normal growth and
replication.
 Deficiency of either cyanocobalamin or folic
acid results in defective DNA synthesis and
cellular maturation abnormalities.
 Consequences of deficiency are most evident
in tissues with high cell turnover rates (eg,
hematopoietic system).
 Deoxyadenosyl cobalamin and
hydroxocobalamin are active forms of vitamin
B-12 in humans.
 Microbes synthesize vitamin B-12, but
humans and plants do not.
 Vitamin B-12 deficiency may result from
intrinsic factor (IF) deficiency (pernicious
anemia), partial or total gastrectomy, or
diseases of the distal ileum.
 Folic acid is an essential cofactor for enzymes
used in the production of red blood cells
(RBCs).
 Prognosis is dependent on several factors.
 The underlying medical condition usually
dictates the prognosis, but comorbid
conditions, the chronicity of the disease, and
the patient’s diet, age, and access to medical
care are contributing factors.
 The majority of complications in chronic
anemia arise from chronic or persistent tissue
hypoxia.
 Pediatric patients, elderly patients, and
patients who are immunocompromised are at
the highest risk for complications, since they
have less physiologic reserve.
 Failure to comply with follow-up and
treatment regimens predisposes patients with
chronic anemia to complications.
 Low Retic count
 High RDW
 Due to chronic blood
loss
 Diet deficiency
 Precipitated RNA
 lead or heavy metal
poisoning
 Ethanol abuse
 Hemolytic anemia
 Altered lipid in cell
membrane
 artifact
 Uremia
 Renal failure
 gastric CA
 transfused old blood
 Abnormal
cytoskeletal proteins
 Hereditary
elliptocytosis
 Nuclear remnant -
DNA
 hemolytic anemia
 absent or
hypofunction spleen
 Fragmented
(mechanical or
phagocytosis)
 DIC
 TTP
 HUS
 Vasculitis
 prosthetic heart valve
 severe burns
 Molecular
aggregation of Hb-S
 SCA/trait
 Common in newborn
 severe degree of
hemolysis
 Absent central
pallor
 look smaller
 Hereditary
spherocytosis
 Other immune
hemolytic anemia
 Mouth like
 Membrane defect
 Smear artifact
 Hereditary
stomatocytosis
 Liver disease
 Due to Increased
redundancy of
membrane
 hemoglobinopathies
 thalassemia
 liver disease
 Distorted ,drop(tear)
shaped
 Smear artifact
 myelofibrosis
 promyeloblastic
leukemia
 space occupying
lesions of marrow
 Inclusion body

Heinz body- G6PD defy.

 Normal to increased
RPI
 Normal RDW
 Target cells
 Confirm by Hb
electrophoresis
 Accumulation of
mitochondrial iron in
erythroblasts
 Hereditary
 Drugs - INH, lead,
zinc, alcohol,
chloramphenicol,
cycloserine,
clopidogrel
 Hypothermia
 Confirm w/ BM Bx
 Round, purple
inclusions in
RBCs.
 Composed of DNA.
 Commonly seen in
in patients with
hypofunctioning
spleens.
 Splenectomy.
 Numerous, small
purple inclusions
in RBCs.
 Aggregates of
ribosomal RNA.
 Most commonly
seen in lead
poisoning.
 Clusters of dark
blue granules,
irregular in size
and shape.
 Composed of iron
and ribosomal
RNA.
 Seen in
sideroblastic and
hemolytic
anemias.
 Anemia is not the final diagnosis
◦ Need to try and find the cause

 Begin with a thorough history and physical

examination
 Remember basic laboratory approach

◦ Hb
◦ MCV
◦ Retic count
◦ smear
 Know your DDX based on MCV

◦ Microcytic
◦ Macrocytic
◦ Normocytic

 Base further investigations on your DDX