APPROACH TO

DIAGNOSIS AND
MANAGEMENT OF A
CASE WITH ANEMIA
DR. DURGESH KUMAR
PUSHKAR
JR III MEDICINE
KGMU
WHO Definition :
Anaemia is a condition in which the
number of red blood cells (and
consequently their oxygen-carrying
capacity) is insufficient to meet the
bodys physiologic needs which vary by
age, sex, altitude, smoking, and
pregnancy status.
It is defined as a hemoglobin level
<130 g/L (13 g/dL) in men and
<120 g/L (12 g/dL) in women.

Khusun H, Yip R, Schultink W, Dillon DH. J Nutr

1999;129(9):16691674
 WHY IS ANEMIA
IMPORTANT?
Anemia is one of the most common disorder
encountered in clinical practice, affecting
around 1.6 billion people around the globe.
It can sometimes be the first clue towards
an underlying disease.
It affects morbidity and mortality in various
chronic diseases in all age groups.
It is mostly a readily correctable disorder
that can influence outcome in the diseased
patient.
CHRONIC EFFECTS OF
ANEMIA
 AETIOPATHOGENESIS
DEFICIEN
T
SUBSTRA
TE
DELIVERY
INCREASE
D LOSS OR DEFECTIV
DESTRUCT E BONE
ION MARROW
ANEMI
A
DEFECTIV
E DEFICIEN
MATURATI T EPO
ON
 CLINICAL APPROACH
fundamental questions that have to be
considered:
What is the rapidity of onset of
symptoms?

What is the cause of the anemia?

What is the urgency for correcting the

anemia, i.e. is a blood transfusion or
other urgent intervention indicated ?
 APPROACH TOWARDS THE DIAGNOSIS

CLINICAL FINDINGS HISTORY OF THE

(SIGNS & SYMTPOMS) PRESENTING
SYMPTOMS
Depend on-
the magnitude and rate of reduction in
the oxygen carrying capacity of the
blood.

the capacity of the cardiovascular and

pulmonary systems to compensate for
the anemia, and
 Clinical manifestations depending on
temporal evolution of symptoms
Classical Classical symptoms
symptoms of of chronic anemia-(
acute anemia- O2 delivery to tissues)
(hypovolemia) Easy fatiguability
shortness of breath Exercise intolerance
tachycardia Lassitude
palpitations Exertional
palpitation
Postural
Exertional dyspnoea
hypotension
extreme fatigue
 Symptoms suggestive of Nutritional
anemia :
Blood in stools
pica
Loose stools/ Clay colour stools
Blood in urine
Pregnancy
Menstrual irregularities
History of Neural Tube Defects in offspring
Tingling and Numbness of bilateral limbs
 Symptoms of Haemolysis :
Yellowish discoloration of eyes and skin
Episodic symptoms
Reversible skin pigmentation

Symptoms suggestive of marrow disorders :

Recurrent upper respiratory tract infections
Episodic jaundice/ abdominal pain/ lumbar pain/
hematuria
Easy bruising/ Gum bleed/ Nose bleed/ Heavy
menstrual flow/ Hemiparesis/ Vision loss
Recent viral illness aggravating anemia symptoms
Stunted growth
Priapism
 Symptoms suggestive of chronic
Inflammation :
Fever
Weight loss
Anorexia
Symptoms related to chronic diseases
like CHF,CKD,CLD, arthritides,
autoimmune diseases and
Endocrinopathies.
 Symptoms suggestive of genetic
disorders :
Early hair greying
Short stature
Dystrophic nails
 Clues from the history
1. Age of Onset-
Early childhood: Genetic disorder of red cells
or hemoglobin producing hemolysis.
Prepubertal age: Nutritional deficiency as
nutrition lags behind growth spurt.
Young people: Chronic infection, chronic
inflammation, malignancy of lymphoreticular
system, inflammatory bowel disease.
In elderly people: Chronic renal failure,
malignancy of G.I. tract, multiple myeloma.
2. Sex-
Female of reproductive age: nutritional
deficiency due to extra demand put by
menstruation, pregnancy and lactation.
Middle-aged female: Hypothyroidism,
chronic inflammatory disease,
including inflammatory bowel disease.
Elderly female/male: Chronic renal
failure, malignancy of genital tract.
3. Family history:
most useful for increasing suspicion of-
hereditary hemolytic diseases (including
hemoglobinopathies)
hereditary bleeding disorders (including
hereditary vascular abnormalities like
hereditary hemorrhagic telangiectasias).
4. History of Bleeding-
Frank bleeding, e.g. bleeding piles, fresh
bleeding with stool, hematuria,
menorrhagia.
Occult bleeding, e.g. drug induced gastric
erosion, undetected esophageal varices or
congestive gastropathy as well as worm
infestation, which may also produce
malabsorption of nutrients.
5. Fever-
Associated with night sweat,
lymphadenopathy, splenomegaly
Chronic infection, chronic
inflammation, malignancy of
lymphoreticular system.
Petechiae, purpura, lympadenopathy,
splenomegaly hematological
malignancy.
Past medical history:
i. Rheumatoid arthritis- anemia of chronic
inflammatory disease or that due to
methotrexate therapy.
ii. Hepatitis or evidence of portal
hypertension-anemia of chronic liver
disease, hypoplastic anemia, or blood loss
from esophageal varices.
iii. Kidney disease or stigmata of chronic
renal disease including hypertension renal
anemia.
iv. Gastric malignancy- Anorexia, persistent
dyspeptic symptoms in spite of continuous
treatment in previously healthy individual
v. HIV infection- multiple sexual exposure,
chronic diarrhea, weight loss.
vi. Hypothyroidism- lethargy, poverty of
thought, sleepiness, feeling of cold
vii. Gastrointestinal operation, chronic
inflammatory bowel disease, may produce
deficiency of intrinsic factor or vitamin B12.
Drug History
i. Prolonged use of analgesic, NSAID, steroid may
produce gastropathy and occult blood loss from G.I. tract.
ii. Use of cytotoxic chemotherapeutic agents may
produce myelosuppression.
iii. Methyldopa may produce immune hemolytic anemia.
iv. Folate antagonists e. g. Methotrexate may produce
folate deficiency
v. Purine and pyrimidine inhibitors like 6-mercaptopurine
or azathioprine and 5-flurouracil may produce folate
deficiency.
7. Occupational Exposure
Lead may produce interference of bone
marrow hemopoiesis, inhibition of hem
synthesis or red cell membrane damage.
8. Dietary habits and addiction-
very young children, those who obtain the
bulk of their nutrition from cows milk (good
for calories, very low in iron) are at great risk
for iron deficiency anemia.
Pure vegetarian diet predisposes to risk of vit
B12 deficiency
Alcoholism also predisposes to megaloblastic
anemia.
 Physical examination

General Systemic
examination: Examination :
Pallor Splenomegaly
icterus
Hepatomegaly
Clubbing
Cyanosis Forceful Heart beat
Lymphadenopath Strong peripheral
y
pulses
Pedal edema
Petechiae/Ecchym Systolic Flow
 Also Look for :
Ascites
Heart failure
Cirrhosis
Endocrinopathies
Neoplasms
To identify the cause of anemia,
information from the medical
history and physical
examination must be integrated
with some key laboratory tests.
 Lab Investigations

Complete Blood counts

Hb :
Occasion Normal Value
(mg/dL)
At Birth 17
Childhood 12
Adolescence 13
Adult Man 16 2
Menstruating 13 2
Adult Female
Post Menopausal 14 2
Adult Female
During Pregnancy 12 2
 Lab Investigations
Hematocrit :
Normal Values
(%)
Adult Male 47 5
Adult Female 42 5
 Lab Investigations
RBC Indices
Indices Normal

MCV 90 8 fL
MCH 30 3 pg
MCHC 33 2 %
RDW 11.5 14.5 %

Other Counts
TLC
DLC
Nuclear Segmentation of Neutrophils
Platelet Count
 Lab Investigations
Red cell Morphology
Cell size
Mirocytic (<80 fL)
Macrocytic (>100 fL)
Anisocytosis ( Variable size )
Poikilocytosis ( Variable Shape )
Polychromasia
( Slightly larger than normal cells,
greyish blue in Wright Giemsa stain
Prematurely released Reticulocytes
having residual ribosomal RNA
After EPO stimulation/ architectural
damage of BM )
 Lab Investigations
Iron Studies

Study Normal Range

Serum Iron 50-150 g/dL
TIBC 300-360 g/dL
Serum Ferritin Males 100 g/ L
Females 30 g/
L
Transferrin 25-50 %
Saturation
 Lab Investigations
Marrow Examination:
Aspirate :
M/E ratio (1:1)
Cell Morphology
Iron Stain
Biopsy
Cellularity (1:1)
Morphology
Signs of Hemolysis:
Unconjugated bilirubin, urobilinogen, S.LDH
Haptoglobins
Positive Urine hemsiderin
 Reticulocyte Count
By Supra vital stains Blue, black
punctate spots (precipitated rRNA)
Life 24 to 36 hrs
Normal range 1-2%
Daily replacement 0.8 to 1%
Response depends on
Availability of EPO
Availability of Iron
Healthy Bone marrow
 Reticulocyte count
Correction for Anemia

Correction for prematurely released

reticulocytes (only when you see
shift cells)
 Evaluation of Basic Hematology
Laboratory Data
Is Anemia Associated with Other
Hematologic Abnormalities?

Thrombocytopenia
or
YE abnormalities in
S white blood cell
numbers or the
presence of NO
Bone marrow abnormal
leukocytes?
examination to
assess for:
Is there an
Leukemia
Aplastic anemia
appropriate
Myelodysplasia reticulocyte response
Myelofibrosis to anemia?
Myelophthisis
 CBC, reticulocyte
count
Index Index <
<2.5 2.5
Red cell
morphology Hemolysis/
Normocytic Micro or hemorrhage
normochromi macrocytic Blood loss
c Maturation Intravascular
Hypoproliferat disorder hemolysis
ive Cytoplasmic
Metabolic defect
defects
Marrow Membrane
Iron deficiency
damage abnormality
Thalassemia
Hemoglobinopat
Sideroblastic
Infiltration/fibros hy
anemia
is Immune
Nuclear defects
Aplasia destruction
Folate deficiency
Iron Fragmentation
Vitamin B12
deficiency hemolysis
deficiency
Dec Drug toxicity
 Is there an appropriate reticulocyte
response to anemia?
YES NO

Is there evidence of What are the

hemolysis? red blood cell
inc. bilirubin, inc. LDH, indices?
dec. haptoglobin,
hemosiderin in urine
YES NO MCV MCV 80- MCV
>100 100 <100

Evaluate Evaluate Evaluate Evaluate Evaluate

for cause for for for for
of Hemorrh macrocyt normocy microcyti
hemolysi agic ic tic c
s Causes anemia anemia anemia
 Diagnostic approach to a
patient with macrocytic
anemia
Does the peripheral blood smear
reveal
hypersegmented neutrophils or
macro-ovalocytes?
 Yes

Megaloblastic anemia
Bone
marrow examination to
confirm; test for vitamin
Vitamin B12 B12 and Nofolate Folate
deficiency deficienc deficiency
y
Schilling Inherited
test disorders
corrects of DNA Poor diet
with synthesis Drug-induced
Yes
Intrinsic No Drugs that malabsorption
factor interfere Jejunal resection
Pernici with DNA
Ileal disease Tropical sprue,
ous Previous ileal surgery gluten sensitivity
anemia Small bowel bacterial Increased needs
Gastric overgrowth associated with
resecti Fish tapeworm pregnancy or
on Drug-induced chronic hemolysis
 No

Nonmegaloblastic anemia

Reticulocytosis
Increased Normal or decreased

Consider:
Hemolytic anemia Alcohol toxicity
Hemorrhagic anemia Hypothyroidism
Liver disease
If above negative,
get bone marrow
examination
Myelodysplasia syndrome
Red cell aplasia
Acquired sideroblastic anem
Hereditary dyserythropoieti
anemia (types I and III)
 Pathogenetic Classification Of
Megaloblastic Anemia
Vitamin B12 Folate deficiency Inherited
deficiency Dietary disorders of DNA
Dietary deficiency deficiency synthesis
(rare) Increased Orotic aciduria
Pernicious anemia requirements: Lesch-Nyhan
Pregnancy syndrome
Gastric surgery
Chronic hemolytic Transcobalamin II
Biologic anemia deficiency
competition for Alcoholism Homocystinuria
vitamin B12: Drug-induced and MMA
Small-bowel bacterial folate deficiency Drug- and toxin-
overgrowth Extensive induced-
Fish tapeworm intestinal Folate antagonists
disease (jejunal) resection Purine
Chronic Combined folate antagonists
pancreatitis and vitamin B12 Pyrimidine
ZES deficiency antagonists
Tropical sprue Alkylating agents
Diseases of the
 Nonmegaloblastic Macrocytic
Anemias
Hemolytic anemia/reticulocytosis
Posthemorrhagic anemia
Alcoholism
Liver disease
Myelodysplastic syndrome
Myelophthisic anemias
Acquired sideroblastic anemia
Congenital dyserythropoietic anemia (CDA) I
and III
Diamond-Blackfan anemia
Hypothyroidism
Spurious macrocytosis (paraproteinemia,
 Diagnostic approach to a
patient with microcytic anemia

RETICULOCYT
ES
 Pathogenic Classification Of
Microcytic Anemias
Disorders of iron metabolism
Iron deficiency anemia
Anemia of chronic disorders
Disorders of globin synthesis
a- and b-thalassemias
Hemoglobin E syndromes (AE, EE, E-b-thalassemia)
Hemoglobin C syndromes (AC, CC)
Sideroblastic anemias
Hereditary sideroblastic anemia
Acquired sideroblastic anemia
Refractory anemia with ringed sideroblasts
Malignancies
Myeloproliferative disorders
Lead intoxication (usually normocytic)
Diagnostic approach to
a patient with
normocytic anemia

Reticulocytes
 Classification Of The Normocytic Anemias
Anemia associated with
appropriately increased
erythrocyte production
Posthemorrhagic anemia
Hemolytic anemia
Decreased erythropoietin
secretion
Impaired source:
Renal: anemia of renal
insufficiency
Hepatic: anemia of liver
disease
Reduced stimulus (decreased
tissue oxygen needs)
Anemia of endocrine
deficiency
Anemia with impaired
marrow response
Red blood cell aplasia
Acquired pure red cell
aplasia in adults
Transient erythroblastopenia
of childhood
Transient aplastic crises
associated with hemolysis
Aplastic anemia
(pancytopenia)
Bone marrow infiltrative
disorders
Leukemia
Myeloma
Other myelophthisic anemias
Myelodysplastic anemias
Congenital dyserythropoietic
 Approach to haemolytic
anemia
A. Establishing the Presence of
Hemolytic Anemia
most common manifestations of
chronic hemolytic anemia include
anemia and reticulocytosis, often
associated with various signs of
excessive blood destruction.
 Laboratory Signs Of Hemolysis
Accelerated red cell destruction
Decreased erythrocyte lifespan
Increased serum unconjugated bilirubin level
Increased rate of urobilinogen excretion
Increased serum lactate dehydrogenase
Decreased serum haptoglobin
Hemoglobinemia
Hemoglobinuria
Hemosiderinuria
Methemalbuminemia
Fall in blood hemoglobin level at a rate >1.0
g/dl/wk
 B. Determining the Specific Cause
of Hemolysis:
Those patients in whom the diagnosis
is clear because of medical history
such as obvious exposure to infectious,
chemical, or physical agents.
Some infections, such as malaria, can
cause hemolysis directly, whereas in other
cases it is more indirect, associated with
an underlying G6PD deficiency or an
unstable Hb, such as Hb H.
Those patients with a positive
direct antiglobulin test.
Such individuals may be presumed to
have immunohemolytic anemia.
The subsequent investigation
requires a search for an underlying
disease as well as a serologic study
of the nature of the antibody.
Those patients with antiglobulin-
negative, spherocytic hemolytic anemia.
Such patients probably have hereditary
spherocytosis.
It is appropriate to confirm the presence of
spherocytes by the osmotic fragility test.
Immunohemolytic anemia may be
associated with spherocytosis and is
occasionally associated with a negative
antiglobulin reaction. Exposure to chemical
or infectious agents producing
spherocytosis may not always be easy to
establish.
Those patients with other specific
morphologic abnormalities of
erythrocytes.
The significance of various types of
abnormally shaped red cells was
discussed previously. Some
poikilocytes, such as elliptocytes and
sickle cells, are virtually
pathognomonic findings.
Those with no specific morphologic
abnormalities and a negative reaction
to the antiglobulin test.
These patients warrant a battery of
screening tests, including:
Hb electrophoresis,
the heat denaturation test for unstable Hb
disease,
G6PD
Pyruvate kinase, and a screening test for
paroxysmal nocturnal hemoglobinuria.
 Classification of Hemolytic Anemias
Inherited Hemolytic Disorders
RBC Membrane abnormalities
Hereditary spherocytosis
Hereditary elliptocytosis syndromes
Hereditary stomatocytosis
Hereditary xerocytosis
RBC Enzyme disorders
Glucose-6-phosphate dehydrogenase (G6PD) deficiency
Pyruvate kinase (PK) deficiency
Glucose-phosphate isomerase (GPI) deficiency
Pyrimidine 5 nucleotidase deficiency
RBC Hemoglobin disorders
Sickle cell anemia syndromes
Thalassemia syndromes
Unstable hemoglobin disorders
Acquired Hemolytic Disorders
Immunohemolytic anemias
Autoimmune hemolytic anemia
Hemolytic disease of the newborn
Transfusion of incompatible blood
Traumatic and traumatic hemolytic anemia
Prosthetic valves and other cardiac abnormalities
Hemolytic uremic syndrome (HUS)
Thrombotic thrombocytopenic purpura (TTP)
Disseminated intravascular coagulation (DIC)
Infection
Protozoa (Malaria, Toxoplasmosis, Leishmaniasis,
Babesiosis)
Bacteria (Clostridial infection, cholera, bartonellosis)
Other causes
Paroxysmal nocturnal hemoglobinuria (PNH)
Associated with hemodialysis and uremia
Thermal red blood cell (RBC) injury
 Management of common
Anemias
IRON DEFICIENY ANEMIA
B12 AND FOLATE DEFICIENCY
ANEMIA
ANEMIA OF CHRONIC DISEASE
HEMOLYTIC ANEMIA
APLASTIC ANEMIA
IRON DEFICIENCY ANEMIA
Absolute & functional iron
deficiency
Depleted body iron stores
Absolute iron Low serum ferritin (<100ng/ml) or
deficiency
TSAT <20%

Inadequate iron supply to meet demand despite

normal or abundant iron stores
Functional
iron Most frequently occurs during ESA therapy
deficiency Normal or high ferritin levels 100 299 ng/ml
TSAT <20%
59 5
9
 Iron Deficiency Anemia

Red cell infusion

Oral Iron
(Symptomatic/ CV
instability/ Elder/ (Young/ Asymptomatic)
Continued blood loss)
R
x Iron
Parenteral
(Oral iron intolerance/ Acute need/
Persistent GI loss/ Malabsorption/ EPO
therapy
ORAL IRON PREPARATIONS
AVAILABLE
Generic Name Tablet (Iron
Content), mg
Ferrous sulfate 325 (65)
195 (39)
Ferrous fumarate 325 (107)
195 (64)
Ferrous gluconate 325 (39)
Polysaccharide iron 150 (150)
50 (50)
 Iron Deficiency Anemia
Oral Iron:
200mg elemental Iron/day
Absorption will be upto 50mg/d (with good
retention capacity)
Supports 2-3x production
Add Ascorbic acid for increased absorption (if
cost effective)
3-4 tabs/day for 6-12 months
GI disturbances (15-20%)
First response : Retic count in 4-7 days;
peak in 7-10 days
 Iron Tolerance test
2 Iron tabs on empty stomach
Serial S.Iron for 2 hrs
At least 100 mcg/dL increase
 Parenteral iron therapy
Intravenous iron can be given to patients who
are-
i. unable to tolerate oral iron;
ii. whose needs are relatively acute; or who need
iron on an ongoing basis,
iii. usually due to persistent gastrointestinal
blood loss.
. The amount of iron needed by an individual
patient is calculated by the following formula:
. Body weight (kg) 2.3 (15 patients
hemoglobin, g/dL) + 500 or 1000 mg (for
stores).
 PARENTERAL FORMS OF IRON

Proper Ideal Iron Iron Ferric Iron

ty dextr sucros Carboxy Isomalt
an e maltose oside
1000
Type Robust Robust Semirobu Robust Robust
st
Half life Long 3-4 6 hours 16 hours 20 hour
days
pH Neutral Neutral High Near- Neutral
Neutral
Osmolal Isotonic Isotonic High Isotonic Isotonic
ity
Antigeni Low High Low Low Low
city
Time for Short 4-6h 3.5 h for 15 min for 15 min -30
injectio for 7mg/kg 1000mg min
B12 DEFICIENY ANEMIA
Replenishment with Hydroxocobalamin 6 x
1000 g IM/ week
For maintenance therapy, 1000 g
hydroxocobalamin IM once every 3 month is
satisfactory.
FOLATE DEFICIENCY
Oral 5-15 mg/ day For 4 months
Pregnancy
i. Preventive 400 g/day
ii. Prev NTD history 4 mg/day
Anemia of chronic
disease
treatment:
Transfusion : symptomatic/ terminal
disease
Wait up to 7-8 g/dL
If compromised, maintain at 11 g/dL
Liberal use in ICU leads to morbidity
& mortality
EPO : Glycoprotein, from peritubular
capillary cells in kidney & hepatocytes,
regulated by HIF 1
Normal 10-25 U/L; t - 6-9 hrs
Up to 4-5x production in 1-2 weeks
 Anemia of chronic
inflammation
Recombinant EPO therapy :
Check for iron stores
50-150 U/kg 3 times/week IV
Up to 300 U/kg, (in chemo induced anemia)
10-12 g/dL Hb in 4-6 weeks
Stop if acute inf/ iron depletion/ Al toxicity/
hyperparthyroidism
Thrombo-embolic events, Tumor
progression
Long acting : DARBEPOETIN
 Anemia in various endocrinopathies
usually corrects by itself when the
primary disease is managed
adequately.
THRESHOLD FOR PRBC TRANSFUSION

The guidelines from the AABB (formerly

the American Association of Blood
Banks) are based on a systematic
review of randomized, controlled trials
evaluating transfusion thresholds.
These guidelines recommend
adhering to a restrictive transfusion
strategy and consider transfusion
when Hb is 7 to 8 g/dL in hospitalized,
stable patients.
Management of haemolytic Anemias

Hereditary spherocytosis
Thalassemias
Sicle cell anemia
G6PD deficiency
PNH
 Hereditary Spherocytosis
Treatment-
No causal treatment
Splenectomy
Mild cases : Defer Splenectomy
Moderate cases : delay until puberty
Sever cases : delay until 4-6 years of
age
Anti pneumococcal vaccination
before surgery
 Thalassemia
Mild No treatment
Hb H
Folate 1mg/day oral
No oxidative drugs/ iron
Transfusion
Splenectomy (if hypersplenism is seen)
Iron chelation
Oral DEFERASIROX 20 30mg/kg/day
Allogenic BMT ( Definitive )
 Sickle cell anemia
Allogenic BMT (Curative in child)
Folate 1mg/day
Transfusions
Pneumococcal vaccination
Iron chelation
Hydroxy Urea 500-750 mg/OD
Painful crisis :
Hydration, NSAIDS, O2
Vaso-occlusive/ Intractable pain/ Acute
chest synd/ priapism/ stroke
Exchange transfusion
 G6PD Deficiency
Diagnosis :
DNA testing
Enzyme levels
Rx :
No cure
Severe Transfusions, Splenectomy.
Good prognosis if No Kidney damage
Avoiding drugs that causes hemolysis
 AIHA
Medical Emergency, needs transfusion.
Abs are commonly non specific against
e Ag of Rh system.
So all most all the blood groups will be
incompatible
Start incompatible blood transfusion to
keep the pt alive (with hold when
condition improves)
Prednisolone 1mg/kg/day +
Rituximab 100 mg/week x 4
Splenectomy, Allogenic BMT.
 PNH
Life long condition
S. Iron maintanence
Folate >3mg/d
Never long term corticosteroids
ECULIZUMAB IV/ Fort night
(Compliment mediated hemolysis)
Extra vascular hemolysis
Allogenic BMT (definitive)
 Aplastic Anemia
Supportive
Epoetin/ Darbepoetin + Filgrastim/
Mild Sargramostim
Transfusions, AMD
Severe
(<500/L <40 yrs + HLA matched donor =
neutrophils allogenic BMT
<20000/L
thrombocytes <40 yrs HLA matched donor/
<1% retic >40 yrs
count =Immunosuppressive
therapy
<20% BM
cellularity)
Transfusions
Refractory ELTROMBOPAG
 Aplastic Anemia
Immunosuppressive therapy

Equine Anti thymocyte globulin

(40mg/kg/day x 4)
Initially Cyclosporin A (6mg/kg BD x 6months)
Methyl prednisolone (1-2mg/kg/day x 7day)

After 1-3 Patient becomes partially transfusion free

months

After 4 Complete remission can be seen

months
 TAKE HOME MESSAGE
Anemia in clinical practice should not be ignored, as
the most common causes of anemia are generally
readily treatable.
A detailed history and thorough examination should
be undertaken as a part of good clinical practice.
A stepwise approach in lab tests should be followed
to avoid unnecessary & costly investigation.
Liberal PRBC transfusion should always be avoided.
Since some anemias results from difficult to treat
etiology, hence proper counselling and timely
referral to a Hemtologist/Hematoncologist should be
done.
THANK
YOU
 REFERENCES
Kasper, Dennis L.,, et al.Harrison's Principles of
Internal Medicine. 19th edition. New York: McGraw Hill
Education, 2015.
Wintrobe, M. M., & Greer, J. P.Wintrobe's clinical
hematology. 13th edition. Philadelphia: Wolters Kluwer
Health/Lippincott Williams & Wilkin, 2014.
RS Hillman et al: Hematology in Clinical Practice, 5th
ed. New York, McGraw-Hill, 2010.
1. All of the following laboratory values
are consistent with an intravascular
hemolytic anemia except
A. increased haptoglobin
B. increased lactate dehydrogenase (LDH)
C. increased reticulocyte count
D. increased unconjugated bilirubin
E. increased urine hemosiderin
2. A 24-year-old man with a history of poorly
treated chronic ulcerative colitis is found to have
anemia with a hemoglobin of 9 g/dL and a reduced
mean corpuscular volume. His ferritin is 250 g/L.
Which of the following is the most likely cause of
his anemia?
A. Folate deficiency
B. Hemoglobinopathy
C. Inflammation
D. Iron deficiency
E. Sideroblastic anemia
3. All of the following statements regarding the
anemia of chronic kidney disease are true
EXCEPT:
A. The degree of anemia correlates with the
stage of chronic kidney disease.
B. Erythropoietin levels are reduced.
C. Ferritin is reduced.
D. It is typically normocytic and
normochromic.
E. Reticulocytes are decreased.
4. Which of the following hemolytic
anemias can be classified as
extracorpuscular?
A. Elliptocytosis
B. Paroxysmal nocturnal
hemoglobinuria
C. Pyruvate kinase deficiency
D. Sickle cell anemia
E. Thrombotic thrombocytopenic
purpura