10 / 11 / 2009
Important point in anaemia:
The most common cause of anaemia is iron deficiency anaemia.
female in child bearing age (Menses and pregnancy).
It is usually hypo chromic microcytic anaemia.
Always we should know the cause of anemia- the explanation.
(eg. 25 years old Female with anemia, we should ask about menses).
And always any pnt with anemia we’ve to look for ferretin and B12 and
folic acid, to correct any deficiency.
Vitamin B12 associated with neurological damage.
Reduction in the total number of RBCs, hemoglobin, and/or hematocrite.
(generally low Hb).
SOoo.. In CBC.. first of all.. we look for Hb: (low Hb = anemia), with take in
consideration that female Hb < male Hb.
- Symptoms are related to the rapidity of anemia.
♦ Symptoms of Anemia depend on:
- General status of the pnt. (ex: young person can tolerate anemia more,
or pnt with IHD can’t tolerate anemia).
- Medical status : young, fitness, cardiac disease.. etc.
- Rapidity of anemia.
♦ Causes of sudden drop of Hb:
- Aplastic crises: caused by ribovirus.
In examination.. firstly: take history
♦ Common questions you’ve to ask pnt with anemia:
- Bleeding: melena, hematuria, rectal bleeding, mense.
- Jaundice: related to hemolysis.
- Diet: (vegetarian people have iron deficiency anemia).
- Drugs: (eg: NSAID cause gastric bleeding which cause anemia).
- Neurological symptoms: means B12 deficiency.
♦ CBC indices: v. IMP
♦ In CBC:
- We look firstly to Hb to determine if there’s anemia or not.
- Then, MCV: mean corpuscular volume(= size of RBC).
- Then, MCH : mean corpuscular Hb.
- MCHC : mean corpuscular Hb concentration itz not important.
- RDW : red cell distribution width:
In iron deficiency anemia there’s variation in RDW(cells differ in
shape and size), but in thalasemia RDW is normal.
* Classification of anemia:
♦ Morphological :
Clinical finding of
- Micro cytic: low MCV.
- Normo cytic: normal MCV.
- Macro cytic: high MCV.
- Decrease production: in bone marrow problems.
- Increase destruction: peripheral destruction (hemolysis).
- Sequestration of blood , usually, in spleen.
e.g: pnt with schistosomiasis or portal hyper tension will be presented
with spleenomegaly bcz blood is sequestrated in spleen, and this will
♦ Underlying mechanism:
- Impaired production (proliferation/differentiation/maturation).
- Increased destruction – hemolytic.
- Blood loss:
- WBC: fighting infection so any pnt with WBC loss will be presented
- Platelet: homeostasis (thrombosis) so any pnt with platelet loss will
be presented with bleeding.
- RBC: O2 carrying capacity so presented with general weakness,
In pnt with anemia:
1. Take history(ask about menses, and GI bleeding and NSAID).
2. Physical examination: pallor, jaundice, spleen & L.N exam, neurological
3. Investigation: look for this slide:
* Anemia Workup:
• Iron/TIBC/Ferritin (feritin is acute phase reactant: used for IDA diagnosis)
• Folate/B12. (we’ve serum folate & red cel folete(which is more accurate))
• LDH/Bilirubin. (high LDH & high unconjugated bilirubin in hemolytic anemia)
• Haptoglobin (low in hemolytic anemia)/Urine for hemosiderin.
• Coombs Test (direct anti globulin test) – Direct & indirect.
• Hemoglobin electrophoresis (test for thalasemia & sickle cel anemia/ IDA
can mask Hb electophoresis that’s why we don’t use this test for IDA).
• Acid hemolysis.
• Osmotic fragility (test for hereditary spherocytosis).
• Rx iron/folate/B12.
• Type & Cross.
• Transfuse 2-4 units.
• GI Consult.
• Hematology Consult –
• Bone Marrow.
The BEST investigation of anemia after CBC is BLOOD FILM which
is the most important tool for diagnosis of anemia.
- Reticulocyte Count = Retic % x RBC Count.
- Absolute Value.
– eg 0.01 x 5x1012/l = 5x 1010/l
- Normal up to 1.2x1011/l (120,000/μl)
- More accurate way to assess body’s response to anemia
- Give us indication about bone marrow activity.
Iron Deficiency Anemia (IDA):
- Hypochromic Microcytic Anemia.
- Common in women.
- The most common cause is bleeding, and intravascular
hemolysis(common in pnt with G6PD or prosthetic valve).
* Causes of IDA:
2. GI bleeding: gastric ulcer, duodenal ulcer.
3. Poor diet.
4. Increase requirements: infant, children, pregnancy.
5. Chronic blood loss: GI and GU bleeding: gastric CA, colon CA, hemorrhoid,
Do endoscopy to know the cause.
6. Impaired absorption: gastrectomy, celiac disease:v.common(cause IDA
associated sometimes with folate & B12 dificiency).
* How to diagnose IDA:
The 1st test
- Take history.
- CBC: Low Hb, MCV, MCH, MCHC and high RDW.
- Blood film: hypochromic microcytic, El iptocytes or pencil cells,
its low then
- Low reticulocytes.
- Low serum iron, low ferritin, increased TIBC, < 15% saturation.
Treatment: treat the underlying cause, then administer iron orally, or IV iron
in pnt with malabsorption or cant tolerate oral iron.
Differential Diagnosis of Hypo chromic Microcytic Anemia:
1. IDA (low ferritin).
3. Sederoblastic syndrome.
4. Anemia of chronic illness.
Complication of thalassemia major:
- Hemochromatosis: Iron overload (HIGH FERRITIN): which wil cause:
1. Grey color.
2. Deposition of iron in pituitary gland pituitary failure (e.g:
3. Deposition of iron in pancreas diabetes mel itus.
4. Liver overload.
* Ferritin is a reflection of iron store:
Low ferritin: IDA.
High ferritin: Thalassemia.
Anemia of Chronic Illness :
- Like in pnt with rheumatoid arthritis, Cancer, inflammatory bowel disease
- Normal or High ferritin.
Megaloblastic Anemia Haemolytic anemia:
* Macrocytic Anemia:
- Megaloblastic: B12 deficiency and folate deficiency.
we can differentiate between B12 & folate deficiency that B12
deficiency 1.cause neural damage(numbness, weakness.. etc), 2. B12
stores for 3 years, so anemia start to appear after 3 years.
- Non- megaloblastic: hypothyroidism, liver disease, hemolytic anemia.
* Crohn disease common cause of megaloblastic anemia.
E.g.: 70 years old male presented with general weakness, numbness, Hb=3,
MCV= 130, pancytopenia, high LDH, high unconjugated billirubin, low
soo this pnt has megaloblastic anemia, and high LDH & billirubin means
ineffective erythropioses/hematopioses which means that cells produce
and die in bone marrow so we’ll find hyper-cellular bone marrow.
And low retic. tell us that its not hemolytic anemia.
B12 Deficiency Anemia:
*High MCV: RBC size > neutrophile size,
pancytopenia or anemia alone.
*Blood film: hyper-segmented neutrophils
*Bone marrow: giant cell, hyper-cel ular marrow
bcz of ineffective erythropioses.
* ineffective erythropioses: high LDH,
*Etiology: impaired absorption(stomach/terminal ilium problems), increased
requirement, inadequate diet(in vegetarian people: bcz the exclusive source
of B12 is dietary animal product).
*Don’t forget to do neurological examination.
- Endoscopy: to know the cause, E.g. atrophy gastritis cause pernicious
- Look for anti- intrinsic factor antibodies, antiparietal antibodies.
* Treatment of pernicious anemia: B12 injection (loading dose and
Folate Deficiency Anemia :
Doesn’t cause neurological damage.
Associated with hemolytic anemia , pregnancy(bcz of increase
demand, and to prevent neural tube defect).
Normal survival for RBC IS 100-120 days.
But in hemolytic anemia there’s shortening
If the liver is palpable
in RBC survival.
this doesn’t mean that its
enlarged for sure, BUT if
- Jaundice, change in urine color.
the spleen is palpable
- Splenomegaly: by palpation or by ultrasound. this mean that its
- Ankle ulcers.
* Lab finding:
MCV: normal or high.
Serum LDH Increased, Serum unconjugated bil irubin
Increased. but remember Gilbert disease: in which all test is
normal except high indirect billirubin.
Serum haptoglobin Decreased.
After we know that the pnt has hemolytic anemia, we’ve to know is it immune
(auto-immune), or non-immune hemolytic anemia:
So, we do COOMB’S TEST (direct anti-globulin test):
- if it’s positive, then it’s immune: then it’s maybe primary or secondary
immune (the most common secondary is SLE).
- if it’s negative, then it’s non-immune.