ANAEMIA

DR AFOLABI, O.F
Outline
Definition
 Aetiology Of Anemia.
Patho-physiology Of Anemia.
Epidemiology
Symptoms And Signs
Evaluation
Treatment
Prognosis
Definition

 Anemia is strictly defined as a decrease in

red blood cell (RBC) mass.
Anemia is a reduction in hemoglobin (Hb) or
hematocrit (HCT) or RBC count with
reference to age and sex of individuals.
Definition

 The World Health Organization (WHO) chose

12.5 g/dL for both adult males and females.
 Normal Hb ranges from lab
13.5 to 18.0 g/dL in men
11.5 to 15.0 g/dL in women
11.0 to 16.0 g/dL in children
Patho-physiology of Anemia
 The function of the RBC is to deliver oxygen
from the lungs to the tissues and carbon
dioxide from the tissues by using hemoglobin
.
 In anemia, a decrease in the number of RBCs
transporting oxygen and carbon dioxide
impairs the body’s ability for gas exchange.
Erythrocyte Life Cycle

Erythroid precursors develop in bone marrow at

rates usually determined by the requirement for
sufficient circulating Hb to oxygenate tissues
adequately.
Erythroid precursors differentiate sequentially
from stem cells to progenitor cells to erythroblasts
to normoblasts in a process requiring growth
factors and cytokines.
This process of differentiation requires several day’
 erythroid precursors are released into circulation
as reticulocytes.
Erythrocyte Life Cycle
 They remain in the circulation for
approximately 1 day before they mature into
erythrocytes, after the digestion of RNA by
reticuloendothelial cells.
The mature erythrocyte remains in
circulation for about 120 days before being
engulfed and destroyed by phagocytic cells of
the reticuloendothelial system.
Aetiology of Anaemia
Aetiology of anaemia is broadly divided into
3:
 Anemia caused by blood loss
 Anemia caused by decreased or faulty red
blood cell production
 Anemia caused by destruction of red blood
cells
Blood loss

Acute-
 hemorrhage
 surgery
 trauma
 menorrhagia
Blood Loss
• Chronic-
 heavy menstrual bleeding
 , chronic gastrointestinal blood losses in the
setting of, ulcers , gastritis, Non-steroidal anti-
inflammatory drugs (NSAIDs) such as aspirin or
ibuprofen, which can cause ulcers and gastritis,
hookworm infestation, hemorrhoids and cancers

 urinary losses (BPH, renal carcinoma,

schistosomiasis)
Anemia Caused by Decreased or Faulty Red Blood Cell
Production

Conditions associated with these causes of

anemia include:
Iron-deficiency anemia
Vitamin-deficiency anemia, specifically b12 or
folate
Bone marrow and stem cell problems
Aplastic anemia due to medications,
radiation, chemotherapy or infection.
Anemia Caused by Decreased or Faulty Red Blood Cell
Production

Drugs or chemicals commonly cause the

aplastic and hypoplastic group of disorders.
 Certain types of these causative agents are
dose related and others are idiosyncratic.
 sufficient dose of inorganic arsenic, benzene,
radiation, or the usual chemotherapeutic
agents used for treatment of neoplastic
diseases can cause bone marrow depression
with pancytopenia.
Anemia Caused by Decreased or Faulty Red Blood Cell
Production

chloramphenicol may produce pancytopenia,

granulocytopenia is more frequently
observed with toxicity to sulfonamides or
antithyroid drugs
 myeloma or leukemia.
Sometimes, there’s no clear cause of aplastic
anemia.
· Lead poisoning.
Anemia Caused by Decreased or Faulty Red Blood Cell
Production

The idiosyncratic causes of bone marrow

suppression include antibiotics,
antimicrobials, anticonvulsants,
antihistamines.
 The other idiosyncratic causes are viral
hepatitis and paroxysmal nocturnal
hemoglobinuria.
 In approximately one half of patients
presenting with aplastic anemia, a definite
etiology cannot be established, and the anemia
must be regarded as idiopathic
Anemia caused by destruction of red blood cells

Hemolytic anemia
Acquired- immune-mediated, infection,
microangiopathic, blood transfusion-related,
and secondary to hypersplenism
Hereditary- enzymopathies, disorders of
hemoglobin (sickle cell), defects in red blood
cell metabolism (G6PD deficiency, pyruvate
kinase deficiency), defects in red blood cell
membrane production (hereditary
spherocytosis and elliptocytosis)
Nutritional Aetiologies
Nutritional etiologies include the following:
Iron deficiency
Vitamin B12 deficiency
Folate deficiency
Starvation and generalized malnutrition
Physical Aetiologies
Physical aetiologies include the following:
Trauma
Burns
Frostbite
Prosthetic valves and surfaces
Chronic disease and malignant aetiologies
Chronic disease and malignant etiologies
include the following:
Kidney disease
Liver disease
Chronic infections
Neoplasia
Collagen vascular diseases
Infectious aetiologies
Infectious aetiologies include the following:
Viral - Hepatitis, infectious mononucleosis,
cytomegalovirus
Bacterial - Clostridia, gram-negative sepsis
Protozoal - Malaria, leishmaniasis,
toxoplasmosis
Epidemiology

Anemia is an extremely common

disease affecting up to one-third of the global
population.
 In many cases, it is mild and asymptomatic
and requires no management.
The prevalence increases with age .
it is more common in women of reproductive
age, pregnant women, and the elderly.
Epidemiology
The prevalence is more in individuals who
are older than the age of 85
In the elderly, approximately one-third of
patients have a nutritional deficiency as the
cause of anemia, such as iron, folate, and
vitamin B12 deficiency.
In another one-third of patients, there is
evidence of renal failure or chronic
inflammation
Epidemiology
 mild iron-deficiency anemia is seen in
women of childbearing age, usually due to
poor dietary intake of iron and monthly loss
with the menstrual cycles.
Other at-risk groups include alcoholics, the
homeless population, and those experiencing
neglect or abuse.
 the race is also an important determinant of
anemia, with the prevalence increasing in the
African American population
Epidemiology
 geographic diseases, such as sickle cell
anemia, thalassemia, malaria, hookworm, and
chronic infections, are responsible for a portion
of the increase in africans
 nutritional factors with iron deficiency , folic
acid deficiency also contribute to the increased
prevalence of anemia in africans.
 anemia of chronic disorders is commonplace in
populations with a high incidence of chronic
infectious disease (eg, malaria, tuberculosis,
acquired immunodeficiency syndrome
Types of Anaemia
Microcytic
Normocytic, normochromic
Macrocytic
Symptoms of Anemia

Classically depends on the rate of blood loss.

Symptoms usually include the following:
Weakness
Tiredness
Lethargy
Restless legs
Shortness of breath, especially on exertion, near
syncope
Chest pain and reduced exercise tolerance- with more
severe anemia
Pica- desire to eat unusual and nondietary substances
Mild anemia may otherwise be asymptomatic
Signs of Anaemia
Skin may be cool to touch
Tachypnea
Hypotension (orthostatic)
 Pallor conjunctiva ,buccal mucosa, palms

 “Boxcars” or “sausaging” of retinal veins: suggestive

of hyperviscosity which can be seen in myelofibrosis

 Jaundice- seen in hemoglobinopathies, liver

diseases and other forms of hemolysis
Signs of Anaemia
Lymphadenopathy: suggestive of lymphoma or
leukemia

Glossitis (inflammation of the tongue) and

cheilitis (swollen patches on the corners of the
mouth): iron/folate deficiency,
alcoholism, pernicious anemia
Signs of Anaemia
Abdominal exam:
 Splenomegaly: hemolysis, lymphoma, leukemia,
myelofibrosis

 Hepatomegaly: alcohol,myelofibrosis

 Scar from gastrectomy: decreased absorptive

surface with the loss of the terminal ileum leads to
vitamin B12 deficiency
 Scar from cholecystectomy: Cholesterol and pigmented
gallstones are commonly seen in sickle cell anemia and
hereditary spherocytosis
Signs of Anaemia
Cardiovascular:
Tachycardia

Systolic flow murmur

Severe anemia may lead to high output heart

failure
Signs of Anaemia
Neurologic exam: Decreased proprioception/vibration:
vitamin B12 deficiency
Skin:
 Pallor of the mucous membranes/nail bed or palmar
creases: suggests hemoglobin < 9 mg/dL

 Petechiae: vasculitis

 Dermatitis herpetiformis (in iron deficiency due to

malabsorption- Celiac disease)

 Koilonychia (spooning of the nails): iron deficiency

Signs of Anaemia
Rectal and pelvic exam:
 If a patient has heavy rectal bleeding, one
must evaluate for the presence of
hemorrhoids
 hard masses that suggest neoplasm as
causes of bleeding.
Evaluation

Approach to anemia includes identification of the

type of anemia
1. Complete blood count (CBC) including
differential
2. Calculate the corrected reticulocyte count =
percent reticulocytes x (patient's HCT/normal HCT)
For normal HCT, use 45% in men and 40% in
women
If result > 2, this suggests hemolysis or acute blood
loss, while results < 2 suggests hypoproliferation.
Evaluation
3. After calculating the reticulocyte count,
check the MCV- Mean corpuscular
volume ;MCH- Mean corpuscular HB
MCV (<80 fl) - Microcytic
Iron deficiency- decreased serum iron, percent
saturation of iron, with increased total iron-
binding capacity (TIBC), transferrin levels, and
soluble transferrin receptor
Lead poisoning- basophilic stippling on the
peripheral blood smear, ringed sideroblasts in
bone marrow, elevated lead levels
Evaluation
Anaemia of Chronic Disease- may be
normocytic
Thalassemia- low MCV, target cells, and
basophilic stippling are on peripheral smear.
Alpha thalassemia is differentiated from beta-
thalassemia by a normal Hgb electrophoresis
in alpha thalassemia. Elevated Hb A2/HbF is
seen in the beta-thalassemia trait.
Sideroblastic anemia- elevated serum iron and
transferrin with ringed sideroblasts in the bone
marrow
Evaluation
MCV (90-100fl) - Normocytic
Renal Disease: BUN/Creatinine
Aplastic anemia- ask for drug exposure, check
for infections (EBV, hepatitis, CMV, HIV), test
for hematologic malignancies and paroxysmal
nocturnal hemoglobinuria (PNH)
Myelofibrosis- check bone marrow biopsy
Multiple myeloma- serum and urine
electrophoresis
Pure red cell aplasia- test for Parvovirus B19,
exclude thymoma
Evaluation
MCV (>100 fl) - Macrocytic
 B12/folate levels- B12 and folate deficiency can be
differentiated by an elevated methylmalonic and
homocysteine level in B12 deficiency and only an
elevated homocysteine level in folate deficiency.
Methylmalonic levels are relatively normal.
 Haematological disorders e.g aplastic anaemia

 Hypothyroidism- TSH, free T4

 Liver disease- check liver function
 Alcohol- assess alcohol intake
 Drugs e.g hydroxyurea, azathioprine, zidovudine
Steps to Evaluate for Hemolytic Anemia
1) Confirm the presence of hemolysis- elevated
LDH, corrected reticulocyte count >2%, elevated
indirect bilirubin and decreased/low haptoglobin
2) Determine extra vs. intravascular hemolysis-
Extravascular
 Spherocytes present
 Urine hemosiderin negative
 Urine hemoglobin negative
Intravascular
 Urine hemosiderin elevated
 Urine hemoglobin elevated
Steps to Evaluate for Hemolytic Anaemia
3) Examine the peripheral blood smear
Spherocytes: immune hemolytic anemia (Direct
antiglobulin test DAT+) vs. hereditary spherocytosis
(DAT-)
Bite cells: G6PD deficiency
Target cells: hemoglobinopathy or liver disease
Schistocytes: ThromboticThrombocytopenic
Purpura/Heamolytic Ureamic Syndrome,
Disseminated Intravascular Coagulopathy, prosthetic
valve, malignant HTN
Acanthocytes: liver disease
Parasitic inclusions: malaria, babesiosis, bartonellosis
Steps to Evaluate for Hemolytic Anaemia
 If spherocytes +, check if DAT is +
DAT(+): Immune hemolytic anemia (AIHA)
DAT (-): Hereditary spherocytosis
Evaluation
Other investigations include
esophagogastroduodenoscopy for the determination
of an upper GI bleed
 colonoscopy for the determination of a lower GI
bleed.
 If a menstruating woman has heavy vaginal
bleeding, evaluate the presence of fibroids with a
pelvic ultrasound
Other imaging studies when indicated
Bone marrow studies- cellullarity, type of
erythropoiesis, iron stores, infiltration of the
marrow
Management

Management depends primarily on treating the

underlying cause of anemia.
1) Anemia due to acute blood loss- Treat with IV
fluids, crossmatched packed red blood cells,
oxygen.
 Always remember to obtain at least two large-bore
IV lines for the administration of fluid and blood
products.
 Maintain hemoglobin of > 7 g/dL in a majority of
patients.
Those with cardiovascular disease require a higher
hemoglobin goal of > 8 g/dL.
Management
 Anemia due to nutritional deficiencies:
Oral/IV iron, B12, and folate.
Oral supplementation of iron is the most
common method of iron repletion.
 The dose of iron administered depends on
the patient's age, calculated iron deficit, the
rate of correction required, and the ability to
tolerate side effects.
The most common side effects include
metallic taste and gastrointestinal side effects
such as constipation and black tarry stools.
Management
 The hemoglobin will usually normalize in 6-8
weeks, with an increase in reticulocyte count
in just 7-10 days.
 IV iron may be beneficial in patients
requiring a rapid increase in levels.
 Patients with acute and ongoing blood loss
or patients with intolerable side effects are
candidates for IV iron
Management
 Anemia due to chronic disease: Anemia in
the setting of renal failure, responds to
erythropoietin. Autoimmune and
rheumatological conditions causing anemia
require treatment of the underlying disease.
) Anemia due to defects in the bone marrow
and stem cells: Conditions such as aplastic
anemia require bone marrow transplantation.
Management
 Anemia due to increased red blood cell
destruction:
Hemolytic anemia caused by faulty mechanical
valves will need replacement.
Hemolytic anemia due to medications requires the
removal of the offending drug.
Persistent hemolytic anemia requires splenectomy.
Hemoglobinopathies such as sickle cell anemia
require blood transfusions, exchange transfusions,
and even hydroxyurea to decrease the incidence of
sickling.
Prognosis

The prognosis for anemia depends on the

cause of anemia.
In iron deficiency, replacements must
continue for at least three months after the
normalization of iron levels, in order to
restore iron stores. Usually, nutritional
deficiencies have a good prognosis if treated
early and adequately.
Anemia, due to acute blood loss, if treated
and stopped early, has a good prognosis
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