ANEMIA-INTRODUCTION
“Anemia” is not a diagnosis in itself, but merely an objective sign of the presence
of disease. The correct diagnostic terminology for a patient with anemia requires the
inclusion of the pathogenesis of the anemia. The reason for this is simple and
fundamental: the correct treatment requires an understanding of the pathogenesis of
the condition. The term “anemia”, as it is generally used in clinical medicine, refers to
reduction below normal in the concentration of hemoglobin or red blood cells in the
blood. It must be remembered that the mean normal value and the lower limites of the
“normal” range depend upon the age (childhood or adult life) and gender of the
subjects, as well as the altitude of residence.
I. Classification of Anemia
1. Pathogenetic Classification
(1) Blood loss
A. Anemia after recent hemorrhage (acute)
B. Anemia after persistent hemorrhage (chronic)
(2) Excessive destruction of erythrocytes (hemolytic disease)
A. Extracorpuscular factors
B. Intracorpuscular factors
(3) Inadequate production of mature erythrocytes
A. Deficiency of essential substances
B. Deficiency of erythroblasts
C. Infiltration of bone marrow
D. Endocrine abnormality
E. Chronic renal disease
F. Chronic inflammatory diseases
a. Infections
b. Noninfectious disease, including granulomatous
G. Cirrhosis of liver
2. Morphologic Classification
(1) Macrocytic (MCV>94, MCHC>31)
Vitamin B12 deficiency, Folic acid deficiency
(2) Hypochromic-microcytic (MCV<80, MCHC<31)
A. Iron deficiency
B. Disorders of globin synthesis
C. Disorders of porphyrin and heme synthesis
D. Other disorders of iron metabolism
(3) Normochromic-normocytic (MCV82-92, MCHC>30)
A. Recent blood loss
B. Overexpansion of plasma volume
C. Hemolytic diseases
D. Hypoplastic bone marrow
E. Infiltrated bone marrow
F. Endocrine abnormality
G. Chronic disorders
H. Renal disease
I. Liver disease
II. Manifestations of Anemia
Symptoms in patients with anemia depend on five factors: 1. The reduction in the
oxygen-carrying capacity of the blood; 2. The degree of change in total blood volume;
3. The rate at which 1. And 2. have developed; 4. The associated manifestation of the
underlying disorder that resulted in the development of anemia, and 5. The capacity of
the cardiovascular and pulmonary systems to compensate for the anemia. The
symptoms of acute hemorrhage, are chiefly related to hypovolemia, rather than to
anemia.
In chronic anemia, the reduction in the concentration of the oxygen-carrying
pigment in the blood has a more meaningful correlation with the cardivascular
adjustments that must be made than does the magnitude of the deficit in the total
quantity per se of red blood cells or of hemoglobin in the circulation.
The binding and release of oxygen by hemoglobin are profoundly affected by the
variations in the concentration of 2,3-diphosphoglyceric acid (2,3-DPG), which are
known to occur in the cell in disease. The oxygen affinity of hemoglobin is reduced as
the concentration of 2,3-DPG increases, and the converse is also true. An increase in
red cell 2,3-DPG is found in chronic anemia. It has been calculated that DPG-induced
changes in hemoglobin affinity for oxygen may compensate for up to half the oxygen
deficit in anemia.
1. Cardiovascular Adjustments
The cardiac index generally is increased in anemia, and the arteriovenous oxygen
difference is narrowed. When the hemoglobin concentration is less than 70g/L the
cardiac output is nearly always increased, and when it less than 50g/L, the increase in
cardiac index has been found to be due mainly to an increase in stroke volume and, to
a lesser extent, in heart rate, even with exercise.
In chronic anemia, only moderate dyspnea or palpitation may occur. Salt and
water retention in anemia may result when blood flow to the kidneys is diminished.
Heart murmurs are a very common cardiac sign in anemia. These are usually systolic
in time and are most often heard in the pulmonic area, or else at the apex.
Electrocardiographic changes have been ascribed to severe anemia; they are corrected
as anemia is relieved. The most common are depression of the ST junction and a
U-shaped deformation of the ST segment, and flat or inverted T waves.
Changes in the duration of the electrical systole (QT interval) and abnormalities
of A-V conduction have been noted. Atrial fibrillation has been attributed to severe
anemia per se; this reverted to a normal sinus thythm when the anemia was relieved
by transfusion of packed red cells.
2. Integument Manifestations
Pallor is the most evident sign of anemia. Pallor can be detected most constantly
in the conjunctivae and the lips, and in the nailbeds. In the hands, the skin of the
palms first becomes pale, but the creases may retain their usual pink color until the
hemoglobin concentration is less than 70g/L. Other changes in the integument occur
with anemia, loss of normal skin elasticity and tone, resulting in a dry, shriveled
appearance, has been described. The nails may lose their luster, become brittle, and
break easily.
3. Neuromuscular Signs
Headache, vertige, tinnitus, faintness, scotomata, lack of mental concentration,
drowsiness, restlessness, and muscular weakness are common symptoms of anemia.
4. Alimentary system Manifestations
Glossitis and atrophy of the papillae of the tongue commonly occur in pernicious
anemia and much less often in iron-deficiency anemia. The nonspecific symptoms in
iron-deficiency anemia. The nonspecific symptoms of anorexia, naused, flatulence,
abdominal discomfort, vomiting, and constipation of diarrhea are also common
complaints in anemic patients.
5. Genitourinary Signs
Slight proteinuria is not uncommon when anemia is marked.
6. Metabolic Signs
In severe anemia, the basal metabolic rate may be increased.
7. Fever
Fever of mild degree rarely may be present without cause, other than the anemia,
when anemia is severe. It may not necessarily connote infection. However, except for
acute hemolytic episodes, fever of 38℃ or greater should be taken as a sign to search
for infection, lymphoma, and other disorders.
III. Diagnosis
The first step in the diagnosis of anemia is the detection of the presence of
anemia. The second step is the investigation of the pathogenesis of the anemia.
1. History
The duration of the symptoms and whether they were insidious or acute in onset
should be established. One should inquire about the family history with special
reference to anemia, spells of jaundice, splenectomy, bleeding disorders, and
abnormal hemoglobins. The patient’s occupation, household customs, and his hobbies
be known in seeking out possible injurious agents.
2. Physical Examination: Jaundice---Hemolytic anemia, Secondary anemia due to
liver disease.
Hepatomegaly--- Liver disease, Lymphoma, Leukemia.
Splenomegaly---Hemolytic anemia, Lymphoma, Leukemia, Liver disease.
Sternal tenderness---Leukemia.
Flatting of finger nail--- Iron deficiency anemia.
3. Laboratory examination:
(1) Hematologic examination--- Hematocrit (VPRC), Hb, red cell indices, leukocyte
count, platelet count, ESR, examination of stained blood film, including leukocyte
differential count, reticulocyte count.
(2) Urine Analysis--- Routine test, bence-jones protein, billirubin, urobilinogen,
occult blood.
(3) Stool---Routine, occult blood, ova.
(4) Serum or plasma---BUN, creatinine, bilirubin, protein, iron and TIBC.
4. Treatment of Anemia
The optimum treatment of anemia requires the eradication of its cause or, if that
is not possible, at least modification of the underlying disorder.
(1) Drug: Vit B12 or folic acid---Vit B12 or folic acid deficiency, Megaloblastic
anemia.
Iron--- Iron deficiency anemia.
Vit B6--- Sideroblastic anemia.
Prednisone--- AIHA, Aplastic anemia.
Testesterone--- Aplastic anemia.
(2) Blood Transfusion
Transfusion of blood is a valuable temporary measure for the treatment of chronic
anemia if the cardiovascular compensation is inadequate, or if the magnitude of the
magnitude of the anemia is such that cardiovascular collapse is threatened.
(3) Splenectomy
Splenectomy is of greatest value in the treatment of the patient with anemia of
hereditary spherecytosis. It is sometimes helpful, but not curative, in the hemolytic
anemia of pyruvate kinase deficiency and in some patients with acquired hemolytic
anemia who have a positive reaction to coombs’ antiglobulin test, when
adrenocorticosteroid hormones are required in such large doses and for so long a time
that their use is impractical. Splenectomy is sometimes of benefit in aplastic anemia
and rarely so in thalassemia.
(4) Bone marrow transplantation--- Acute Aplastic Anemia.
Zhonglu