The class of diseases which are referred to as the Anemias are those in
which there is an actual, or apparent, decrease in the oxygen carrying
element or hemoglobin. This may not be due to an actual decrease in
amount of hemoglobin, but rather to a decrease in the ability of
the red cells to carry it. This decrease in ability may be due to
alteration in the erythrocytes themselves, or to effects of change in
the molecular concentration of the plasma in which they are suspended.
The plasma may also contain certain poisons probably protied, which
may make impossible the efficient carrying of hemoglobin by the
erythrocytes.
The simplest form of anemia is that due to removal of a large
percentage of erythrocytes from the body. This condition is fulfilled
in acute hemorrhage. If the amount of blood lost does not exceed the
amount necessary to maintain circulation, roughly fifty per cent of
the total quantity, the fluid portion lost is quickly replaced from
the fluids of the body and from material ingested. The formed elements
and proteids are less rapidly replaced by a compensatory increase in
function of the hematopoietic tissues so that there is a gradual return
to the original number and proportion.
A blood cell may be considered as passing through a life cycle of
infancy, adolescence, maturity, and senility before it is finally
destroyed. If the demand for new cells is not too great it will be met
with mature cells. If the call is more urgent, younger and older cells
will both be put into the conflict, while in a time of extreme stress
all types of cells, from the “school boys” to the “gray-beards”, will
have to be utilized to maintain life. So, roughly, we can judge the
severity of the anemic process by the reaction which the body makes to
it as indicated by the character of the cells in service.
The pigment, hemoglobin, is slowly regenerated even as compared to
erythrocytes, so that the color index is usually the last finding
to return to normal after a hemorrhage. The leucocytes are usually
increased after hemorrhage, probably as a protective mechanism, nature
having learned by hard experience that she has less resistance to
infection, when there is loss of a considerable quantity of blood.
To be considered, also, is the fact that constantly blood cells are
outliving their usefulness—some must be disposed of. The extra function
required of these older cells gives the same results as over work
upon an old man—hurries his time of demise so that there is a greater
percentage than usual to be sent to the salvage shops. The regeneration
of blood after hemorrhage depends upon the severity of the loss, the
nutrition, upon the treatment given, and indirectly the ability of
resistance developed by the patient.
In the chronic anemias we may have either defective development of
erythrocytes, or defective function of them, or a relatively too great
destruction of these same agents.
A bank account may be depleted either by too small deposits to account
for current expense, or by extravagant withdrawals. It is sometimes
difficult to determine on which side the fault lies. It seems to be
nature’s plan not to subject to active work an erythrocyte until after
the nucleus has disappeared, judged by ordinary methods of staining.
A sudden call for an increased number of erythrocytes may force the
organism to send in some with nuclei, but the circulation does not
receive those which have not been standardized, as to shape and
staining reaction, unless the crisis is of grave import. Evidence of
increased destruction of these cells is shown by broken forms—shadow
forms, and by an increased excretion of the pigments derived from the
breaking down of hemoglobin, namely bilirubin and urobilin. A great
deal of information can be obtained by a study of the other formed
elements of the blood.
In general the symptomatology of all the anemias will be that of
lessened metabolism because of deficient oxygenation. This is
accompanied by imperfect nutrition and general impairment of function.
Among the usual results are muscular weakness, malaise, headache,
dizziness, anorexia, and cutaneous and membranous pallor, with tendency
to local hemorrhages. The heart is often rapid, easily disturbed in
rhythm, may possess a hemic or functional murmur, and gives a soft
compressible pulse of low pressure. As a compensatory attempt the
respiration may be rapid, but is likely to be shallow, and dyspnea
results from disproportionately small exertions.
There may be either troublesome constipation, or diarrhea; often there
are alternating periods of each. In the severer forms convulsions,
coma, delirium, stupor, localized edema of the ankles or eyelids may be
seen.
In general the treatment of the secondary anemias will concern the
removal of the cause followed by measures tending to increase the
decreased element or elements in the blood stream. In the anemia
resulting from hemorrhage the thirst which follows is the body’s
method of calling for more fluid with which to maintain pressure in
the arteries and capillaries sufficient to develop new formed elements
to take the place of those lost. If the loss is severe enough to give
rise to shock, emergency measures are necessary of introducing into
the venous stream an artificial fluid to make up for the fluid part of
the blood lost. If the condition can be predicted and a suitable donor
obtained, blood transfusion is of greatest advantage to the patient.
More often the urgency of the condition will require an artificial
fluid to be given in haste. Probably the best so far devised solution
is Fischer’s physiological salt solution. In the anemias due to chronic
metal poisoning as from lead and mercury, or from systemic poisoning
such as syphilis or malaria, or from the retention of metabolic
products as in some of the diseases of the kidneys or of the liver,
the anemia can only be successfully treated by normalizing its primary
cause—as it occurs in the role of a symptom or result, and hence is
only indirectly a blood condition.