By Earl R. Hoskins
General Considerations:—It has been said that each individual is a part of all the generations which have preceded him. In the same way it might be said that every drop of our blood is a part of every other cell in our bodies. The other tissues are able to maintain their existence only through the ministrations of the blood and in turn the blood derives its own substance from tissues which it supplies. We are accustomed to speak of certain organs as being those of blood formation, yet it is true that every tissue furnishes its quota of blood composition, making up the mass which we call blood.
It is in one way an algebraic sum of good and baneful substances, without which there can be no normal function, and sometimes being of itself a menace as well as an aid to other tissues, as in sepsis. There can be no perverted function of any tissue without there being a direct effect upon the blood. We may not always be able to measure this effect with our present laboratory methods. We may not be able to detect clinically the result of this alteration of the blood stream because of compensatory influences, dilution, phagocytic action, enzymatic action, oxidation, and the intricate processes of excretion. It must also be remembered that normal blood is not of a certain definite chemical or physical composition. It must vary from minute to minute according to the normal metabolic phenomena which make up our succession of events associated with life.
But comparatively little is known about this most important fluid. We have accumulated data regarding morphology and relative numbers of its formed elements and their behavior when sufficient abnormality is present to upset their wonted balance of arrangement. We have an ever widening field of investigation in the blood plasma in which we are constantly being told of newly discovered complexities. Certainly the field of the unknown is big enough to contain our unexplained blood reactions.
It is probable that as our knowledge increases our number of diseases really considered as true blood diseases will decrease and be shown to be the effect of blood passing through certain pathologic tissues of the body. We can measure the number and proportion of formed elements, and the relative efficiency of the erythrocytes by the amount of hemoglobin which they carry. The genesis of the formed elements is to be kept in mind in considering therapy. The erythrocytes and granular cells developing in adult life, principally from the red marrow, leads our attention in decrease or increase of these particular cells to the greatest aggregation of red bone marrow which happens to be in the ribs. The anatomical relation of the ribs to the spine would seem to render them very liable to disturbances of nutrition and nerve control as a result of structural maladjustment and clinically this presumption is verified. Limitation of the motion of the thoracic spine is perforce accompanied by costal inactivity with disuse effects upon the red marrow and eventually upon the relative content of the blood stream.
We can measure the efficiency of the erythrocytes in carrying oxygen to the tissues by measuring the relative amount of hemoglobin which a given volume of blood contains. The actual changes taking place in blood character are often thus sufficiently indicated for us in terms of our present methods of examination, to at least aid in the arrival at a diagnosis. We sometimes have to remember that the adaptation to abnormality may be efficient enough to keep the apparent significance from telling the “whole truth.”
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.
(Burns’ Anemia)
Costogenic Anemia is a result of functional disuse-atrophy of the hematopoietic organs, there being an insufficient supply of erythrocytes to meet the demands of the metabolism of the body. It results from insufficient opportunity for nutrition and drainage of the red marrow of the ribs, and gives the clinical picture of an anemia due to too slow production of erythrocytes.
Etiology.—The condition is predisposed to by any factor which tends to limit the action and nutrition of the ribs. We are too prone to forget that the function of the ribs is to produce erythrocytes; it is really a matter of secondary importance that they make up part of the thoracic wall. The change from the horizontal to the upright position has tended to a drooping of the whole chest from gravity. The human animal seldom develops the free hinge rib motion as often seen in quadrupeds. The passage of both arterial and venous blood, is not normally free and copious, and as a consequence the tissue supplied functions less efficiently. This function of the red marrow is to produce erythrocytes. Any structural lesion of the dorsal vertebral column, or its costal articulations, which interferes with the free motion of the rib thus interferes directly with the efficient function of these particular ribs. The severity of the condition varies with the number of ribs affected and the impedance to nutrition and drainage.
Diagnosis.—The condition may be of gradual onset, and may be associated or coincident with some other condition leading to a loss of tone or opportunity for free rib action. The systemic symptoms are due to a deficient oxygenation of all tissues as a result of the above disuse. The thorax is usually rigid—forced respiration requires unusual effort without proportionate thorax expansion. The type of breathing tends toward diaphragmatic. The quantities of tidal and supplemental air are both markedly decreased. The lack of tissue oxidation renders elimination less active, hence constipation. Gas accumulation, weakness, insomnia, with slightly increased amount of urine, and low in total solids, is the rule.
“The blood itself is rather characteristic. Coagulation time is increased; specific gravity and viscidity diminished; red cell count normal or only slightly diminished; hemoglobin 6 to 10 grams per 100 c. c. of blood (Meischer); 40% to 80% (Dare). The red cells are small, pale, vacuolated, sometimes nucleated. The white cell count is normal, slightly increased or slightly diminished. The hyaline cells are normal, or slightly relatively increased. (These, being formed in lymph nodes, tonsils, etc., are not affected by rib changes.) The mononuclear neutrophiles are relatively increased. The nuclear average of the polymorphonuclear neutrophile is low. Vacuolated and atypical neutrophiles are often found. Basophiles, myelocytes and amphophiles may be found in considerable numbers. Nuclei in all granular forms present evidences of immaturity or degeneration—they may be swollen, vacuolated, extruded, ragged, or with variable staining reaction” (Clinical Osteopathy).
Treatment.—The treatment is to obtain a normal function in the inactive tissues. This is done by getting better rib hygiene. Whatever is interfering with rib function and metabolism is to be removed. Breathing exercises are given not only to “ventilate the thorax, but to exercise its walls”. Carefully selected horizontal bar work is often of great value. The diet should be of such nature as to supply material for manufacture of erythrocytes and for loading them with hemoglobin as well. Hence the foods with high chlorophyl or hemoglobin content should be emphasized.
Prognosis.—This depends on patient’s desire for improvement of his condition. He can be improved by correction of whatever lesions there may be interfering with his freedom of thoracic motion. He can be benefited by manipulations which adjust the ribs, but his cooperation is essential. Lack of cooperation on the part of the patient, which would tend to increase the mobility and metabolism of the ribs, renders him more liable to any of the intercurrent pulmonary infections, as a result of his deficient thoracic ventilation.
Encourage free thoracic respiration especially when in school, or when under conditions which ordinarily would tend to slovenly habits of breathing.
(Green Sickness)
An anemia characterized by great reduction in the amount of hemoglobin. It most frequently occurs in adolescent girls. It seems to be associated with neurotic manifestations and menstrual irregularities.
Etiology.—Its cause is not well understood. Poor hygienic conditions may be a factor, but it is a condition found in all stations of life. The age and sex have led to investigation as to probability of lack of an ovarian internal secretion. The reports of workers are contradictory. The name of the condition is derived from the color of the skin, which usually ranges from a pale greenish tint to a slight pallor. Occasionally there is localized vasodilation of the cheeks giving brilliant color. Constipation accompanied by copremia seems to be either a causative factor or result. In many cases it appears to act in the dual role. Fixation of the middle and lower ribs accompanied by osteopathic lesions from the mid to the lower dorsal spine seem to be constant findings. The costal fixation leads to lessened respiratory excursion and resulting diminished oxygenation.
Diagnosis.—Chlorosis may be suspected from the color of the skin, perverted appetite, wandering neuralgias, heart palpitation, edematous infiltration, and shallow type respiration, but the diagnosis is not to be made without the aid of the blood count. The striking part of the blood picture is the great reduction in amount of hemoglobin carried by each erythrocyte. There is usually some reduction in the erythrocyte percentage but not in proportion to the decrease in color index.
There are usually many pessary-shaped and shadow erythrocytes. These are of all sizes, but seldom is the condition of such gravity as to cause more than an occasional nucleated red cell, and when found are most likely to be normoblasts. The staining reaction is of wide limits. Cells of all degrees of relative alkalinity are found and often there is a wide variation of staining reaction in the same cell. The number of erythrocytes is usually slightly decreased but not in the proportion that the hemoglobin percentage is, so that the color index is therefore strikingly low. Probably, the average color index for a typical case of chlorosis is 50, with an erythrocyte count of 4,000,000 and a hemoglobin of 40 per cent (Dare.) This drop in color index in chlorosis is far out of proportion to the clinical symptoms which would be expected from a similar reduction resulting from the ordinary causes of secondary anemia. The blood plasma is increased and the specific gravity is lowered, sometimes reduced from 1.055 to about 1.030.
Treatment.—The treatment of any malady in which the etiology may be apparently of widely different natures will naturally rationally vary with the apparent cause. If there is copremia, which seems to be a definite causative factor, this should be at once corrected. These patients form the cathartic habit readily, so physical and dietary methods of returning the digestive motility to normal should logically be given first trial. If it is a matter of lessened metabolism as a result of insufficient exercise, or blood oxygenation, outdoor gymnastics and breathing exercises may incite the stimulus to normal erythrocyte hemoglobinization. The diet should be of such nature as to furnish material both for erythrocyte formation and iron in form for ready absorption by them. The organic iron compounds of animal hemoglobin and vegetable chlorophyl are our most common and cheapest as well as most effective sources.
The medical treatment of chlorosis is based on the empiric use of inorganic iron. “The exact method in which iron exerts a favorable influence upon chlorosis still remains unsettled. It is difficult to understand why iron salts in the food which are sufficient for all ordinary needs, are insufficient in chlorosis. It seems most probable that iron cures chlorosis by acting as a stimulant to the blood forming organs” (Beifeld, The Basis of Symptoms.)
Clinically, osteopaths are daily obtaining rationally the necessary stimulus to the blood forming organs by removing all impedance from these organs caused by vertebral and costal lesions and by obtaining better digestive and respiratory hygiene.
Prognosis.—Recovery is to be expected and its rate will depend upon the thoroughness of the osteopathic work and the patient’s ability to respond to the stimulus. The blood may show chlorotic relapses with concomitant symptoms if in later life secondary anemia develops from hemorrhage, hook-worm infection, or other causes.
This anemia is of obscure etiology, characterized by progressive destructive hemolysis of the erythrocytes, usually with fatal termination. The cells retain their hemoglobin carrying ability, so that while the hemoglobin is decreased in percentage, the proportionately greater decrease in the number of erythrocytes leads to a marked increase in the color index. The destructive influence upon the red cells may be sufficient to allow only a small percentage of the erythrocytes to appear normal and show the greater number to be deformed, or in various stages of degeneration. Cells which in times of health would have been sent to the “salvage station” are retained to carry an over-load for them of hemoglobin to the needy tissues. Immature nucleated cells of all types are drawn into the battle long before they can be efficient carriers to help supply oxygen to the tissues. Seldom will a secondary anemia be severe enough to produce megaloblasts in the blood stream yet they are a rather constant finding in pernicious anemia. With these cells of irregular carrying capacity and development, anisocytosis and polychromatophilia are expected findings.
Symptoms.—The condition must be regarded as a symptom complex or a result of pathologic process or processes. A type of anemia very similar in symptoms and blood findings to the pernicious anemia is produced by the toxins of advanced malignancy, and by at least two forms of intestinal parasites, the ankylostoma duodenale and the bothriocephalus latus. In the true pernicious anemia we have similar results but are not able to locate the primary pathology. There are present synchronously, enormously increased destruction of erythrocytes and enormously increased production of them but we are unable to determine which is primarily at fault. The belief that the cells are more fragile and too easily broken up has led to the removal of the erythrocyte destroying spleen in the hope that destruction would be delayed until regeneration of even imperfect cells would balance the need. Occasionally, the algebraic sum of regeneration and destruction may be apparently balanced and not tell the tremendous amount of pathology both productive and destructive, that the body is going through.
The first symptoms are of easily produced fatigue of all the body, brain, muscles, diminished digestive secretion, and dyspnea. As a result of poor tissue oxygenation, fatty degeneration takes place in the more active organs as the heart, kidneys and liver. There may be extensive degeneration of varying areas of the central nervous system. Some of these areas are due to hemorrhages from the general tendency to breaking down of vessel walls. Often these areas of destruction affect the posterior horns of the spinal cord, and, occasionally, a blood count differentiates between similar symptoms of pernicious anemia and tabes dorsalis. There is seldom any emaciation; usually the patient appears “puffy” with a “pasty” color. There is variable subcutaneous edema. The symptoms being of such wide distribution and character, the patient is usually treated for all sorts of supposed conditions until some one makes a blood count at a time when there is enough disturbance of equilibrium to give the findings of pernicious anemia.
Treatment.—The treatment of the form due to intestinal parasites gives striking results on removal of the causative organisms. Some advise treating all cases having these blood findings on the assumption that the presence of these parasites is responsible for the condition. The treatment of the idiopathic form resolves itself into building up the ability of the body to resist disease and the removing of all possible agents for depressing the vitality of the body. Rest in bed coupled with the digestible and assimilable limit of nutrition often gives temporary improvement. Removal of questionable teeth also often aids for a time. Correction of troublesome osteopathic lesions is often accompanied by the same result. The symptomatic osteopathic treatment always makes the patient more comfortable, often gives temporary improvement, and, occasionally, has given a return to normal that has persisted for several years.
Prognosis.—It is nearly always possible to obtain transient improvement, but the pernicious anemia patient is usually dead within two years from the time the diagnosis is well established.
As a result of any inflammatory process, there is a physiological reaction or stimulus leading to an increase in the number of neutrophilic leucocytes found in the peripheral circulation. As long as this increase does not crowd out other cells, red and white, sufficiently to interfere with their ability to function there is nothing but gain to the body of the character of more efficient bacterial destruction. After the need for these cells has passed, their number is decreased by destruction and the lessening of their production, until an equilibrium is reached which will be maintained.
This same process of making and destroying is constantly going on for all of the different classes of cells found in the blood stream. Over-production of any type will lead to actual increase of that sort of cell in circulation, and, if unaccompanied by over-production of other types, will lead to a relative decrease of the other elements.
It is very difficult for the body to furnish normal cells very much in excess, relatively, of the normal number, so that when the stimulus leading to immense over-production is at work immature cells in great numbers are apt to be thrown into the blood stream. As an example, the case of leucocytosis which has a white count of 60,000 is extreme and the patient nearing death, yet it may not show many, if any, abnormal types of cells. A case of myelogenous leucemia with a white count of 60,000 would not be proportionately sick, and would be a mild case—yet the greater part of his white blood content would be made up of cells not found in normal blood. The leucocytosis patient is suffering more from the cause of his increase in number of cells, while usually the leucemia patient suffers because of the increase of cells. In one, the cause is usually extrinsic, and, in the other, it is intrinsic as far as the blood is concerned.
In general, then, the symptoms of a leucemia parallel in intensity the increase in cells. It takes energy to make these cells—other tissues are made to suffer from lack of this energy. Erythrocytes and white cells cannot occupy the same space at the same time. The increase in white therefore crowds the red cells out of function. Disease in relative and absolute content of erythrocytes decreases the oxygen carrying capacity of the blood stream. Hence, metabolism of the whole body suffers. Often, then, the whole apparent symptomatology of a severe leucemia is that of a secondary anemia.
The primary pathology is of hyperplasia of the particular genetic tissue of the type of cells which are in excess, and is proportionate in amount to the excess developed.
(Myeloid Leucemia; Myelemia)
Myelemia is a disease characterized by an enormous increase in the white cell content with proportionate changes in the spleen, liver, and the blood marrow.
Etiology.—It is a disease occurring at all ages, but the majority of cases are recognized in adult males.
Heredity, trauma to the spleen, malaria, syphilis, and rapid repetition of pregnancies seem to be at least exciting factors. A few cases have been reported in which tenth, eleventh, and twelfth rib lesions were definite etiologic factors by pressure.
Diagnosis.—The patient goes through a period of vague, indefinite, and wandering symptoms. General malaise, weakness often accompanied by dyspnea, and emaciation similar in many ways to incipient pulmonary tuberculosis, except that the slight temperature changes are not typical. At the same time there may be digestive discomfort of various kinds without typical pathology. Of these early symptoms the most persistent is the dyspnea which is a structural result of the increase in size of the spleen. As a direct pressure result of this hyperplasia, there may develop dropsical infiltration of the lower extremities and ascitic accumulation in the abdominal cavity.
With the changes in the blood itself, the blood vessel walls break down more easily, and subcutaneous hemorrhages, epistaxis and hematemesis are common.
In an attempt to destroy the excessive amount of white cells, the liver may become enlarged. But this occurs later and of much less degree than the enormous increase in size of spleen. There may be areas of hemorrhage with resulting softening in the spinal cord. The most likely areas to suffer are the posterior and lateral horns, with resulting paraplegia, spastic or ataxic.
Usually, the course is slow, and the condition is truly chronic. But, occasionally, the rapid increase and succession of symptoms, with concomitant blood changes, change the diagnosis to acute myelogenous leukemia.
The total cell count, red plus white, is diminished, for while there is enormous relative increase of the white cells a greater actual decrease takes place in the reds. This decrease in reds is partially relative from crowding out of erythrocytes by leucocytes, but there is also actual decrease in their formation, so that there is an actual anemia present as well as a leukemia.
In some respects the red cells behave as in chlorosis, each carrying a diminished percentage of hemoglobin, resulting in a low color index. Atypical staining reactions and morphology, together with many fractured forms, are the rule. Normoblasts are common throughout the course of the disease, but megaloblasts seldom appear until near fatal termination.
The changes in the white cells are enormous, both as to numbers and character of cells found. The total white count often exceeds 350,000. This, with the accompanying reduction in number of erythrocytes, leads to a reduction of the ratio between reds and whites to as low as 1 to 5 or 3, or occasionally 1 to 1. There is an actual increase in number of all the white cells with the possible exception of the lymphocytes. In the actual increase of polymorphonuclear neutrophiles and eosinophiles is rendered a sharp relative decrease by the enormous production of myelocytes. Basophiles are usually both relatively and absolutely increased. In a white count of 350,000 it is not unusual to have present 325,000 myelocytes, with 25,000 as the actual number of ordinary leucocytes. There is, therefore, a mild leucocytosis coupled with a violent leukemia. These two are combined with an anemia that varies with the course of the disease.
Treatment.—The treatment is largely hygienic, including thorough osteopathic attention to the lower dorsal and costal area. Symptomatic treatment is often followed by temporary improvement both clinically and in the blood picture, but complete recovery seldom takes place. Occasionally, roentgen therapy has given a “cure” lasting several years.
Prognosis is not good. These patients are frequently carried away quickly by some oftentimes slight intercurrent infection. Even if carefully guarded from such, the course of the process usually leads to death from exhaustion in two or three years.
Clinically, this is a parallel condition to myelogenous leucemia, except that the hyperplasia of cells occurs in lymphoid tissue, and leads to an enormous over-production of lymphocytes rather than myelocytes. It is more readily divided into acute and chronic forms than myelogenous leucemia from differences in symptomatology.
In the acute form, adolescents are usually affected, the condition beginning with tumefaction of the lymph glands, first noted in the cervical region, but usually a general involvement. Dyspnea results from pressure upon trachea and bronchi by the enlarged glands of the mediastinum. There is pyrexia of 103 to 105 degrees, intermittent in character.
The pressure upon nerve trunks and plexuses in the thorax leads to variable anginas distributed not only in regions actually imposed upon but over all sorts of possible reflex paths. The blood vessels of the skin are easily broken down so that slight injuries result in great suggillation. The patient rapidly develops anemia, and later goes into a syndrome similar to the cachexia of malignancy. In fact, the rapid termination and clinical course of acute lymphatic leukemia is parallel to the action of malignancy. Probably the condition will eventually be properly classified as a neoplasm of the blood itself.
The chronic form occurs in later life, and, instead of being an abrupt rapid process, is slow, progressive and painless. It has the lymph gland hyperplasia, but the enlargement is so gradual that compensation is established to a remarkable degree. It is usually a generalized process, first noted in the cervical and axillary glands because of their accessibility. Usually both the spleen and liver are enlarged, but this also is a slow and later development.
There may be exacerbations of temperature, but they are not constant or usually severe. Hemorrhages into the skin are not common, but pruritus may be very troublesome.
The patient comes to a physician because of symptoms resulting from his secondary anemia, dyspnea, dyspepsia, and palpitation.
The diagnosis cannot be made without the aid of a blood study. The blood picture shows a severe anemia with both the number of erythrocytes and the hemoglobin percentage very much lowered. Of the two findings, the hemoglobin percentage is relatively more decreased, so that the color index is markedly lowered.
In the acute form nucleated reds are common. Just before death these may show various forms and sizes as well as the normoblasts. In the chronic form normoblasts do not appear except as the case grows decidedly worse. As compared to myelogenous leucemia the anemia of lymphatic leukemia is of greater severity.
In the leucocyte count there is great increase in numbers, the greater part being composed of the lymphocytes. The lymphocytes may be either of the large or small variety, and occasionally are found in about equal proportions. In contra-distinction to the myelogenous type, the increased type of cells are of the mononuclear nongranular types. It is not very unusual to find a well advanced case of lymphatic leucemia without abnormal cells in the blood count, the expression of pathology being in the shape of disturbance in number and proportion of cells rather than in development of abnormal types. The actual number of leucocytes does not go as high in proportion to the gravity of the condition in lymphatic leukemia as it does in the myelogenous. In other words, a patient with lymphoid leucemia showing a count of 90,000 leucocytes with 90% of these lymphocytes is a much sicker man than the myelogenous case showing a 350,000 leucocyte count.
Usually there is an actual as well as relative decrease of all the granular types of leucocytes with the polymorphonuclear neutrophiles especially decreased.
The treatment is systemic and symptomatic. Recovery is not to be expected, but these unfortunates can be made relatively comfortable and given occasional respite by judicious osteopathic care.
(Lymphadenoma; pseudo-leucemia)
In a general way, the several conditions which are clinically leucemia, yet do not possess leukemic blood, can be classified as pseudo-leukemias. We do not definitely know the cause of leucemia as yet and can but little more than speculate on the various etiologic factors of the pseudo-leucemias.
Syphilis, malaria, tuberculosis, and malignancy are all considered as factors, and probably certain cases can be definitely associated with these conditions.
All of this group of pseudo-leucemias are characterized by early swelling of cervical lymph glands, followed by general gland enlargement, and by great destruction of the erythrocytes. There may be metastatic-like growths of lymphoid tissue in other organs. The enlargement of cervical glands usually begins on one side near the angle of the jaw, and most commonly in young male adults. These glands progressively increase in size, first are soft, then later become hard through fibrous proliferation. Each gland tends to increase in size by itself, not to coalesce with its neighbors, so that each separate gland can be palpated. This is more readily done as there is little tendency to fibrous adhesion formation to the overlying skin. These glands are painless throughout the course of the disease, and tend neither to caseate nor to suppurate.
The excised glands show a combined hyperplasia and connective tissue proliferation. In the soft stage of the tumefaction, the lymphoid hyperplasia is in preponderance, while, at the stage of hardening, the fibrous tissue derived from the trabeculae and capsule of the gland is in prominence. There is increase in the size of the spleen, and occasionally of the liver, but these are never as marked as those resulting from leucemia.
The symptoms are, first, those due to the glandular enlargement in the order of: dyspnea, hydrothorax, dysphagia, ascites, swelling of the extremities, and jaundice.
The destruction of red cells gives a resulting anemia which goes with and exaggerates the pressure symptoms.
A process of this kind to induce such grave changes over as well protected organs as make up the lymph system, must be virulent enough to set up other symptoms, to be associated with those due to pressure or to anemia. These are usually emaciation (giving greater prominence to glandular tumefaction), cachexia, and the implantation of masses of lymphatic tissue in organs where normally only traces of this tissue exist.
Fever is dependent upon the disturbed thermic metabolism and may be practically absent or subject to wide variations.
The erythrocyte count shows a progressive decrease with a greater proportion of broken down cells and abnormal types as the condition advances. The actual count is usually between 2,000,000 and 3,500,000 per cubic millimeter. The hemoglobin usually reduces in proportion to the erythrocytes, so that there is little change in color index.
The leucocytes are not markedly changed in number (seldom over 10,000), and this is often the diagnostic finding between leukemia and the pseudo-leukemias. Hodgkin’s disease usually has a high percentage of lymphocytes, so that there is an actual as well as relative decrease of the granular leucocytes.
The treatment is unsatisfactory, and is in the main symptomatic. Roentgen therapy has given temporary improvement, in some cases lasting several years. In general the prognosis is hopeless, the end occurring within four years of the time the condition is recognized.