Complete Text (Part 18)

to .7. Platelets gone. Pronounced leukopaenia (1,200 to 2,000). At autopsy one finds metaplasia of bone marrow. Xo islands of actively func tioning red or white cells. (Musser) : 1. Coagulation time distinctly delayed. 2. Xo reticulated blood cells ever found. 3. Minimal resistance unchanged. Maximal resistance increased. Etiological factors in aplastic anaemia : Three groups : 1. So-called aplastic anaemia from chronic repeated hemorrhages, characterized chief- ly by history. 2. Destructive property of some toxin, hemo lytic in origin. They include all the chronic hemolytic anaemias. The clinical history is very important. 3. Aplastic P. A. In the aplastic stages of P. A. there is a constantly dropping W. B. C. count and no evidences of E. B. C. re- generation. Xaegeli says a better name for aplastic anae- mia is aregenerative anaemia. Imi^ortant points in all cases : 1. Clinical history. 2. Barely reduction of B. B. C. is as great as in P. A. 3. Age — usually under 30 or over 60. V. Carcinoma of the stomach. Possible existence of pain. Patient's historv' — same general symptoms, but usually loss of weight. G. I. findings may or may not have free HCl. (Pvloric end do not.) , 235 . Occult blood apt to be absent in P. A. Stomach Inperniotile in P. A. Blood : Allow to clot — likely to look normal in car- cinoma. In P. A. serum lias high color, but not same proportion between clot and serum. R. B. C. rarely below 2,000,000. Poikilocytosis and anisocytosis less marked as a rule. C. I. hovers around 1, varies more than in P. A. Platelets usually plentiful. W. B. C. usually normal or above. P. M. N. increase. X-raj^ does not always show distinction. Leukemia s. A leukemia is a disease characterized by an in- crease in the Avhite cells of the blood usually abnor- mal, and by a general hyperplasia of the leukopoie- tic organs of the body. The blood condition is a symptom of this hyperplasia. There may be a digres- sion between hyperplasia and leucocytosis. Leuke- mias may have a count as low as 50,000, and a leuco- cytosis may reach 100,000. Leukemias were recog- nized by Virchow in 1845 and clinically in 1850. The classification at that time was : 1. Splenic, 2. Lymphatic; depending upon which was enlarged. There are no true transitional stages between tlie lymphatic and the myeloid which speaks for the dual origin of these cells. In lymphoid leukemia the bone marrow^ is involved very late. Possible sources of origin : 1. Parasitic — amoeba. 2. Cancer. 240 lymph glands, exophthalmos, periosteal' infil- trations, etc. 31yeloses. ^[yeloid lenkemias are general hyperplasia of the myeloid tissue . They have the same general group- ing as the lymphatic lenkemias. 1. Chronic myeloid leukemia. 2. Acute myeloid leukemia. :>. Chloromyelosis (myeloid chloroleukemia ) . 4. Aleukemic myelosis. 1. Chronic Myeloid Leukemia. Occurs chiefly in people in middle lite, more in men than in women, rarely in children. It is char- acterized by slow development with gastric symp- toms, weakness, poor sleep, often marked sweating. (Often tuberculosis is suspected.) Special symptomatology. ( a I Enormous enlargement of spleen, with smooth surface, hard, and notch preserved. Usually sensitive. (b) Liver enlarged, smooth, hard, keeps normal shape. Rarely jaundice. (c) Lymph glands not enlarged and inconspicu- ous. (d) Bones frequently tender and patient often has bone aches. (e) Ascites. (f) No enlargement of tonsils (except late). (g) Irregular fever. (h) Hemorrhagic diathesis rare, however, ten- dency to skin eruptions. (i) Priapism. (j) Amenorrhea. Blood findings : Gross color unchanged at first. Blood thick, coagulation time increased. Oxidase reaction marked. 233 Remission stage — decrease in AY. B. C. Usually well marked anaemia, but never so severe as P. A. Characteristics of Secondary Anaemia. C. I. low, cells pale, if nucleated tend to be nor- moblasts. Nucleated forms tend to be pres- ent more than they ever are in P. A. Differential count shows greater peculiarities than P. A. III. Leukanaemia. Larger number of megaloblasts. Severe anaemia with leucocytosis. Probably atypical forms of Von Jaksch's (may occur in older people). Rapid course — usually die within 2 months. IV. Aplastic anaemias. An anaemia different from any pernicious or secondary anaemia, characterized by retro- gressive changes in the bone marrow. ( At autopsy one finds all the bone marrow re- placed by fat.) 1. Primarily of young people. (May be seen from 5 to 60. ) Well under 30 as a rule. 2. Clinical course different. Jlapid and pro- gressively fatal. (Two months and as low^ as 6 days.) 8. From the start tendency to subcutaneous and mucus hemorrhages. 4. High and persistent fever. 5. Blood picture: R. B. C. — severe and intense anaemia. (1,000,000.) No poikilocytosis or anisosytosis. May be slight general increase in size. Absence of polychromasia of any type. No nucleated reds. 238 protoplasm is basic and seems almost absent in many. Blood platelets — diminisbed. Diagnosis — blood picture. Difterential diagnosis : Lympbosarcoma, tbc, and myeloid leukemia . l^rognosis : Fatal after remissions. -. Acute Lympliatic Leukemia. 1. r^ever, witb prostration. -. (iangrene and ulcer in G. I. tract. ^1 Hemorrbagic tendency. J. Rapid course of disease. Anaemia, cacbexia, deatb in one to tAvo montbs. (Minimum one week.) 5. More acutely fatal and common in cbildren. (5. Tbere is higb irregular fever. 7. Progressive splenic and lympbatic enlargement. Diagnosis : Ulcerative tonsilitis and stomatitis. Prodromal period, witb occasional mild attacks of fever and general malaise, followed in a few weeks witb cervical glandular enlargement, tben witb a flare up and extensive bemorrbage and tbe picture above given. Blood picture — abounds in lympboid cells. Otber groups : 1. Like acute rbeumatic fever — polyarticular, usu- ally painless involvement. 2. Like typboid — diarrbea and abdominal pain. 3. Like pleurisy. 4. Like meningitis. 3. Cblorlympbadenoses. In tbis condition tbere are tumors in various parts of tbe body witb cbar- acteristic greenisb tinge. Tbey are divided into groups according to location. 1. Tumors in or on tbe skull. Symptoms — exopbtbalmos, generally symmetrical, witb swelling of tbe occipital and temporal regions. 239 2. Subperiosteal infiltration of the spinal column, ribs and pelvic bones. 3. Lymphatic leukemia Avith tumors, but only at autopsy does the green color of the tumors be- come apparent. In all the cases the blood picture is that of chronic and acute lymphatic leukemia, and the tumors show chronicity, which runs with leukemia. Most cases are rapidly fatal and show no remissions. Over 50 per cent of the cases are in children. 4. Aleukemic Lymphadenoses. This is a leukemic state with low AY. B. C. count. Clinical differences— lymph glands not as swollen, course of disease is quite chronic and may develop into chronic lymphatic leukemia. Blood picture is practically the same, qualitative- ly, as lymphatic leukemia, but absolute numbers are lower. Naegeli groups into six types: I. General lymphatic hyperplasia (aleukemic blood picture). II. Lymph hyperplasia more localized^glands adhere to one another and the un<lerlying tissues so that the diagnosis of h^mphosar- coma is sometimes made. III. Very large splenic tumor with oniy slight lymphatic hyperplasia. Spleen shows uni- form enlargement and keeps normal form. IV. Localized lymphatic infiltrations in pharynx, larynx, eyelids and cheeks. Spleen may be large or small. V. Slight anaemia and low fever, aleukemic state. Suddenly acute leukemia, severe hem- orrhagic diathesis and death in a few hours. Actual bleeding from skin. Vl. Chloroma in skull with aleukemic blood picture. Enlargement of spleen, liver and 236 3. luleclious — present view. Facts wliicli suj)- port view: (a) StoruiT, rapidly progressive, febrile con- dition. lb) Apparently follows septic conditions. (c) Apparently contageous in a few cases at least. Similar condition can be trans- mitted in animals. Lymphadenoses. These are conditions associated with lymphatic hyperplasia and with characteristic blood picture. Kinds : 1, Chronic lymphatic lenkemia. 2. Acute lynix)hatic leukemia. 8. Aleukemic lymphadenoses. 4. Chlorlymphadenoses. 1. Chronic Lymphatic Leukemia. Begins in childhood or in young adults with slow onset and probably aleukemic states, Avith only qualitative blood picture changes during period of hyperplasia. Sexes evenly distributed. Symptoms : 1. Marked enlargement of tonsils. 2. General symmetrical enlargement in neck and axilla. 3. Splenic enlargement with perisplenitis. 4. Hemorrhagic diathesis (bleeding from any mucus membrane). 5. Severe headache and visual disturbances. G. Usually anaemic symptoms (languor, slight loss of weight, etc.). 7. Stitch in side and signs of pleurisy. Glands : There are generally enlargements some- where, sometimes ahead of the other symptoms. Sometimes only the retroperitoneal glands are in- volved. They are usually soft, isolated, not adher- ent, rarely matted together. They are grayish, fria- 241 E. B. r. :],50(),000 to 4,000,000. rolychromasia, large numbers of nucleated reds. Hb. reduced pro- portionately— therefore about normal C. I. Platelets markedly increased. W. B. C. Increased and may go up to 1,000,000. Large myelocytes abundant. Larger types pre- dominate with basic protoplasm, irregular in size and staining reactions. Nuclei show a fine network structure. Some myeloblasts. Typical P. M. N. is ]n'edoniinating celL Eosinophiles increased in abso- lute count. Mast cells in no other cases seen so frequently. L. M. and Transitionals increased in actual numbers. Lymphocytes only in small num- bers (absolute count little changed!. Frequently find true megakaryocytes, but so fragile as to be only recognized by the nucleus. There are three changes of interest: 1. Changes under X-ray and arsenic treatment. Cell count may drop to normal or may be same general count, with immature cells almost dis- appearing. 2. Changes during infectious diseases — may loose all abnormal cells. 3. Appearance of myeloblasts. Increase markedly as disease grows worse. Increased enormously in cases treated by X-ray and influenced un- favorably. In agonal stage may rise to 20-50%. Prognosis. There are stages of remission. An apparently slight case, perhaps lasting for years, may suddenly become acute, and some slight cause may bring about a change for the worse. Etiology unknown. Treatment : Arsenic. Benzol — great care should be exercised. Give small doses in a bland oil and stop when the count reaches 242 20,000 to 30,000. Wait till the count stops falling before giving again. X-ray and radium — in vogue. 2. Acute M} eloid Leukemia. Kuns a course like acute lymphatic leukemia. Has a clinical picture of lymphatic. Distinguished only by blood picture. The more acute the disease the less typical the characteristics. The course of the disease is steadily progressive and fatal. 3. and 4. Same thing is true as in other tAvo groups. It is to be remembered that any leukemia may un- dergo an aleukemic stage either normally or in- duced. Distinguish chronic myeloid leukemia from : 1. Hyperleucocytosis due to infection — u^r./Zy in children. 2. Severe anaemias may show high leuc \ytosis — rarely hyperleucocytosis. 3. Metastasis of malignant tumors in bone mar- row. Picture more distorted. Blood findings in infectious diseases : 1. Leucocj^tosis with absence of eosinophiles points to pyogenic infection, the so-called "sep- tic factor." The reappearance of eosinophiles is a favorable sign. 2. Lymphocytosis occurs in pertussis, rickets, con- genital lues, tbc, measles, typhoid, influenza, diseases of endocrine glands. 1. Pertussis — hyperleucocytosis, lymphocytosis, B. Pertussis in the sputum, R. B. C. unchanged. W. B. C. 22,000 to 25,000. 40 to 60% snuill lymphocytes. 2. Poliomyelitis— leucocytosis, 20,000 to 50,000 W. B. C. count with 80% P. M. N. Spinal ihiid with cell increase, especially small lym- phocytes. Absence of ^'septic factor." 243 ?). Epidemic ineniiioitis — leucocytosis, constant septic factor, bacteraemia, spinal fluid shows specific organism with purulent fluid. K. B. C. unclumged, W. B. C. 12,000 to 55,000. P. M. X. 85 to 90%. Eosinophiles diminished. Spinal fluid cell count shows almost exclusively pus cells. 4. Malaria — leucopaenia, absence of septic factor. Increase in L. M. Pigmented leucocytes, and presence of organism. R. B. C. show anaemia usually, C. T. constantly low. Usually signs of regeneration. W. B. C. increased before par- oxysm, after chill rapidly developing leuco- paenia (2,000 to 3,000). P. M. X. decreased. Phagocytes of L. M., with marked amoeboid activity. Thayer's classification of blood findings in malaria : (a) Ordinary S. A., with abundant regeneration. (b) Blood picture essentially P. A. (c) Rapidly fulminating. (d) Severe, chronic, aregenerative S. A. 5. Measles — leucopaenia, diazo reaction in urine. Moderate pre-emptive leucocytosis. Platelets decreased or absent. (5. Diphtheria — leucocytosis, septic factor, bacilli from throat, albuminuria, hig'h R. B. C. at first, later mild anaemia. W. B. C. 14,000 to :>0,000, present from early stage, and falls- slowly. Eosinophiles absent. P. M. X. 90%. Leucocytes should fall rapidly after antitoxin. 7. Scarlet fever — leucocytosis, absence of septic factor^ eosinophiles increased. Diazo reaction. Streptococci in smears or blood cultures. . R. B. C. unchanged. W. B. C. show a consistent increase especially before the rash, normal at three weeks. P. M. X. 90 to 95%. Glandular infections (P. M. X\ go up). If leucocytes do 244 not respond it means severe infection. Plate- lets increased. Dalil's leucocytic inclnsions may be present. 8. Typhoid fever — S. A., leucopaenia, increase in lymphocytes, blood cnlture, Widal abont tenth day, late diazo, no septic factor. R. B. C. 5,500,- 000 to 4,500,000. Hb. rednced more than E. B. C. always. Nucleated forms rarely. W. B. C. — the greater the leucopaenia the more severe the case. P. M. X. 50%, eosinophiles absent in three-quarters of the disease. Mono increase. Favorable findings are moderate leucopaenia, with a return of eosinophiles in three Aveeks. Hemorrhage and perforation: 1. Liver dullness. 2. W. B. C. going up from the depths. The count may go down. It may remain stationary Avith alteration in liver dullness. Hemorrhage — W. B. C. increase and then leucopaenia. 9. I*neumonia — hyperleucocytosis, septic factor, fibrin increase. Rusty sputum, chloride reac- tion, pneumococci in the blood and sputum. R. B. C. 4,000,000. W. B. C. increased 15,000 to 25,000. The count may diminish at first. P. M. N. 80 to 85%. Septic factor marked. Hodgkin's Disease. Hodgkin in 1832 described this disease Aery im- perfectly. Three theories as to origin : 1. Cohnheim and Sternberg. A tbc. origin based on (a) acid fast organism, (b) Tbc. elseAA'here. (c) Perhaps human reaction to bo\ine. Still an open question. Probably coincidental rather than true etiological fact. 2. True tumor. Described as pseudo-leukemia. Against it: (a) Histology, (b) Attempts to transplant a failure. o. True infectious granuloma. Bunting and 245 Yates) Diphtheroid organism and vaccine treat- ment. jS^ow stands as follows : (a) The diphtheroid can be cultivated from glands. (b) The diphtheroid can be cultivated else- where. (c) Glands in general have a normal flora (Bloomfield). Blood picture (Bunting and Yates). 1. Kelative or complete absence of anaemia. •2. Kelative and positive increase in L. M. 3. Platelets increased notoriously. 4. Eosinophilia. 5. Leucocytosis with P. M. X. increase. Many observers fail to get this picture. They get a slight tendency to this with many variations. There is no consensus of opinion as to etiology or blood picture. Only positive diagnosis is removal and examination of gland. Conditions with anaemia and si)lenomegaly : 1. Banti's disease — splenic enlargement, tendenc}^ to hemorrhage, occurs after 25 to 30. Blood picture is not characteristic. 2. Splenic anaemia — see above. 3. Gaucher's disease — in young children, progres- sive splenic enlargement, anaemia, no jaundice, no blood destruction, no characteristic blood picture, familial disease. 4. Hemolytic anaemia, acquired or inherited. True bone marrow dystrophy, hemolytic function of the spleen. Icterus, constant urobilin in acho- luric urine. Moderate secondary anaemia, de- creased resistance of R. B. C. Reticulated, vitally staining R. B. C. Splenectomy curative. 5. Pernicious Anaemia with splenic enlargement. Paroxysmal Hemoglobinuria. The patient either has hemorrhage after exposure 246 to cold or lias secondary anaemia from unexplained hemorrhage. 95% have lues, and it responds to sije- cific therapy. The diagnosis is often made by sub- jecting patient to cold. Experiment: Use patient's serum and his washed corpuscles. Patient's serum ]3lns K. B. 0. at 37 deg. C. gives no hemolysis. Patient's serum plus R. B. C. at 0 deg. C. gives no hemolysis. Patient's serum i^lus R. B. C. at 37 deg. C, after chilling at 0 deg. C, gives hemolysis. Purpura and Pathological Hemorrhages. 1. Definition of purpura: A tendency to spon- taneous hemorrhages developing in and be- neath the skin and mucus membrane in any part of the body. The size varies from i)in point to several cm. in size. (a) Pin point, small areas — petechiae. Chiefly on extremities, especially legs. (b) Lines or streaks — vibices. (c) Large areas — ecchymoses. (d) Extensive areas — suggilation (covering whole thigh, etc.). When recent they are usually bright red, but later become livid and purple. No remnants in time. The}^ are generally not elevated, no indura- tion, cannot bepressed out, differing from erythremia in this respect. Gangrene and ulceration common. They frequently come in crops, and are commonest on the legs and arms, and occur mostly on the ex- tensor surfaces. N 247 2. Occurrence: 1. Symptomatic — secondary. 2. Idiopathic — primary blood trouble, 1. Symptomatic purpura. (a) Acute infectious diseases. It may occur in any infectious disease, especially where there is bacteraemia : 1. Typhus. 2. Small- pox. 3. Epidemic meningitis. 4. Endocar- ditis, Avhere it is especially valuable in con- nection with the clinical history. (b) Chronic malnutrition — cachexia and malig- nant states in general (especially of the bone). (c) Conditions associated with jaundice. Con- nection not known, but may be due to some impaired function of the liver. (d) Blood diseases. (e) Chronic nephritis — rare. (f) Drugs — rare. (lodin, mercury, antipyrene, aromatic drugs as copaiba, turpentine, etc.). (g) Mechanical injuries. Trauma and also due to the bite of parasites, etc. (h) Nervous forms — with hysterical seizures or along nerve trunks in neuritis. Only when all these causes are excluded can one go to the 'Trimary purpuras" in which the funda- mental cause is