Thrombocytopenia

THROMBOCYTOPENIA, a decrease in thrombocytes in the circulating blood. The circulating blood normally contains a definite number of blood plates or thrombocytes (Bizzozero's plates). Various counting methods give different figures; thus, according to Fonio's method (^<nonio) on a blood smear, 1 cm³ contains from 200,000 to 300,000 blood plates, while counting in a chamber according to Hofmann-Flossner gives from 600,000 to 900,000. A significant decrease in the amount of blood plates below the above-mentioned norms is designated as thrombocytopenia. A decrease in the amount of blood plates is accompanied by a symptom-complex of hemorrhagic diathesis (see). Markedly expressed symptoms of hemorrhagic diathesis are usually revealed when the amount of plates falls to 30,000 and below—the so-called critical Frank boundary. In thrombocytopenia, qualitative changes of the plates are also usually discovered—among the normal size of plates, large and giant plates are encountered, exceeding the size of erythrocytes and lymphocytes. In addition, plates and tails of syncytium, which have not divided into individual plates, are encountered. Occasionally, clotted granularity and marked basophilia of the protoplasm are observed. Prolonged bleeding time in thrombocytopenia is explained by the fact that on the wound surface of the vessel, adherent plates do not deposit and thus, if the vessel has not contracted, the wound opening remains open. The insufficient contractility of vessels some authors partly connect with the loss in thrombocytopenia of the tonifying action of plates on the smooth muscle of the vascular wall. Platelet-poor blood in vitro gives poor retraction of the blood clot. Physiologically, the amount of plates may decrease during the day; for instance, after a meal, regardless of its composition, most researchers have observed a fall in the amount of blood plates, which they explain by the influence of increased tone of the vagus nerve. In newborns, marked thrombocytopenia is noted, which is sometimes observed in infants. With old age, the amount of plates decreases on average to 85,000. In women during the menstrual period, the number of thrombocytes falls two, and sometimes even five times. Morawitz observed a fall of plates to 30,000. With parenteral administration of protein, the amount of plates first decreases, then increases. With anaphylactic shock, a sharp thrombocytopenia occurs, caused not only by redistribution of plates through the bloodstream, but also by disintegration of plates, as well as by the formation of thrombi from plates. Among medicinal substances, the following substances lead to thrombocytopenia, sometimes occurring rapidly (Plattchensturz): salvarsan, arsenic, bismuth, calcium, atropine, saponin, pepton, histamine, gelatin, corpus luteum extract, and others. Large doses of X-rays, radium, thorium, and polonium with a single action, as well as repeatedly acting small doses, often lead to thrombocytopenia; a similar symptom-complex headed by thrombocytopenia is the result of avitaminosis A and B; benzol acts analogously. In this case, a characteristic picture of the disease develops with hemorrhagic diathesis standing out prominently—cutaneous hemorrhages, hemorrhages from mucous membranes, anemia, stomatitis, necrotizing angina, and finally with the addition of secondary infection with high temperature and often with a fatal outcome. With respect to the blood in this so-called malignant thrombocytopenia of Frank (thrombopenia maligna, or aleukia haemorrhagica Frank—see Aplastic anemia), marked leukopenia, neutropenia, marked lymphocytosis, often monocytosis, and an eosinophilia are noted. Regeneration of red blood may be weak, therefore the amount of reticulocytes is sharply reduced; in other cases, reticulocytes hold at high figures. The bone marrow, varying in its regenerative status, and accordingly in its cellular composition, is also in thrombocytopenia. While in a number of cases the bone marrow even in flat bones at autopsy is yellow-fatty, poor in cellular elements (so-called aplastic bone marrow), in other cases it turns out to be red, containing many erythroblasts. Introzzi and Aubertin therefore propose to distinguish two forms in the group of malignant thrombocytopenia—aplastic and pseudo-aplastic anemia. The cellular composition of the bone marrow of the latter form often includes only histiocytic plasma cells, lymphoid elements, and a small amount of granulocytes. Megakaryocytes—giant cells, from the protoplasm of which, according to the opinion of most authors, blood plates are formed by off-shoelining—are sharply reduced in number, and in some cases it is difficult to find individual specimens. Megakaryocytes are also qualitatively changed—the majority of them represent young forms, so-called megakaryoblasts with basophilic protoplasm without granularity. Regarding the pathogenesis of malignant thrombocytopenia, there is no generally accepted opinion. Thus, Frank considers the primary toxicosis of the bone marrow, while Naegeli, Turk, and others consider that exhaustion, aplasia of the bone marrow occurs secondarily as a result of hemolytic, resp. toxic, action on the blood of various pathologic processes. The opinion of Barinstein deserves attention, that hypofunction of the adrenal system leads to a decrease in the function of the bone marrow, in particular to thrombocytopenia. Freyfel'd also considers that changes in the bone marrow in this disease are functional, not locally degenerative; in the ganglia of the marginal column they were found in this disease to be sharp changes, mainly of an inflammatory nature. Thrombocytopenia of Werlhof, the so-called essential or benign thrombocytopenia (see Werlhof's disease), is not accompanied by changes in other formed elements of the blood; the amount of megakaryocytes in the bone marrow in this disease does not decrease. In individual cases, degenerative changes on the part of the protoplasm of megakaryocytes are noted, in particular its granularity; in other cases, these changes are absent. The erythroblastic system suffers only secondarily as a result of significant and repeated hemorrhages; changes on the part of leukoblastic tissue are also not discovered in typical cases. Frank, Glanzmann, Oberling consider the cause of thrombocytopenia to be the reduced production of plates by megakaryocytes. Kaznelson, on the contrary, sees the cause of thrombocytopenia in the increased destruction of plates by the spleen. Regarding the heredity of this disease, see Werlhof's disease. A great significance in the symptom-complex of hemorrhagic diathesis has the state of the neurovascular apparatus; this is also evidenced by the positive therapeutic effect obtained in some cases of Werlhof's disease from hypnosis. To the number of symptomatic thrombocytopenias belong thrombocytopenia in various forms of splenomegaly, in Wilson's disease, in pernicious anemia, in acute leukemia. Among acute infectious diseases with signs of hemorrhagic diathesis, thrombocytopenia is observed in measles, scarlet fever, in typhoid diseases, in dysentery, smallpox, and chickenpox, as well as in various septic diseases. Rare cases of thrombocytopenia occur in tuberculosis, syphilis, and lymphogranulomatosis.