[Skip to Content]
Access to paid content on this site is currently suspended due to excessive activity being detected from your IP address 54.161.216.242. Please contact the publisher to request reinstatement.
[Skip to Content Landing]
Article
April 1955

Management of Thrombocytopenic States

Author Affiliations

Boston

From Saint Elizabeth Hospital, the New England Center Hospital, and the Department of Medicine, Tufts College Medical School; Established Investigator, American Heart Association.

AMA Arch Intern Med. 1955;95(4):543-556. doi:10.1001/archinte.1955.00250100049005
Abstract

Either defect of production of platelets from the bone marrow megakaryocytes or excess of their destruction or utilization in the peripheral circulation may result in thrombocytopenia. These two basic pathogenetic mechanisms are reflected into two main types of this syndrome, amegakaryocytic and megakaryocytic (Table 1). Whatever the pathogenetic mechanism of thrombocytopenia in the individual patient may be, platelet deficiency results in serious breakdown of the hemostatic process, involving all of its phases and mechanisms 1: A. The "resistance" of the vascular wall appears decreased. The tourniquet test becomes positive. B. The ability of the vessel to contract effectively after injury is also impaired, owing to lack of serotonin, an agent liberated by platelet disintegration. Perhaps for this reason, the bleeding time is prolonged. C. The fibrin clot retracts poorly. D. The coagulation of blood becomes abnormal, since platelet deficiency causes impaired formation of thromboplastin, and this, in turn, results in

First Page Preview View Large
First page PDF preview
First page PDF preview
×