Platelet Count

Whole blood. Peripheral blood smears prepared at the time of collection may also be useful, particularly when platelet aggregation is a problem.

Tube fill capacity

0.5 mL (500 μL for pediatric microtainer capillary tubes; fill tube to capacity.) (Note: This volume does not allow for repeat testing.)

Lavender-top (EDTA) tube.

Evaluate, diagnose, and/or follow up bleeding disorders, drug-induced thrombocytopenia, idiopathic thrombocytopenia purpura (acute or chronic), disseminated intravascular coagulation, leukemia states, chemotherapeutic management of malignant disease states; investigate purpura, petechiae; evaluate response to platelet transfusions, steroids, or other therapy

Clumping may cause false low count.¹ Platelet satellitism around neutrophils will cause a pseudothrombocytopenia. RBC or WBC fragments including fragmented fragile leukemic cells and neutrophil pseudoplatelets² may cause falsely elevated counts.

Automated cell counter; microscopic exam of peripheral smear if specific criteria are met

The platelet, of growing practical clinical importance in hemostatic considerations and a variety of medical/surgical processes is also fundamental to etiologic considerations of arteriosclerotic³ and malignant disease.⁴

Careful estimate of platelet number from stained peripheral blood smear can provide useful information. A variety of factors affect the distribution of platelets on a peripheral blood smear, and thus platelet estimates lack precision. Capillary blood platelet counts (c.f. to venous blood counts) may be significantly underestimated. Platelets are often clumped on smears obtained from capillary blood, contributing to imprecision. A small whole blood clot or very small fibrin clots in the EDTA anticoagulated specimen will usually be associated with clumping of platelets on the slide, and with a false low platelet count.

Quantitative platelet disorders have varied etiology. Thrombocytopenia may have an immunologic basis, the result of production deficiency due to the effect of drugs or physical agents, abnormal platelet pooling or increased destruction (eg, sequestration by large vascular tumor), or result from a variety of probably nonimmunologic mechanisms (eg, hypersplenism). Decreases may occur after bleeding, transfusion, infections, or relating to defective production of or regulation by thrombopoietin.

Drugs and chemicals associated with thrombocytopenia, often on an immune mediated basis⁵ or as the result of marrow suppression, include quinidine, quinine, heparin, gold salts, sulfas, rifampicin, ASA, digitoxin, apronal, chlorothiazides, chlorpropamide, meprobamate, antihistamines, chloramphenicol, penicillin, DDT, benzol, a variety of other industrial organic chemicals, diphenylhydantoin, PAS, hydrochlorothiazide, phenylbutazone, and a variety of antineoplastic chemotherapeutic agents. ASA acts by acetylating cyclo-oxygenase.

Thrombocytosis is less common, but likewise varied in etiology: physiologic (eg, postpartum, or after exercise); myeloproliferative syndromes (eg, thrombocythemia, some cases of chronic myelogenous leukemia, myelofibrosis with myeloid metaplasia); rebound following thrombocytopenia, marrow regenerative activity after bleeding episode, hemophilia, iron deficiency; asplenism, infections, inflammatory or malignant disease, especially carcinomatosis. Oral contraceptives may cause slight increase.

Congenital causes of thrombocytopenia include Wiskott-Aldrich syndrome, May-Hegglin anomaly, thrombocytopenia with absent radius, and Bernard-Soulier syndrome. See table.