Platelet Count

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.

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 Order 115345 for citrated platelet count.

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.

1. Solanki DL, Blackburn BC. Spurious leukocytosis and thrombocytopenia. A dual phenomenon caused by clumping of platelets in vitro. JAMA. 1983 Nov 11; 250(18):2514-2515. PubMed 6632146

2. Merz B. Newly identified particle may explain spurious platelet count. JAMA. 1983 Jun 17; 249(23):3146-3147. PubMed 6854834

3. Halushka PV, Knapp DR, Grimm L. Prostaglandins, thromboxanes, and platelet function. Curr Top Hematol.1979; 2:75-143.

4. Doolittle RF, Hunkapiller MW, Hood LE, et al. Simian sarcoma virus onc gene, v-sis, is derived from the gene (or genes) encoding a platelet-derived growth factor. Science. 1983 Jul 15, 221(4607):275-277. PubMed 6304883

5. Moss RA. Drug-induced immune thrombocytopenia. Am J Hematol. 1980; 9(4):439-446. PubMed 6452056

Rajasekhar A, Gernsheimer T, Stasi R, James AH.2013 Clinical Practice Guide on Thrombocytopenia in Pregnancy. Available at: http://www.hematology.org/Clinicians/Guidelines/Quick-Reference.aspx. Washington, DC: American Society of Hematology; 2013. Accessed June 30, 2014.