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Chapter 171: Quantitative Abnormalities of Platelets: Thrombocytopenia and Thrombocytosis

Theodore E. Warkentin

THROMBOCYTOPENIA

Key Clinical Questions Thrombocytopenia

  • image Does the patient have true thrombocytopenia or pseudothrombocytopenia?

  • image What is the timing of onset, progression, and severity of the thrombocytopenia?

  • image Is the thrombocytopenia isolated, or is there concomitant anemia, leukopenia, or both?

  • image What are the findings of the peripheral blood film?

  • image What tests and studies are useful to evaluate each etiology?

  • image What is the frequency of specific causes of thrombocytopenia in defined clinical circumstances?

  • image Is the thrombocytopenia a marker of bleeding risk, thrombosis risk, or adverse prognosis?

  • image What treatments are available for each etiology?

Thrombocytosis

  • image Is the thrombocytosis newly acquired during the hospitalization?

  • image Is there concomitant splenomegaly and/or abnormalities in hemoglobin or white blood cell levels?

  • image Does the thrombocytosis predate the hospitalization?

  • image Is the red cell size (mean corpuscular volume) increased or decreased?

INTRODUCTION

The normal platelet count range is approximately 150 to 400 × 109/L (150,000-400,000/mm3). An individual’s platelet count usually remains relatively constant during life. The platelet count decreases normally during pregnancy (gestational thrombocytopenia). The platelet count increases to above the usual value following an acute self-limited thrombocytopenia. For example, after major surgery, an early postoperative platelet count nadir is observed; subsequently, thrombocytosis occurs, with the peak platelet count reached approximately 2-week postsurgery, with a late postoperative platelet count nadir occurring 2 weeks later (ie, approximately 1-month postsurgery) (Figure 171-1). As discussed later in this chapter, these postsurgery platelet count changes are expected, and reflect physiological consequences of changes in thrombopoietin-induced (TPO-induced) platelet production triggered by the initial acute surgery-associated platelet count fall.

Figure 171-1

Serial platelet counts in an 81-year-old male who underwent coronary artery bypass surgery (day 0). The patient’s usual platelet count (“baseline”) was ~160 × 109/L. Following acute surgery-associated thrombocytopenia (early postoperative platelet count nadir, day 1), the platelet count rose, peaking by day 15 at 294 × 109/L (ie, almost twice the preoperative value). The platelet counts then progressively declined, resulting in a late postoperative platelet count nadir (99 × 109/L) observed on day 29, with a second, much less marked, platelet count peak (191 × 109/L) reached on day 38. The platelet count value of 99 approximately 1-month postcardiac surgery prompted a hematology consultation. The hematologist’s opinion was that these postoperative platelet count fluctuations were expected, reflecting physiological increases and subsequent later decreases in blood thrombopoietin (TPO) concentrations (as blood TPO levels correspond inversely with platelet count levels), with corresponding increases and decreases in platelet production by the bone marrow megakaryocytes. The over- and undershooting of the platelet counts—in relation to the patient’s baseline platelet count value—are explained by the lag time of several days required for changes in TPO levels to produce corresponding changes in marrow platelet production. As predicted by the hematology consultant, the platelet counts began to recover, indeed overshooting the baseline platelet count one more time (days 38-44).

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