Assessing thrombocytopenia in the intensive care unit: the past, present, and future

Abstract

Thrombocytopenia is common among patients admitted to the intensive care unit (ICU). Multiple pathophysiological mechanisms may contribute, including thrombin-mediated platelet activation, dilution, hemophagocytosis, extracellular histones, ADAMTS13 deficiency, and complement activation. From the clinical perspective, the development of thrombocytopenia in the ICU usually indicates serious organ system derangement and physiologic decompensation rather than a primary hematologic disorder. Thrombocytopenia is associated with bleeding, transfusion, and adverse clinical outcomes including death, though few deaths are directly attributable to bleeding. The assessment of thrombocytopenia begins by looking back to the patient's medical history and presenting illness. This past information, combined with careful observation of the platelet trajectory in the context of the patient's clinical course, offers clues to the diagnosis and prognosis. Management is primarily directed at the underlying disorder and transfusion of platelets to prevent or treat clinical bleeding. Optimal platelet transfusion strategies are not defined, and a conservative approach is recommended.

Figure 1.

Mechanisms of thrombocytopenia in sepsis. Multiple mechanisms have been proposed to contribute to the thrombocytopenia of sepsis. The relative contribution of each potential mechanism may vary among patients and within a given patient over time. DIC, disseminated intravascular coagulation.

Figure 2.

Time course of thrombocytopenia in septic shock. Mean platelet count (±95% confidence interval) in patients with septic shock who developed thrombocytopenia after ICU admission. Time axis is anchored to the day that vasopressors were discontinued (day 0). Only data for survivors are included.