Assessment of Risk Factors and Outcome of Thrombocytopenia in Intensive Care Unit Patients in Assiut Pediatric University Hospital
Assessment of Risk Factors and Outcome of Thrombocytopenia in Intensive Care Unit Patients in Assiut Pediatric University Hospital
The many comorbidities in the severely ill patient also make thrombocytopenia very common (∼ 40%) in intensive care unit patients. The risk of bleeding is high with severe thrombocytopenia and is enhanced in intensive care patients with mild or moderately low platelet counts when additional factors are present that interfere with normal hemostatic mechanisms (eg, platelet function defects, hyperfibrinolysis, invasive procedures, or catheters).
The many comorbidities in the severely ill patient also make thrombocytopenia very common (∼ 40%) in intensive care unit patients. The risk of bleeding is high with severe thrombocytopenia and is enhanced in intensive care patients with mild or moderately low platelet counts when additional factors are present that interfere with normal hemostatic mechanisms (eg, platelet function defects, hyperfibrinolysis, invasive procedures, or catheters). Even if not associated with bleeding, low platelet counts often influence patient management and may prompt physicians to withhold or delay necessary invasive interventions, reduce the intensity of anticoagulation, order prophylactic platelet transfusion, or change anticoagulants due to fear of heparin-induced thrombocytopenia.
The many comorbidities in the severely ill patient also affect platelet homeostasis, and, consequently, thrombocytopenia is very common in critically ill patients treated in the intensive care unit (ICU). Thrombocytopenia is usually defined as a platelet count of < 150 × 109/L, whereas severe thrombocytopenia is considered as platelet counts < 50 × 109/L. Thrombocytopenia has six major mechanisms, and it can be induced by hemodilution, increased platelet consumption (both are very common in the ICU after tissue trauma, bleeding, and disseminated intravascular coagulopathy [DIC]), increased platelet destruction (ie, immune mechanisms), decreased platelet production, increased platelet sequestration, or by the laboratory artefact of pseudothrombocytopenia .
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