الفهرس 
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Abstract
Thrombocytopenia is commonly seen in critically ill patients. In addition, some patients, such as those with uremia or von Willebrand disease (vWD), may have dysfunctional platelets despite normal counts. When mild, thrombocytopenia may not increase the bleeding risk substantially, but severe thrombocytopenia is associated with both increased bleeding risk and higher mortality (Rice et al., 2009).
As the most common coagulopathy in the ICU, the etiology of low platelet counts is often multifactorial resulting from the underlying disease state, medications, or as a result of consumption of thrombi. Although thrombocytopenia often improves with treatment of the underlying illness, an in-depth understanding of the causes of thrombocytopenia and subsequent action may raise platelet counts and prevent unnecessary delay of invasive procedures or exposure to platelet transfusion risks in critically ill patients (Rice et al., 2009).
Thrombocytopenia may also be a manifestation of a disease that promotes clotting, such as heparin induced thrombocytopenia (HIT) or disseminated intravascular coagulation (DIC) (Strauss et al., 2002).
The cause of thrombocytopenia in most ICU patients is multifactorial, involving some combination of the following four mechanisms: increased destruction or consumption; decreased production; dilution; and sequestration (Drews, 2003).
The present study was conducted in Theodor Bilharz Research Institute’s ICU throughout 6 months. Patients who experienced even a single episode of thrombocytopenia of less than 150×109 cells/L during ICU stay were classified as ”group A”. The rest of the patients included in the study and didn’t develop thrombocytopenia during ICU stay were classified as ”group B”.
During the study period, 40 of the 100 studied ICU patients developed thrombocytopenia of less than 150×109 cells/L, producing a global incidence rate of 40 episodes of thrombocytopenia per 100 admissions.
All patients were subjected to thorough clinical assessment (including history taking and clinical examination) and laboratory examinations (including CBC, coagulation profile, kidney functions tests and liver functions tests).
The severity of illness was evaluated with the first-day APACHE II score (Acute Physiology and Chronic Health Evaluation) and SOFA scoring (Sequential Organ Failure Assessment) daily during ICU stay starting from the 2nd day.
This study showed that the incidence of thrombocytopenia in ICU patients in Theodor Bilharz Research Institute was 40% and that sepsis was the first cause of thrombocytopenia while heparin induced thrombocytopenia (HIT) was the second cause.
The group of patients who developed thrombocytopenia showed higher mortality and morbidity as denoted by higher 1st day APACHE II, more ICU stay, higher incidence of mechanical ventilation and for longer duration.
This leads us to the fact that thrombocytopenia can be considered an important prognostic factor for ICU patients and frequent assessment of the platelets count must be taken in consideration during ICU patients management.
Our study has several shortages as it was limited to a single hospital, in a short duration and on limited number of patients. So, further studies should be performed in the future to evaluate the impact of platelet count declines on mortality and morbidity. It is better for further studies to be performed in multiple centers, for longer duration and to include more candidates with more subgroups.