الفهرس 
Evaluation of platelet functions
Pathophysiology of sepsisOnly 14 pages are availabe for public view
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Abstract
Coagulation disorders are common among intensive care patients and may range from isolated thrombocytopenia or prolonged global clotting tests to complex defects, such as disseminated intravascular coagulation. There are many causes for coagulation disorders and each of these underlying disorders may require specific therapeutic management. Hence, a proper differential diagnosis and the initiation of adequate treatment strategies are crucial to reduce morbidity and mortality in critically ill patients with coagulation abnormalities.
Activated platelets secrete numerous compounds from their α granules, dense granules, lysosomes and cytoplasmic stores, all contributing to platelet adhesion, aggregation and modulation of endothelial function and inflammatory processes. Nowadays, platelets are considered vital to host immunity.
In the intensive care unit, approximately 40% of the patients develop thrombocytopenia,and INR is increased in 30%. Disturbed coagulation and its consequences may lead to organ dysfunction Platelets are consumed intravascularly by the activation of the coagulation process (diffuse disseminated intravascular coagulation) [DIC] or by deposition on damaged endothelial cells (microangiopathy). Production defects result from those diseases that cause bone marrow failure, such as aplastic anemia, infiltration by leukemia or another malignancy, fibrosis, granulomatous disorders, or tuberculosis. Causes of thrombocytopenia related to increased destruction include immune thrombocytopenias (e.g. autoimmune, alloimmune, drug-induced) and increased consumption (e.g. DIC, TTP). Causes of thrombocytopenia related to decreased production include bone marrow depression.
The unexpected occurrence of thrombocytopenia in a patient with a recent history of drug exposure should always give rise to the suspicion of DIT.
A medical history taking and physical examination are vital, since many different conditions can produce similar laboratory abnormalities. For example, end-stage liver failure and disseminated intravascular coagulation produce thrombocytopenia and similar changes in standard tests of coagulation, and yet the management of and prognosis for these conditions are very different. A peripheral-blood smear is a vital investigation tool in most cases to confirm a low platelet count and the presence or absence of other diagnostic features, such as red-cell fragmentation, platelet morphologic abnormalities, or evidence of dysplasia or hematinic deficiency.
Thrombocytosis or thrombocythemia is a condition characterized by the presence of elevated platelet counts (>450 x 109 /L) in the blood. One must first distinguish reactive from primary thrombocytosis.The presence of acute or subacute infection, a connective tissue disorder, vasculitis, hemolysis, active bleeding, recent surgery, history of splenectomy, or iron deficiency anemia favors the diagnosis of reactive thrombocytosis.
Patients with essential thrombocythemia (ET) are at risk for vascular events and transformation to myelofibrosis or leukemia. Cytoreduction in symptomatic patients is usually achieved with hydroxyurea, anagrelide, or interferon. Recently, the megakaryocyte telomerase enzyme from patients with ET was found to be more sensitive to inhibition than the enzyme from healthy individuals.
Every patient‘s medical situation is different and should be evaluated individually by a hematologist or oncologist who specializes in treating blood cancers.Patients with low risk for clotting are observed without any therapy; low-dose aspirin can be considered.Patients with high risk for clotting require medical therapy to decrease platelets to normal levels, and are given low-dose aspirin to prevent clotting. A risk factor for bleeding include a very elevated platelet count (over 2 million platelets per microliter).