BLEEDING RELATED TO REDUCED PLATELET NUMBER: THROMBOCYTOPENIA

Reduction in platelet number constitutes an important cause of generalized bleeding. Normal platelet counts range from 150,000 to 300,000/μL. A count below 100,000/μL is generally

considered to constitute thrombocytopenia. However, spontaneous bleeding does not become evident until the count falls below 20,000/μL. Platelet counts in the range of 20,000 to 50,000/

μL can aggravate post-traumatic bleeding. Bleeding resulting from thrombocytopenia alone is associated with a prolonged bleeding time and normal PT and PTT.

The important role of platelets in hemostasis is discussed in Chapter 4 . It hardly needs reiteration that these cells are critical for hemostasis, as they form temporary plugs that quickly stop

bleeding and promote key reactions in the clotting cascade. Spontaneous bleeding associated with thrombocytopenia most often involves small vessels. The common sites of such

hemorrhage are the skin and the mucous membranes of the gastrointestinal and genitourinary tracts. Intracranial bleeding is a threat to any patient with a markedly depressed platelet count.

The many causes of thrombocytopenia can be classified into the four major categories listed in Table 13-9 .

• Decreased production of platelets. This can accompany generalized diseases of bone marrow such as aplastic anemia and leukemias or result from diseases that affect the

megakaryocytes somewhat selectively. In vitamin B12 or folic acid deficiency, there is poor development and accelerated destruction of megakaryocytes within the bone marrow

(ineffective megakaryopoiesis) because DNA synthesis is impaired.

• Decreased platelet survival. This important cause of thrombocytopenia can have an immunologic or nonimmunologic etiology. In the immune conditions, platelet destruction is

caused by circulating antiplatelet antibodies or, less often, immune complexes. The antiplatelet antibodies can be directed against a self-antigen on the platelets (autoantibodies) or

against platelet antigens that differ among different individuals (alloantibodies). Common antigenic targets of both autoantibodies and alloantibodies are the platelet membrane

glycoprotein complexes IIb-IIIa and Ib-IX. Autoimmune thrombocytopenias include idiopathic thrombocytopenic purpura, certain drug-induced thrombocytopenias, and HIVassociated

thrombocytopenias. All of these are discussed later. Alloimmune thrombocytopenias arise when an individual is exposed to platelets

of another person, as may occur after blood transfusion or during pregnancy. In the latter case, neonatal or even fetal thrombocytopenia occurs by a mechanism analogous to

erythroblastosis fetalis.[52]

Nonimmunologic destruction of platelets may be caused by mechanical injury,in a manner analogous to red cell destruction in microangiopathic hemolytic anemia. The underlying

conditions are also similar, including prosthetic heart valves and diffuse narrowing of the microvessels (e.g., malignant hypertension).

• Sequestration. Thrombocytopenia, usually moderate in severity, may develop in any patient with marked splenomegaly, a condition sometimes referred to as hypersplenism

( Chapter 14 ). The spleen normally sequesters 30% to 40% of the body's platelets, which remain in equilibrium with the circulating pool. When necessary, hypersplenic

thrombocytopenia can be ameliorated by splenectomy.

• Dilutional. Massive transfusions can produce a dilutional thrombocytopenia. Blood stored for longer than 24 hours contains virtually no viable platelets; thus, plasma volume and

red cell mass are reconstituted by transfusion, but the number of circulating platelets is relatively reduced.

TABLE 13-9-- Causes of Thrombocytopenia

Date: 2016-04-22; view: 715