PLT 184 - 370 LOW
The abnormality chosen is:
THROMBOCYTOPENIA, a platelet count less than 150,000 cells/microL. Normally, platelets survive in the peripheral circulation for 10 days. When platelet survival is shortened, the marrow may respond eight-fold so that a normal platelet count may be maintained even when platelet survival is as short as 1 to 2 days. Thrombocytopenia may result from impaired platelet production, increased platelet destruction, posttransfusion (dilutional), or platelet sequestration. Examination of bone marrow aspirate will show normal or increased numbers of megakaryocytes if either increased peripheral platelet destruction or sequestration are the etiology whereas a low megakaryocyte count is indicative of decreased platelet production. Medications, alcohol ingestion, and cocaine use are frequent causes of thrombocytopenia. Medications commonly associated with this condition include thiazide diuretics, estrogens, trimethoprim-sulfamethoxazole, chemotherapeutic agents, heparin, rifampin, sulfonamides, gold salts, quinine, and quinidine.
An increased bleeding tendency is the sole manifestation of thrombocytopenia. Ecchymosis, petechiae, menorrhagia, or mucosal membrane hemorrhaging are the most common manifestations. Usually, platelet counts greater than 50,000 cells/microL are asymptomatic, and severe, spontaneous bleeding is a concern only when the platelet count decreases to below 20,000 cells/microL. However, patients with idiopathic thrombocytopenic purpura (ITP) often have platelet counts well below 20,000 cells/microL without symptoms because their low platelet counts are comprised of a low number of large, functional platelets. ITP has been shown to have an association with HIV infection, and persons with ITP should undergo HIV testing.
Thrombocytopenia is associated with megaloblastic anemias secondary to folate or B12 deficiency. Folate deficiency is common in alcoholic patients. Alcohol may also produce thrombocytopenia independent of folate deficiency. Alcohol may be marrow toxic, decrease peripheral platelet survival time, or may cause increased sequestration in patients with hypersplenism secondary to alcohol induced liver cirrhosis with portal hypertension. Consideration should be given to the possible diagnosis of hypersplenism of any cause when the thrombocytopenia is associated with concomitant leukopenia. A left upper quadrant ultrasound that demonstrates splenomegaly is convincing evidence to support the diagnosis of hypersplenism in the proper clinical setting. Multilineage cytopenias in the absence of hypersplenism, should cause consideration of vitamin/mineral deficient states (B12, folate, copper), aplastic anemia, systemic lupus erythematosus, paroxysmal nocturnal hemoglobinuria, and marrow failure. Acute viral infections by rubella, cytomegalovirus, or Epstein-Barr virus are often associated with low platelet counts. Iron deficiency, which often causes thrombocytosis, is associated with thrombocytopenia in up to one-third of cases.
Before beginning an extensive workup, it is important to exclude pseudothrombocytopenia as a cause of a low platelet count. Pseudothrombocytopenia refers to a low platelet count that results secondary to in vitro clumping of platelets. Examination of the peripheral smear for clumped platelets will help confirm the diagnosis. This abnormality occurs because counting machines identify the clumped platelets as a single large platelet, thus resulting in false thrombocytopenia.
Platelet transfusions are given when bleeding can not be controlled or when an invasive procedure is anticipated in cases of acute thrombocytopenia. Patients with chronic thrombocytopenia may derive some benefit from prophylactic platelet transfusions. For patients who may require long term transfusion therapy, it is prudent to use single-donor platelets as they reduce the risk of alloimmunization. Aminocaproic acid is another treatment option, other than transfusions, for thrombocytopenia. A 5-gram intravenous loading dose is followed by oral therapy (1 gram PO QID, which can be decreased once an effect is noted). An effect should be noted 24 to 48 hours into therapy. If no benefit is appreciated, then therapy should be discontinued.