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Thrombocytopenia
Thrombocytopenia: Excerpt from Professional Guide to Diseases (Eighth Edition)
The most common cause of hemorrhagic disorders, thrombocytopenia is characterized by deficiency of circulating platelets. Because platelets play a vital role in coagulation, this disease poses a serious threat to hemostasis. (See What happens in thrombocytopenia, pages 1044 and 1045.) The prognosis is excellent in drug-induced thrombocytopenia if the offending drug is withdrawn; in such cases, recovery may be immediate. In other types, the prognosis depends on the patient’s response to treatment of the underlying cause.
Causes
Thrombocytopenia may be congenital or acquired; the acquired form is more common. In either case, it usually results from decreased or defective production of platelets in the marrow (such as occurs in leukemia, aplastic anemia, or toxicity with certain drugs) or from increased destruction outside the marrow caused by an underlying disorder (such as cirrhosis of the liver, disseminated intravascular coagulation, or severe infection). Less commonly, it results from sequestration (hypersplenism and hypothermia) or platelet loss. Acquired thrombocytopenia may result from certain drugs, such as sulfonamides, antibiotics, gold salts, estrogens, or chemotherapeutic agents. (See Causes of decreased circulating platelets, page 1046.)
An idiopathic form of thrombocytopenia commonly occurs in children. A transient form may follow viral infection (such as Epstein-Barr virus or infectious mononucleosis).
Thrombocytopenia typically produces a sudden onset of petechiae or ecchymoses in the skin or bleeding into any mucous membrane. Nearly all patients are otherwise asymptomatic, although some may complain of malaise, fatigue, and general weakness. In adults, large, blood-filled bullae characteristically appear in the mouth. In severe thrombocytopenia, hemorrhage may lead to tachycardia, shortness of breath, loss of consciousness, and death.
Diagnosis is based on the results of the patient history (especially a drug history), physical examination, and laboratory tests. Coagulation tests reveal a decreased platelet count (in adults, less than 100,000/µl), prolonged bleeding time, and normal prothrombin time and partial thromboplastin time. If increased destruction of platelets is causing thrombocytopenia, bone marrow studies will reveal a greater number of megakaryocytes (platelet precursors) and shortened platelet survival (several hours or days rather than the usual 7 to 10 days).
Treatment varies with the underlying cause and may include corticosteroids or immune globulin to increase platelet production. The treatment of choice is removal of the offending agents in drug-induced thrombocytopenia or treatment of the underlying cause. Platelet transfusions are helpful only in treating complications of severe hemorrhage.
When caring for the patient with thrombocytopenia, take every possible precaution against bleeding.
❑ Protect the patient from trauma. Keep the side rails up and pad them, if possible. Promote the use of an electric razor and a soft toothbrush. Avoid invasive procedures, such as venipuncture or urinary catheterization, if possible. When venipuncture is unavoidable, be sure to exert pressure on the puncture site for at least 20 minutes or until the bleeding stops.
❑ Monitor platelet count daily. A 1- to 2-hour postplatelet count will aid assessment of response.
❑ Test stool for guaiac; dipstick urine and vomitus for blood.
❑ Watch for bleeding (petechiae, ecchymoses, surgical or GI bleeding, and menorrhagia).
❑ Warn the patient to avoid aspirin in any form and other drugs that impair coagulation. Teach him how to recognize aspirin or ibuprofen compounds on labels of over-the-counter remedies.
❑ Advise the patient to avoid straining at stool or coughing, as both can lead to increased intracranial pressure, possibly causing cerebral hemorrhage in the patient with thrombocytopenia. Provide a stool softener to avoid constipation.
❑ During periods of active bleeding, maintain the patient on strict bed rest if necessary.
❑ When administering platelet concentrate, remember that platelets are extremely fragile, so infuse them quickly. Don’t give platelets to a patient with a fever.
❑ During platelet transfusion, monitor for febrile reaction (flushing, chills, fever, headache, tachycardia, and hypertension). Histocompatibility locus antigen-typed platelets may be ordered to prevent febrile reaction. A patient with a history of minor reactions may benefit from acetaminophen and diphenhydramine before transfusion.
❑ If thrombocytopenia is drug-induced, stress the importance of avoiding the offending drug.
❑ If the patient must receive long-term steroid therapy, teach him to watch for and report cushingoid signs (acne, moon face, hirsutism, buffalo hump, hypertension, girdle obesity, thinning arms and legs, glycosuria, and edema). Emphasize that steroid doses must be discontinued gradually. During steroid therapy, monitor fluid and electrolyte balance, and watch for infection, pathologic fractures, and mood changes.
Review other book chapters online related to Thrombocytopenia:
Copyright notice for book excerpts: Copyright © 2008 Lippincott Williams & Wilkins. All rights reserved.
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More About This Book:
Title: Professional Guide to Diseases (Eighth Edition)
Authors: Springhouse
Publisher: Lippincott Williams & Wilkins
Copyright: 2005
ISBN: 1-58255-370-X
» Next page: Thrombocytopenia (The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter)
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