Thrombocytopenia
Thrombocytopenia: Excerpt from Handbook of Diseases
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.
The prognosis is excellent in drug-induced thrombocytopenia if the offending drug is withdrawn; in such cases, recovery may be immediate. Otherwise, the prognosis depends on response to treatment of the underlying cause. (See Precautions in thrombocytopenia.)
Causes
Thrombocytopenia may be congenital or acquired; the acquired form is more common. In either case, it usually results from the following:
❑ decreased or defective production of platelets in the marrow (such as occurs in leukemia, aplastic anemia, or toxicity with certain drugs)
❑ increased destruction outside the marrow caused by an underlying disorder (such as cirrhosis of the liver, disseminated intravascular coagulation, or severe infection)
❑ less commonly, sequestration (hypersplenism, hypothermia) or platelet loss.
Acquired thrombocytopenia may result from certain drugs, such as nonsteroidal anti-inflammatory agents, sulfonamides, histamine blockers, alkylating agents, heparin, alcohol, or antibiotic chemotherapeutic agents.
An idiopathic form of thrombocytopenia commonly occurs in children. A transient form may follow viral infections (Epstein-Barr or infectious mononucleosis).
Signs and symptoms
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, the brain and the gastrointestinal tract are the most common sites of hemorrhage while large blood-filled bullae characteristically appear in the mouth. The bullae are another site of hemorrhage, but they may not herald GI or brain hemorrhage. In severe thrombocytopenia, hemorrhage may lead to tachycardia, shortness of breath, loss of consciousness, and death.
Diagnosis
To diagnose thrombocytopenia, obtain a patient history (especially a drug history), a physical examination, and the following laboratory tests:
❑ Coagulation tests reveal a decreased platelet count (in adults, < 100,000/µl), prolonged bleeding time, and normal prothrombin time and partial thromboplastin time. Platelet-associated antibodies may be present.
❑ 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
Effective treatment varies with the underlying cause and may include corticosteroids or immune globulin to increase platelet production. When possible, treatment consists of correction of the underlying cause or, in drug-induced thrombocytopenia, removal of the offending agents. Platelet transfusions are helpful in thrombocytopenia only in treating complications of severe hemorrhage. Splenectomy may be performed in patients whose thrombocytopenia was caused by platelet destruction.
Special considerations
❑ 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.
❑ Test stool for guaiac; urine and emesis for blood.
❑ Watch for bleeding (petechiae, ecchymoses, surgical or GI bleeding, menorrhagia).
❑ 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, because fever destroys blood products.
❑ During platelet transfusion, monitor for febrile reaction (flushing, chills, fever, headache, tachycardia, hypertension). HLA-typed platelets may prevent febrile reaction.
CLINICAL TIP: A patient with a history of minor reactions may benefit from acetaminophen and diphenhydramine before platelet transfusion.
❑ During steroid therapy, monitor fluid and electrolyte balance, and watch for infection, pathologic fractures, and mood changes.
❑ A 1- to 2-hour postplatelet count will aid assessment of response.
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Book Source Details
- Book Title: Handbook of Diseases
- Author(s): Springhouse
- Year of Publication: 2003
- Copyright Details: Handbook of Diseases, Copyright © 2003 Lippincott Williams & Wilkins.
More About Thrombocytopenia
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Medical Books Excerpts
- Thrombocytopenia
- "The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter" (2000)
- [ read ]
Copyright notice for book excerpts: Copyright © 2008 Lippincott Williams & Wilkins. All rights reserved.
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More About This Book:
Title: Handbook of Diseases
Authors: Springhouse
Publisher: Lippincott Williams & Wilkins
Copyright: 2003
ISBN: 1-58255-266-5
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» Next page: THROMBOCYTOPENIA (Differential Diagnosis in Primary Care)
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