Thrombocytopenia, a deficiency of circulating platelets, is a common cause of hemorrhagic disorders, so assessing platelet count is essential when your patient has bleeding problems. In this article, we'll describe the types of thrombocytopenia, causes of thrombocytopenia in adults, and treatment options.
Decreased platelets via three processes
By definition, thrombocytopenia is a platelet count below 100,000/mm3. Signs and symptoms include nasal or gingival bleeding; bloody urine, sputum, or stool; petechiae; blood blisters; scleral hemorrhage; purpura; and ecchymosis.
A platelet count below 50,000/mm3 increases the risk of hemorrhage with minor trauma. Spontaneous bleeding can occur with a platelet count from 10,000/mm3 to 15,000/mm3, and a count below 10,000/mm3 can be fatal.
Thrombocytopenia most commonly occurs between ages 20 and 40. Three processes can trigger it:
- decreased or defective platelet production. Aplastic anemia, malignant cells in the bone marrow, infection with human immunodeficiency virus (HIV), and the effects of drugs and radiation therapy are some of the conditions that can decrease platelet production.
- excessive platelet pooling in the spleen. Even if platelet production is normal, the spleen generally holds 30% to 40% of platelets before releasing them into the circulation. In cases of splenomegaly, in which the spleen's normal functions become overactive (hypersplenism), up to 80% of the platelets can pool in the spleen. Hypothermia may be a predisposing factor.
- decreased platelet survival. Immune platelet destruction occurs when the body directs antibodies against platelets. Nonimmune destruction occurs when prosthetic heart valves or narrowed blood vessels cause mechanical injury to platelets or when platelets are excessively consumed during acute disseminated intravascular coagulation or thrombotic thrombocytopenic purpura.
Three key types
The key types of thrombocytopenia are drug-induced, idiopathic, and thrombotic.
- Drug-induced thrombocytopenia is an immune-mediated reaction that lowers the number of circulating platelets within 7 or more days of starting therapy with a new drug or within 2 to 3 days of resuming drug therapy. Unfractionated heparin is the most common trigger. Antibodies activate the platelets and remove them from the circulation to decrease the patient's platelet count. If heparin-induced thrombocytopenia isn't quickly identified and treated, intravascular platelet aggregation can cause rapid development of arterial and venous thrombosis. Low-molecular-weight heparin reduces the risk.
- Quinine, quinidine, and sulfonamide antibiotics may destroy platelets by complement-mediated lysis. Many other drugs, including chemotherapy agents, depress platelet production. Discontinuing the drug typically resolves the problem.
- Idiopathic thrombocytopenic purpura is due to an autoimmune disorder that causes formation of antiplatelet antibodies that make the platelets more susceptible to phagocytosis and destruction in the spleen.
- Thrombotic thrombocytopenic purpura, which is relatively rare, most commonly affects women in their 30s. It may originate with endothelial injury and subsequent release of procoagulant substances from the endothelial cells. As a result, widespread thrombi in the arterioles and capillaries in the microcirculation can trigger life-threatening thrombocytopenia, hemolytic anemia, renal failure, and neurologic abnormalities.
What to look for
Early signs of thrombocytopenia and its complications depend on the patient's platelet count. He may develop petechiae and purpura over several days or have a spontaneous major hemorrhage from mucosal sites such as the nose, urinary tract, and gums. Menorrhagia often affects women. The most common sites of severe bleeding include the brain and gastrointestinal tract, although bleeding into the lungs and pericardium may also occur.
If you suspect thrombocytopenia, investigate whether your patient has a history of bleeding; signs and symptoms of complications, such as weight loss, fever, and headache; risk factors such as HIV infection; medication use that can cause thrombocytopenia; or a family history of bleeding. Assess him for signs of infection and thrombosis and obtain a complete blood cell (CBC) count, platelet count, and differential as ordered.
If his platelet count is decreased, he should have additional studies such as a bleeding time, prothrombin time, activated partial thromboplastin time, platelet antibody studies, platelet survival studies, and a bone marrow biopsy.
Keep in mind that a decreased platelet count isn't always the direct result of a pathologic condition. Pseudothrombocytopenia can occur in certain clinical situations. The first is massive transfusions of platelet-poor packed cells, generally more than 10 units in 24 hours, causing a dilutional thrombocytopenia. Bleeding itself causes platelet loss to further contribute to the thrombocytopenic state.
Another cause of pseudothrombocytopenia is hypothermia. The platelet count should return to normal when normal body temperature is restored.
On rare occasions, normal blood may react with the EDTA anticoagulant in the collection tube, causing the platelets to agglutinate and adhere to white blood cells and giving a falsely low platelet count.
Treatment is initiated when the patient's platelet count is 20,000/mm3 to 30,000/mm3, or if he's bleeding or has a high risk of bleeding and his platelet count is below 50,000/mm3. Because thrombocytopenia has different causes, the treatments vary. (See Key treatment options.)
- Drug-induced thrombocytopenia. The offending drug should be withdrawn and a structurally different medication substituted if the patient still requires treatment. His platelet count should return to normal within 7 to 10 days. If he's had severe hemorrhage and his platelet count is less than 20,000/mm3, he may receive temporary support with glucocorticoids, plasmapheresis, or platelet transfusions.
- Platelet transfusions are contraindicated, however, if heparin caused the thrombocytopenia. Heparin should be discontinued immediately and therapy with another potent thrombin inhibitor such as lepirudin, argatroban, or danaparoid should be initiated. After therapeutic anticoagulation has been achieved or the thrombocytopenia resolves, low-dose warfarin should be added to the anticoagulant regimen.
- Idiopathic thrombocytopenic purpura. Treatment with oral glucocorticoids usually controls platelet sequestering and destruction, but relapse may occur when the dose is tapered. The patient may require temporary intravenous immunoglobulins or an antibody preparation. Splenectomy is usually reserved for desperately ill patients who don't respond to medical therapy.
- Thrombotic thrombocytopenic purpura. Treatment consists of exchange transfusions, intensive plasmapheresis, and infusions of fresh-frozen plasma. Steroids may be used initially to manage mild cases or as adjunctive treatment. Platelet transfusions are contraindicated because the disease is associated with enhanced platelet agglutination, which increases the risk of thrombotic complications.
Protecting your patient
Thrombocytopenia can be life-threatening. Until your patient's platelet counts are normalized, he needs frequent assessment and protection from trauma. Perform these nursing actions:
- Frequently monitor for signs of external and internal bleeding, such as petechiae, ecchymoses, hematomas, conjunctival hemorrhages, bleeding from puncture sites or the gums, hemoptysis, epistaxis, abdominal distension, and rectal, vaginal, or urethral bleeding. Your patient may develop hypotension, tachycardia, dizziness, headache, blurred vision, and changes in mental status due to bleeding.
- Obtain CBC and platelet counts and coagulation studies as ordered and monitor trends.
- Test the patient's stool, urine, and vomit for blood.
- Avoid administering aspirin and other drugs that affect platelet function.
- Advise the patient to avoid straining during coughing or bowel movements; administer stool softeners.
- Administer platelet transfusions as ordered and monitor for adverse reactions.
- Protect the patient from trauma by padding his bed rails as needed.
- Avoid invasive procedures, such as insertion of an indwelling catheter, whenever possible. If suctioning is necessary, do it gently.
- Avoid intramuscular injections and perform necessary venipunctures with the smallest possible needle. Afterward, apply pressure to the site for 5 minutes or until bleeding stops.
- Teach your patient to brush his teeth gently, using only a soft-bristle toothbrush—no flossing or commercial mouthwashes. Have him use Toothettes if his platelet count is less than 10,000/mm3 or if his gums bleed. Lubricate his lips with water-soluble lubricant every 2 hours while he's awake to prevent chapping and bleeding.
- Teach him about his risk of bleeding easily and longer than normal and advise him how to modify his activities when he goes home. (See Safety do's and don'ts.)
Out of the danger zone
The nursing measures spelled out here help protect a patient with thrombocytopenia until his platelet count rises and his risk of bleeding complications leaves the danger zone.
Key treatment options
The following measures are used alone or in combination to treat thrombocytopenia:
- treating the underlying cause or withdrawing the causative drug
- corticosteroid and I.V. immunoglobulin to increase platelet production
- lithium carbonate or folate to stimulate bone marrow production of platelets
- platelet transfusion
- splenectomy to inactivate the source of platelet destruction
- plasmapheresis—removing whole blood from the patient to separate out components that may cause disease. Platelets are removed when a patient has a risk of thrombotic thrombocytopenic purpura.
- fresh-frozen plasma, which is rich in clotting factors but contains no platelets.
Safety do's and don'ts
Teach your patient these tips to prevent bleeding.
- Keep your head elevated when you lie down.
- Use only an electric razor for shaving.
- Wear nonlatex gloves when washing dishes, cleaning, and working with tools.
- Take your temperature only by mouth.
- Wear properly fitting shoes and socks.
- Regularly check your urine, stool, and sputum for blood and watch for heavy menstrual bleeding.
- Use a thimble or finger guards while doing needlework or knitting.
- Tell all heath care workers about your condition before you undergo any procedures, including routine dental care.
- Use a nasal spray containing 0.9% sodium chloride or run a humidifier to moisten your breathing passages and prevent nosebleeds.
- Use a soft toothbrush or gauze to clean your teeth.
- Wear a medical-alert tag to inform others of your condition.
- Don't use any substance that increases your risk of bleeding, such as alcohol, nicotine, caffeine, products containing aspirin or ibuprofen, and herbs such as feverfew, ginger, ginkgo, ginseng, or kava.
- Don't use a straight razor.
- Don't floss your teeth unless your health care provider approves.
- Don't go barefoot. Always wear shoes or slippers to protect against cuts.
- Don't leave knives, scissors, thumbtacks, or other sharp objects where they could accidentally cut you. Store them in protective containers.
- Don't participate in contact sports, cycling, in-line skating, or roughhousing. Avoid heavy lifting.
- Avoid straining when having a bowel movement; use a stool softener as directed.
- Don't puncture your skin, including administering I.M. or subQ injections, if possible.
- Don't pluck your eyebrows or other body hair.
- Avoid skin punctures, such as tattoos, body piercing, or recreational drug use.
SELECTED WEB SITES
National Institutes of Health: Immune Thrombocytopenic Purpura http://www.niddk.nih.gov/health/hematol/pubs/itp/itp.htm
U.S. Pharmacist http://www.uspharmacist.com
Pharmacists Planning Service, Inc.: Herbals and Drug Interactions http://www.ppsinc.org/herbals/herbal07.htm
Last accessed on May 3, 2005.
Baldwin PD. Thrombocytopenia. Clinical Journal of Oncology Nursing
. 7(3):349–352, May/June 2003.
Drews RE. Critical issues in hematology: Anemia, thrombocytopenia, coagulopathy, and blood product transfusions in critically ill patients. Clinics in Chest Medicine
. 24(4):607–622, December 2003.
Huether S, McCance K. Understanding Pathophysiology
, 3rd edition. St. Louis, Mo., Mosby, 2004.