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Introduction ⬇

Platelet aggregation is used to evaluate congenital qualitative functional disorders of adhesion, release, or aggregation. It is rarely used to evaluate acquired bleeding disorders. In vivo, the clotting process follows two pathways: blood coagulation cascade and platelet activation (Figure 2.2).

Normal Findings ⬆ ⬇

Full platelet aggregation in response to the following:

Procedure ⬆ ⬇

  1. Obtain a 5-mL venous blood sample (anticoagulated in a tube containing sodium citrate). Label the specimen with the patient’s name, date and time of collection, and test(s) ordered.

  2. Place the sample in a biohazard bag. The sample is kept at room temperature (never refrigerate) and must be run within 30 minutes after the blood is drawn.

  3. Increase the transmission of light through a sample of platelet-rich plasma when platelets aggregate. This increase in light transmission can be used as an index to the aggregation in response to various agonists.

Clinical Implications ⬆ ⬇

  1. Decreased platelet aggregation occurs in congenital diseases:

    1. Bernard–Soulier syndrome (autosomal recessive coagulopathy)

    2. Glanzmann thrombasthenia (abnormality of platelets, resulting in inability for platelets to bridge with other platelets)

    3. Storage pool diseases (e.g., Chédiak–Higashi syndrome, gray platelet disease)

    4. Cyclo-oxygenase deficiency

    5. Wiskott–Aldrich syndrome (X-linked recessive disease, resulting in a low platelet count)

    6. Albinism

    7. Beta-thalassemia major

    8. May–Hegglin anomaly (abnormally large platelets)

    9. Various connective tissue disorders (e.g., Marfan syndrome)

    10. von Willebrand disease

  2. Decreased platelet aggregation also occurs in acquired disorders:

    1. Uremia

    2. Antiplatelet antibodies

    3. Cardiopulmonary bypass

    4. Myeloproliferative disorders

    5. Dysproteinemias (macroglobulinemia)

    6. Idiopathic thrombocytopenic purpura

    7. Polycythemia vera

    8. Use of drugs and aspirin, some antibiotic drugs, antiinflammatory drugs, psychotropic drugs, and others (see Appendix E)

    9. DIC

  3. Increased aggregation occurs in primary and secondary Raynaud syndrome.

Interventions ⬆ ⬇

Pretest Patient Care

  1. Explain test purpose and procedure.

  2. Ten days before test, drugs that inhibit platelet aggregation are contraindicated. These include aspirin, clopidogrel, antihistamines, steroids, cocaine, antiinflammatory drugs, theophylline, and antibiotic drugs.

  3. On the day of the test, avoid caffeine.

  4. Avoid warfarin (Coumadin) for 2 weeks and heparin therapy for 1 week before testing.

  5. Follow guidelines in Chapter 1 for safe, effective, informed pretest care.

Posttest Patient Care

  1. Review test results; report and record findings. Modify the nursing care plan as needed. Counsel the patient regarding abnormal findings; explain the need for possible follow-up testing and treatment.

  2. Have the patient resume medications and normal diet.

  3. Possible treatments include applying pressure to venipuncture site and assessing for bleeding; hematoma may occur.

  4. Follow guidelines in Chapter 1 for safe, effective, informed posttest care.

Interfering Factors ⬆

  1. Platelet count less than 100,000/mm3.

  2. Patient cannot be taking drugs that interfere with aggregation (see Appendix E).

  3. Lipemia will interfere with testing.