Platelets form the initial hemostatic plug whenever hemorrhage occurs. They also are the source of phospholipid needed for the interaction of coagulation factors to form a fibrin clot. Hemostasis is therefore broadly divided into primary hemostasis, ending in the formation of a platelet plug; secondary hemostasis, ending in the formation of a fibrin clot; and tertiary hemostasis, or fibrinolysis, ending in resolution or lysis of the clot. (Also see Hemostatic Disorders in Animals.)
Platelets are produced in bone marrow from megakaryocytes, under the influence of the hormone thrombopoietin. Beginning with invagination of the megakaryocyte cell membrane, platelet production results from subsequent fragmentation of megakaryocytes into individual platelets. (See images of cat, horse, and cow platelets.)
In contrast, thrombocytes in birds (which do not have platelets) are small cells with a round nucleus.
Courtesy of Dr. John W. Harvey.
Courtesy of Dr. John W. Harvey.
Courtesy of Dr. John W. Harvey.
When vessel walls are damaged, collagen and tissue factor are exposed. Circulating platelets adhere to the endothelium via von Willebrand factor, undergo a shape change, and release ADP. Local aggregation of more platelets is stimulated by ADP, resulting in the formation of a primary hemostatic plug—a platelet plug. Ultimately, local accumulation of fibrin and platelets is known as a fibrin clot, which is needed for effective hemostasis at injury sites.
Clot formation is a necessary protective mechanism to stop or prevent bleeding; however, conditions of inappropriate thrombosis (clot formation) can jeopardize health (see Thrombosis, Embolism, and Aneurysm in Animals).
Platelet disorders are either quantitative (thrombocytopenia or thrombocytosis) or qualitative (thrombocytopathy).
Thrombocytopenia is one of the most common bleeding disorders of animals. In general, platelet counts must fall to < 30,000 platelets/mcL before the risk of spontaneous hemorrhage increases, though hemorrhage from minor trauma (venipuncture, cystocentesis) can occur with platelet counts in the range of 30,000–50,000 platelets/mcL. Spontaneous bleeding from severe thrombocytopenia (or thrombopathia) most commonly manifests as mucosal site (eg, gingiva, GI tract, urinary bladder, nasal passages, or eyes) bleeding or bruising (eg, petechiae, ecchymoses).
Consumption, destruction, or sequestration of platelets causes thrombocytopenia associated with increased platelet production by the bone marrow:
Consumptive thrombocytopenia occurs with massive hemorrhage or with DIC, secondary to a variety of diseases.
Destruction occurs in immune-mediated thrombocytopenia, in which platelets become coated with antiplatelet antibodies and are removed from the circulation by the fixed phagocyte system.
Excessive sequestration of platelets by an enlarged spleen (hypersplenism) can occur in conditions such as myeloproliferative diseases.
Decreased production of platelets in the marrow can be caused by drugs, toxins, or primary marrow disorders such as aplasia, fibrosis, or hematopoietic malignancy. In primary marrow disorders, more than one hematopoietic cell line is often decreased, resulting in bicytopenia or pancytopenia.
Congenital macrothrombocytopenia is a hereditary disorder of platelet division during the maturation process. This disorder results in thrombocytopenia (decreased numbers of individual platelets) with preservation of overall platelet mass, as fewer, but larger, platelets are produced; pathological bleeding is uncommon with this disorder. Cavalier King Charles Spaniels are commonly affected, and a genetic test is available.
Platelet activation during blood collection can cause platelets to clump; hematology analyzers can then provide erroneously low platelet counts, especially in cats. Blood film analysis to assess for platelet clumps is important in determining whether low machine-generated platelet counts are accurate.
Pearls & Pitfalls
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Thrombocytopathies comprise a poorly defined group of diseases in which platelet numbers are normal but their function is impaired. Von Willebrand disease is characterized by a deficiency or malfunction of von Willebrand factor, which decreases platelet adhesion to the endothelium and impairs platelet plug formation. While von Willebrand disease is a primary hemostatic disorder that results in bleeding, platelets themselves are normal. Other hereditary disorders of platelet function have been described but are relatively rare.
Certain infections (feline leukemia virus, ehrlichiosis) and diseases (chronic kidney disease, liver failure) can also impair platelet function, in addition to disrupting the hematopoietic and coagulation systems in other ways. Aspirin administration causes a platelet function defect through its irreversible inhibition of thromboxane (which is necessary for platelet aggregation). Clopidogrel also irreversibly inhibits platelet function by binding an ADP receptor subtype necessary for platelet aggregation.
Thrombocytosis (increased platelet number) may be associated with primary marrow disease, such as in megakaryocytic leukemia (rare), chronic blood loss and iron deficiency, or chronic excess corticosteroid exposure (hyperadrenocorticism or exogenous corticosteroid medication).
Key Points
Platelets are produced from megakaryocytes and form the first stage of coagulation (the hemostatic or platelet plug) when a blood vessel is damaged. Fibrin forms in the presence of aggregated platelets, leading to clot formation.
Bleeding associated with thrombocytopenia is often characterized by petechiae, ecchymoses, or mucosal bleeding.
Platelet function disorders are relatively rare and may be inherited or acquired.
For More Information
Boudreaux MK, Spangler EA, Welles EG. Hemostasis. In: Lattimer KS, ed, Duncan and Prasse’s Veterinary Laboratory Medicine: Clinical Pathology. 5th ed. Wiley-Blackwell; 2011:108-111.
eClinpath. Physiology: hematopoiesis.
Also see pet owner information regarding platelets of dogs.
