Clinical Vignette

History

A 3-year-old 6.5 kg female peekapoo is presented because the owner has seen blood in the stool, a “skin rash,” and red “splotches” in the skin. According to the owner, about 4 months ago the skin rash had been treated by another veterinarian with a cortisone injection and cortisone tablets. The dog seemed to improve, but 1 month ago red skin splotches were once again noticed. A cortisone injection was repeated and this time a swelling developed immediately at the injection site.

Physical Examination

The temperature (102.4°F), heart rate (120 bpm), and respiratory rate (20 rpm) were normal. The dog was depressed and petechial and ecchymotic hemorrhages were present on the feet, neck, and abdomen. The mucous membranes were pale and the capillary refill time was less than 3 seconds (normal).

An enlarged spleen was present on abdominal palpation. Auscultation revealed a grade II/VI holosystolic murmur over the mitral valve area.

Initial Plan

Using the problem-oriented approach described in Chapter 1, identify the most important problems and develop an initial plan for each with emphasis on the problems of petechiae and ecchymoses.

Problem Definition and Recognition

Bleeding disorders are conditions in which there is either spontaneous hemorrhage or excessive hemorrhage in response to tissue trauma secondary to one or more abnormalities in hemostasis (see Table 15-1 for definitions). Bleeding disorders must be differentiated from hemorrhage secondary to local tissue factors (i.e., trauma, neoplasia, inflammation). For example, epistaxis may result from bleeding disorders such as thrombocytopenia or nasal disease. The presence of bleeding disorders can usually be confirmed by a combination of history, clinical signs, and screening tests of the hemostatic system. Historical information that would suggest the presence of a bleeding disorder rather than bleeding due to local tissue factors would include a history or numerous prior bleeding episodes, a recognized breed predisposition to congenital hemostatic defects, and known exposure to a drug affecting hemostasis.

TABLE 15-1. Terminology associated with bleeding disorders

Physical examination findings suggestive of a hemostatic defect would include spontaneous hemorrhage (i.e., bleeding that is not associated with trauma/tissue disease), simultaneous bleeding from multiple anatomic sites, and hemorrhage that is excessive in either severity or duration for a given traumatic insult.

Normal Hemostasis

Normal hemostasis is divided into primary (formation of the vascular plug) and secondary (formation of the fibrin clot) mechanisms, which are described in the next sections. The clotting cascade is diagramed in Figure 15-1.

Primary Hemostasis

Primary hemostasis involves platelet plug assembly that is necessary to seal small defects in blood vessels and to help stimulate formation of the fibrin clot. When blood vessels are injured, they initially constrict to slow blood flow. Injury to the vessel wall exposes the highly thrombogenic subendothelial collagen as well as induces changes in the endothelial cells themselves that promote coagulation. Platelets adhere to exposed subendothelial collagen through the action von Willebrand factor (vWf), a large serum adhesive protein with multiple receptors for both components of the wall and platelets.

FIGURE 15-1. The coagulation cascade. The factors responsible for blood clotting are listed for the intrinsic, extrinsic, and common pathways. Note the order in which the various factors interact. The clotting factors are further described in Table 15-2. Coagulation can be triggered by either the intrinsic or the extrinsic systems or both.

Adhered platelets undergo a shape change, which exposes fibrinogen receptors on the platelet surface, allowing aggregation of platelets to each other. In addition to the shape change, platelets become activated and release agonists, which then recruit and activate additional platelets into the growing platelet plug until the endothelial defect is covered. In small injuries, the platelet plug alone is sufficient to stop hemorrhages. With larger damage to the endothelium, this platelet plug must be stabilized by the production of a fibrin clot generated by “secondary hemostasis.”

Secondary Hemostasis—Coagulation

Secondary hemostasis involves the formation of a fibrin clot through activation of a series of soluble clotting factors (most of them enzymes) in the blood, hence the synonym coagulation. Within the body, the activation of these soluble clotting factors occurs most effectively on platelet membranes. Thus, the fibrin clot is produced at the site of the platelet plug, which it serves to stabilize. The soluble coagulation factors involved in secondary hemostasis are classically divided into the intrinsic, extrinsic, and common pathways. While these divisions are artificial with regard to physiologic hemostasis (there is significant cross talk between these systems), they are relevant to interpreting the diagnostic tests used to evaluate secondary hemostasis.

Intrinsic System. The intrinsic system gets its name because its initiating factors are activated by binding negatively charged surfaces such as collagen (i.e., within, or intrinsic to, the vessel wall). The intrinsic system includes the Factors XII → XI → IX → VIII (the sequence of activation). Factors XII, XI, and IX are enzymes, while Factor VII is a nonenzymatic cofactor of Factor IX. Factors VIII and IX form a complex with calcium ions and this complex activates the common system. These factors are named, although with the exception of fibrinogen and prothrombin, they are typically referred to strictly by their numeric designation. The coagulation factors are described in Table 15-2.

TABLE 15-2. Serum proteins involved in hemostasis

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