Cat bleeding disorders

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CHAPTER 172
Approach to Patients with Bleeding

Disorders

Kathryn Webert, MD, MSc, FRCPC

Catherine P. M. Hayward, MD, PhD

Key Clinical Questions

When should a bleeding disorder be suspected?
How should patients suspected of bleeding disorders be evaluated?
How does one interpret the results of hemostasis testing?
What is the general approach to management of an individual with a bleeding
disorder?

INTRODUCTION
In general, severe bleeding disorders are uncommon, unlike mild bleeding problems, which
can be more challenging to diagnose. Most episodes of clinically significant bleeding
requiring medical attention result from local causes (eg, a duodenal ulcer), surgery, or

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trauma. However, it is important to recognize when bleeding problems are more serious or
more frequent due to an underlying hemostatic abnormality.

Abnormal bleeding represents an important health care problem. For example, in the
United States, it has been estimated that at least 5% to 10% of women of childbearing age
seek medical care for menorrhagia and have bleeding severe enough to require medical
intervention. Among the many defects that can cause abnormal bleeding, inherited and
acquired von Willebrand disease (VWD) and platelet function disorders are much more
common than defects in coagulation and fibrinolytic proteins.

PATHOPHYSIOLOGY
REVIEW OF NORMAL HEMOSTASIS

Hemostasis consists of the following steps: (1) initiation and formation of the platelet
plug, also known as primary hemostasis; (2) propagation and amplification of the clotting
“cascade” or secondary hemostasis, which involves activation of a series of coagulation
factors resulting in the generation of thrombin that cleaves fibrinogen to fibrin; (3) cross-
linking of fibrin; (4) termination of procoagulant response by antithrombotic control
mechanisms; (5) removal of the clot by fibrinolysis; and (6) tissue repair and regeneration.

When a vessel is injured, platelets adhere to exposed collagen and other components
of the subendothelium as the first defense against bleeding. This initial adhesion is
dependent on von Willebrand factor (VWF) as well as specific platelet receptors (eg,
glycoprotein IbIXV) for VWF and collagen. This adhesion leads to platelet activation and
shape change as well as platelet aggregation, which promotes recruitment of additional
platelets.

Coagulation is initiated in vivo when endothelial or vascular cells are damaged. This
results in exposure of blood to tissue factor (TF), which binds to factor VII (FVII) and its
activated form, factor VII (FVIIa). TF-FVIIa complexes (extrinsic tenase) then activates
factors IX and X directly. Activated factor IX can also form a complex with factor VIIIa as
well as phospholipids and calcium, cal