CASE HISTORY • Part 1
A 76-year-old man presents with a complaint of headache, which began several hours after a fall and has steadily worsened. His history is notable for hypertension and coronary artery disease, status post-bypass grafting 4 years prior. He denies any history of bleeding or thrombosis other than his previous coronary symptoms. Medications include a cholesterol-lowering agent, beta-blocker, and a daily aspirin. Examination is notable for a tender bruise over the left occipital region. The remainder of the examination is benign.
CBC: Hemoglobin/hematocrit - 13 g/dL/39%
MCV - 94 fL MCH - 31 pg MCHC - 32 g/dL
RDW-CV - 11% White blood cell count - 8,500/μL
Platelet count - 310,000/μL BLOOD SMEAR MORPHOLOGY
Normocytic, normochromic with no aniso- or poikilocytosis or polychromasia. White blood cells are normal and platelets are numerous with normal morphology. Questions
Given the risk of an intracranial hemorrhage, do these laboratory results rule out a coagulopathy?
What other test(s) might be in order?
An abnormality in platelet function can result in bleeding despite the platelet count being normal. Disordered platelet function occurs when there is an abnormality of either the platelet itself or its primary adhesive ligands, for example, von Willebrand factor. Therapeutic inhibition of platelet function is very common in the developed world, and although most platelet function disorders are associated with a relatively mild bleeding tendency, awareness of these conditions can be important in the overall clinical management of these patients.
The steps involved in platelet adhesion, aggregation, and subsequent clot formation are illustrated in Figure 32-1. Important elements of the system include the vessel wall, functional components of the platelet, and both von Willebrand factor (vWF) and fibrinogen. The ability of the vessel to contract and the condition of the subendothelial connective tissue are both important elements. Reflex contraction of the injured vessel reduces flow and encourages adhesion of platelets to exposed collagen. Loss of this reflex because of a distortion in vessel anatomy or an underlying collagen defect will interfere with normal platelet thrombus formation.
Normal platelet function. Important elements in platelet adhesion and aggregation include platelet shape change; adhesion to subendothelial collagen; aggregation of activated platelets; and release of ADP, thromboxane A2 (TxA2), platelet factor 4 (PF4), and β-thromboglobulin (βTG) to stimulate further platelet activation and recruit additional platelets into the aggregate. Thrombin acts as the most potent physiologic platelet activator to accelerate the process. von Willebrand factor bound to subendothelial collagen is essential for platelet adhesion via the GPIb receptor, whereas fibrinogen is the essential cofactor in the GPIIb/IIIa-mediated platelet-platelet aggregation process.
Platelet adhesion, activation, and aggregation play pivotal roles in platelet thrombus formation. A defect ...