The histologic appearance of human skin puncture wounds obtained at biopsy, after measurement of the local bleeding times, has been studied in serial section in 3 patients with normal hemostasis and in 4 patients with idiopathic thrombocytopenic purpura. It is found that agglutinated platelets arrest hemorrhage in normal skin by rapidly sealing the mouths of all cut vessels larger than capillaries. Such platelet thrombi can resist the effective blood pressure in a cut arteriole of 55 micra. The puncture tract is normally filled with red cell-fibrin clot into which the platelet thrombi protrude. The red clot seals the mouth of the few opened capillaries which can be identified. Other capillaries may be sealed by endothelial agglutination. Fibrin does not enter or form within the injured vessels.
Platelet thrombosis does not occur in idiopathic thrombocytopenic purpura. When larger arterioles and venules are cut the bleeding time is greatly prolonged and fibrin fails to form within the wound because of the speed of blood flow. When smaller vessels are cut in purpura the bleeding time is moderately prolonged, but the cut vessels are eventually sealed by fibrin alone. In thrombocytopenic purpura the bleeding time is normal if only capillaries are cut, since these are normally sealed by fibrin.
The similarity of the histologic appearance of human puncture wounds to that described after experimental vascular injury in other mammals, suggests considerable similarity in mammalian hemostatic mechanisms.
Clinical bleeding time tests vary greatly in depth of puncture and in the caliber and number of the vessels cut. Sufficient volume of hemorrhage during the first minute is thought to be the best guide to an adequate test of the entire hemostatic mechanism.