History Of Blood Coagulation

The study of blood coagulation can be traced back to about 400 bc and the father of medicine, Hippocrates. He observed that the blood of a wounded soldier congealed as it cooled. Additionally, he noticed that bleeding from a small wound stopped as skin covered the blood. If the skin was removed, bleeding started again. Aristotle noted that blood cooled when removed from the body and that cooled blood initiated decay resulting in the congealing of the blood. If fibers were removed, there was no clotting. This was known as the cooling theory or blood coagulation. It was not until 1627 that Mercurialis observed clots in veins that were at body temperature. In 1770, William Hewson challenged the cooling theory and believed that air and lack of motion were important in the initiation of clotting. Hewson described the clotting process, demonstrating that the clot comes from the liquid portion of blood, the coagulable lymph, and not from the cells, disproving the cooling theory. It was Paul Morawitz in 1905 who assembled coagulation factors into the scheme of coagulation and demonstrated that in the presence of calcium and thromboplastin, prothrombin (II) was converted to thrombin, which in turn converted fibrinogen (I) into a fibrin clot. This theory persisted for 40 years until Paul Owren, in 1944, discovered a bleeding patient who defied the four-factor concept of clotting. Thus factor V was discovered. Owren also observed a cofactor that was involved in the conversion of pro-thrombin to thrombin. In 1952, Loeliger named this factor VII. Factor VIII was identified as classic hemophilia prior to the identification of VII in 1936/1937. In 1947, Pavlovsky reported that the blood from some hemophiliac patients corrected the abnormal clotting time in others. In 1952, this was called Christmas disease, after the family in which it was discovered, or factor IX. Factor X deficiency was described in 1957 in a woman named Prower and a man named Stuart. Factor XI was described in 1953 as a milder bleeding tendency. In 1955, Ratnoff and Colopy identified a patient, John Hageman, with a factor XII deficiency who died from a stroke—a thrombotic episode, not a bleeding disease. In 1960, Duckert described patients who had a bleeding disorder and characteristic delayed wound healing. This fibrin stabilizing factor was called factor XIII. Prekallikrein (1965) discovered from four siblings in the Fletcher family demonstrated no bleeding tendencies, as well as high-molecular-weight kininogen (1975). These were both identified as contact activation cofactors that participated in the activation of factor XI by factor XII.1

Testing of blood plasma factors and platelets depended on seeing the clotting process directly or microscopically. The first whole blood clotting time was done in 1780 by William Hewson, who noted that blood taken from healthy people clotted in 7 minutes while in some disease states, blood took from 15 to 20 minutes up to 11/2 hours to form a clot.

In 1897, Brodie and Russel begin observing the process on a glass slide. A drop of blood was placed on a glass cone, in a temperature-controlled glass chamber agitated by an air jet. Blood no longer moved microscopically but clotted in 3 minutes and was completed at 8 minutes. In 1905, Golhorm used a wire loop attached to a glass tube. In 1910, Kottman observed an increased viscosity in clotting blood in a Koagulo-viskosimeter. Blood was rotated at 20 degrees 12 to 15 times per minute. In 1936, Baldes and Nygaard added photoelectric tracings called a coagelogram, depicting shape change by light transmittance.

In the 1960s, BBL introduced the Fibrometer. This instrument provided mechanical registration of clots that allowed more reproducible timing and an expression of the clotting process.2

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