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Nurse Anesthesia Question: Thrombin Clotting Time

On Monday, June 2, I provided two 90-minute lectures for Dr. Ingrid Oakley’s graduate Nurse Anesthesia Program students at the University of Alabama at Birmingham (UAB).

The first lecture was “Hemostasis Overview and Managing the Bleeding Patient,” and the second was “Thrombophilia and Managing Antithrombotic Therapy.” It is tough on students to attempt to cover all of hemostasis in four hours, but fortunately, these are bright, advanced students. Working with students of this caliber is fun for me, though perhaps grueling for them.

We provide study questions following lectures to assist students in preparing for their examinations, and I’ve invited the students to post their questions to Fritsma Factor so I can provide the answer for everyone looking in.

The first question I received is to contrast the thrombin clotting time (TCT) with the prothrombin time (PT) assay. In the TCT, we add reagent (bovine) thrombin (IIa) to patient plasma and time the mixture until a clot forms. The TCT activates the very end of the coagulation mechanism; the reaction in which thrombin converts fibrinogen to gel-like fibrin. Consequently the only conditions that prolong the test are the presence of thrombin inhibitors or the absence of fibrinogen.

Therapeutic heparin is the most prevalent thrombin inhibitor, as it activates plasma antithrombin, which neutralizes thrombin. Consequently the TCT is a simple, cheap means to find if heparin is present in the plasma. A typical TCT reference interval is 17-22 seconds, and the TCT is unmistakebly prolonged by heparin to around 40 seconds.

Since heparin is used to clear lines, its use may go unrecorded, so most lab personnel find it counterproductive to contact the unit and attempt to learn if a patient has received heparin. In fact, the administrative time devoted to calling is more expensive than just running the TCT (my opinion, not backed by any kind of study). In another posting it was Sue Osier who wrote “at our institution, heparin is ‘in the air.’”

In contrast, the PT reagent consists of tissue factor, calcium and phosphatidyl serine. This activates the coagulation mechanism at the level of factor VII and is prolonged by deficiencies of VII, X, V, and II (prothrombin). The PT is most often used to monitor the vitamin K antagonist antithrombotic Coumadin (Warfarin) and occasionally turns up an acquired coagulopathy, the most common of which are vitamin K deficiency and liver disease. Geo

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