Postmortem Blood Sugar and Blood Urea Nitrogen Determinations

Glucose and urea nitrogen determinations were made on blood and cerebrospinal fluid samples collected during 160 postmortem examinations in order to determine the usefulness of such tests in diagnosing diabetes and uremia at the time of autopsy. The results indicated that: (1) Blood is unsuitable for postmortem glucose determination, and no postmortem normal can be established. (2) Cerebrospinal fluid gave more uniform but very low glucose values. (3) Diabetics as a group had very high postmortem glucose levels but showed a marked overlap with non-diabetics. (4) Infants less than 3 months of age showed high postmortem glucose values. (5) Postmortem blood urea nitrogen and cerebrospinal fluid urea nitrogen levels were within normal limits in previously healthy persons who died suddenly from accidental causes. (6) Hospital autopsy cases had high urea nitrogen levels. (7) Postmortem urea nitrogen levels higher than 100 mg.% were indicative of uremia.     

Blood Coagulation

The process of tissue factor initiated blood coagulation is discussed. Reactions of the blood coagulation cascade are propagated by complex enzymes containing a vitamin K-dependent serine protease and an accessory cofactor protein that are assembled on a membrane surface in a calcium-dependent manner.These complexes are 10⁵ 10⁹-fold more efficient in proteolyses of their natural substrates than enzymes alone. Based upon data acquired using several in vitro models of blood coagulation, tissue factor initiated thrombin generation can be divided into two phases: an initiation phase and a propagation phase. The initiation phase is characterized by the generation of nanomolar amounts of thrombin, femto- to picomolar amounts of factors VIIa, IXa, Xa, and XIa, partial activation of platelets, and almost quantitative activation of procofactors, factors V and VIII. The duration of this phase is primarily influenced by concentrations of tissue factor and TFPI. The characteristic features of the propagation phase are: almost quantitative prothrombin activation at a high rate, completion of platelet activation, and solid clot formation. This phase is primarily regulated by antithrombin III and the protein C system. Thrombin generation during the propagation phase is remarkably suppressed in the absence of factor VIII and IX (hemophilia A and B, respectively) and at platelet counts <5% of mean plasma concentration. The majority of data accumulated in in vitro models and discussed in this review are in good agreement with the results of in vivo observations.