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New Treatments for Disseminated Intravascular Coagulation

Disseminated intravascular coagulopathy, DIC happens in individuals who, by way of history, are ill and they are seriously ill. Usually systemically ill. It tends to be more common at the extremes of age and there is actually no sex predilection, and itís found worldwide and there is no isolated or particular geographic distribution. The key and the most important feature to be aware of when you see this problem of DIC, there is always an underlying illness. That is key to remember and key to make every effort to vigorously find out what it is that is the underlying disseminated intravascular coagulation.

The hallmark feature of this disorder in that of hemorrhage and it may be just a little bit of petechiae or purpura, or you can see total body-type of oozing. Mucous membranes. Of course one of the areas that is very susceptible is the central nervous system and any recent incisions or punctures, venipuncture sites, may open up and start to bleed because of the activity of the plasminogen plasmin proteolytic enzyme system. Frequently this is accompanied by hypotension, shock, hypoxemia, and less than 50% of the time one can appreciate a thrombosis.

Probably the four or five most common causes of the DIC process is that of sepsis; virtually every and all known microorganism that are found in Bergeyís manual are capable of initiating this process. Itís somewhat interesting, historically; one of the first reported in the literature was with Mycoplasma tuberculosum. Neoplastic disease; again, any that can be recognized as a neoplastic process, very very common. And liver disease very common.

Congenital abnormalities, again, those things that are rich in tissue thromboplastic material; endotheliomatous, hemangiomatous-type lesions, hyalin membrane disease, again aneurysms and pulmonary cardiac defects. Injury. Injury of any type; severe trauma, loads of tissue thromboplastin into the circulation; drowning, heat stroke, burns, envenomation with scorpions, snakes, again those animals are putting in there some tissue thromboplastic material, something that has the capacity to activate simultaneously the coagulation and the fibrinolytic systems. The body tissue that is probably richest of all is the central nervous system and when you damage that Ö this is an individual here with the Kasabach-Merrittís syndrome. Endotheliomatous hemangiomatous lesion which one sees here, and this releasing a large amount of tissue.

Now areas of obstetrics and gynecology, very important very common, again anything that has the capacity to have tissue thromboplastin enter the maternal, in this case, circulation; toxemia, retained placenta, premature separation of the placenta, loads of tissue thromboplastin there. Retained dead fetus. Again the material is circulating into the maternal side and here thrombotic thrombocytopenic purpura, which weíll cover in a moment.

Immune-mediated, immunological. The incompatible blood transfusion reactions. Of course this is a problem, particularly if the patient is undergoing surgery and is asleep. One canít appreciate a large amount of this reaction taking place. The first sign of a problem there is when the patient starts to have generalized oozing out of every place. Not only where the Bard-Parker blade has been but in some other locations; underneath the anesthesiologists.

How does one go about making the diagnosis of this problem? That you are really dealing with this? Of course one can do this relatively easily at the bedside. Take some blood, put it in a plain glass tube and observe for clot formation, what that clot looks like, see if it undergoes a retraction - which it should if itís normal - if there is lysis taking place in the DIC process, that clot if it forms or if you can appreciate formation - usually does form, sometimes itís difficult to appreciate - it fairly rapidly undergoes lysis and it looks like you have some lumpy, red soup. That is the real tip-off that something undesirable is taking place. The peripheral blood; look at the peripheral blood smear, the blood film, and observe red cell morphology and enumerate the number of platelets because the morphology here is seriously disturbed.

Whatís the management? Well thereís really only one satisfactory form of management and that is to make an intense effort to find out what the underlying illness is and if you adequately treat this or remove it, the problem is rapidly solved. If you donít, thereís trouble. Hereís an example with a retained placenta. We see, when we were first called to see this patient, bleeding. Whatís wrong? I asked them, "Is all the placenta out?", "Well, I think so. Take a look." And we draw some blood, we find the fibrinogen here very very low, degradation product titer high. The platelet count here is down, itís not too bad but remember in pregnancy the platelet count.

What about the use of heparin and other things here, of thrombolytic agents, antiplatelet aggregation agents, again no. These are not particularly helpful. They may be if one cannot actually find the cause. In certain situations, particularly in the Trousseau abnormality where you have underlying neoplasm, yes heparin there may be helpful. But again, once you remove the cause it promptly clears itself. There has been some mention of use of antithrombin 3, which is one of the things among others that is depleted.

This is - I mention this because it is a recent thing, maybe somebody will ask you about it - but it really has not found a great home here in utility, as far as treating this problem. It simply is not necessary.