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Disseminated Intravascular Coagulation (DIC) is always a secondary disease and is a consequence of many other primary problems. Historically, DIC referred to secondary activation of the coagulation system with fibrin deposition in the microvascularture. Now DIC that has changed to describe a varying clinical picture.
The most serious clinical form of DIC is shown in extensive consumption of coagulation proteins, significant deposition of fibrin, and bleeding. In the mild forms of DIC there are endogenous markers of thrombin generation with little or no obvious coagulation problems.
Trauma patients are at increased risk for DIC. Widespread areas of tissue damage (particularly the brain), sepsis and multiple organ failure. The head trauma is a particularly common cause of DIC in infants and children because of the high thromboplastin content of the brain and the proportionately increased ratio of surface area of the head to total BSA.
Sepsis may occur in about 40% of trauma patients and is an important primary cause of DIC in all patients. The clinical condition is worsened by secondary fibrinolysis, which results in the formation of FDP's (fibrinogen / fibrin degradation products or "D - dimers) that interfere with normal fibrin formation and platelet function.
Fibrin deposition in DIC may lead to further organ dysfunction. DIC is a major cause of acute renal failure and it also contributes to multiple system organ failure. The converse is also true with damaged organs contributing to DIC.
A variety of tests are used to detect DIC. The most sensitive tests are markers of endogenous thrombin generation. Prothrombin fragment F1.2, is released when thrombin is generated from prothrombin. Thrombin is neutralized by binding to Antithrombin III (ATIII), its most important inhibitor, and fibrinopeptide forming thrombin-antithrombin III complexes. In the practical management of patients, cruder measures of DIC are often used. Some of these tests include: Screening tests such as the prothrombin time (PT) and activated partial thromboplastin time time (aPTT), which may be prolonged reflecting consumptionof many coagulation proteins. Plasma concentrations of coagulation proteins known to be consumed in DIC, such as Fibrinogen, Factor V, and Factor VIII. All show decreases in concentration. Fibrinogen/fibrin degradation products (FDP's) or D-dimers, a fragment from fibrin alone, which are both increased in concentration. Fibrin monomer (the remaining fibrinogen molecule when fibrinopeptide A has been removed) which may be present. The Thrombin clotting time, which may be prolonged, reflecting hypofibrinogenemia and the presence of FDP's.
The cornerstone treatment of DIC remains to be the alleviation of the primary disorder. Without control, DIC will continue despite forms of therapy directed at correcting the bleeding or thrombotic problem. Some patients with DIC probably do not require therapy because there are no significant clinical ramifications from it. In other DIC forms, patients with significant bleeding, replacement therapy with fresh frozen plasma (FFP), cryoprecipitate, and/or platelet concentrates is helpful until the primary problem is controlled. The use of heparin in DIC is highly controversial and at this time not generally indicated in patients with underlying problem of trauma.
DIC - Disseminmated Intravascular
1. Inappropriatied accelerated systemic activation of coagulation.
2. Always a secondary problem
Massive, prolonged spillage of thromboplastin.
Extensive damage or alteration in the vascular endothelium.
Damage to blood cells.
1. Small clots form imparing perfussion.
2. Tissue ischemia
3. Triggering euent.
. Intravascular thrombin reduced.
Fibrinogen converted into ferin.
Fibrin split products increase.
Inability of blood to clot.
> In the small community hospital where I work, we don't
get too many pts with
> DIC. I know a few years ago, the very controversial treatment for DIC was to
> use Heparin, at least in the Boston area hospitals. Is this still the case, or
> have they totally disregarded it's use? Any new treatments plans?
I never heard that heparin use in DIC was controversial? My understanding is
that it interrupts the cascade.
When did it become controversial? I've used heparin many
times for a
patient with DIC, to help prevent microemboli. It is, after all,
disseminated intravascular *coagulation*.
I understand that......and hence the Heparin. However, many
physicians go by
the school of thought that the Heparin only worsens the bleeding, and it's a
matter of what came first.......the chicken or the egg. It's most definitley
controversial, at least it was 3 years ago when I took several critical care
courses and did a lot of reading on the subject. From my understanding, more
docs opt for the Heparin than don't, though.
Okay. The latest I've read is that if the underlying cause is quickly
treatable, like after an amniotic fluid embolus, you should use only replacement
therapy. Heparin use is controversial when there might be an unacceptable
increase in bleeding, like post-op . But---it might be necessary when the
coagulation is producing serious consequences and the underlying cause is not
rapidly reversible. Then they'll use a combination of heparin and replacement
therapy (platelets, cryoprecipitate or plasma, depending on labs) Prognosis
depends on the underlying disease.
If your docs aren't using heparin in DIC "because it
makes the bleeding worse,"
I submit that 1) they haven't read up on hematology lately, like in the last 15
years minimum, and 2) they've never seen how bad DIC bleeds anyway (there is
nothing "worse" besides maybe Ebola). Heparin for DIC has never been, to my
experience or reading, remotely "controversial" nor limited to hospitals in
Heparin rapidly interrupts the clotting cascade, thus preventing further
consumption of clotting products in the body by the DIC while you
(theoretically) try your damnedest to replace blood and products and to reverse
the cause of the DIC. The benefit is that you (hope to) stop the intravascular
clotting to prevent infarcts hither and yon caused by clotted-off little blood
vessels all over (uh, disseminated). Meanwhile, yes, they bleed like stuck
pigs. They were doing that anyway, with their clotting factors all used up on
the intravascular clots.
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