Disseminated intravascular coagulation – causes, symptoms, diagnosis, treatment, pathology

Disseminated intravascular coagulation, or
DIC, describes a situation in which the process of hemostasis, which is when after blood vessel
wall injury, liquid blood rapidly becomes a gel, called coagulation or clotting, starts
to run out of control. When this happens, lots and lots of blood
clots start to form in blood vessels serving various organs, leading to organ ischemia. DIC, though, is also called a consumption
coagulopathy, because all this clotting consumes platelets and clotting factors. Without enough platelets circulating in the
blood, other parts of the body begin to bleed with even the slightest damage to the blood
vessel walls. So paradoxically, patients have too much and
too little clotting. Normally, after a cut and damage to the endothelium,
or inner lining of blood vessel walls, there’s an immediate vasoconstriction or narrowing
of the blood vessel which limits the amount of blood flow. After that, some platelets adhere to the damaged
vessel wall, and become activated and then recruit additional platelets to form a plug. The formation of the platelet plug is called
primary hemostasis. After that, the coagulation cascade is activated. First off in the blood there’s a set of
clotting factors, most of which are proteins synthesized by the liver, and usually these
are inactive and just floating around in the blood. The coagulation cascade starts when one of
these proteins gets proteolytically cleaved. This active protein then proteolytically cleaves
and activates the next clotting factor, and so on. This cascade has a huge degree of amplification
and takes only a few minutes from injury to clot formation. The final step is activation of the protein
fibrinogen to fibrin, which deposits and polymerizes to form a mesh around the platelets. So these steps leading up to fibrin reinforcement
of the platelet plug make up the process called secondary hemostasis and results in a hard
clot at the site of the injury. Now, as soon as the clot is formed, the body
is also initiating pathways to break down the clot so that it doesn’t get bigger than
it needs to be and dissolves when it’s not needed anymore—a process called fibrinolysis. And this process produces fibrin degradation
products. Normally, the formation of new clots and the
process of fibrinolysis are in a steady balance. Now, in serious medical conditions, like for
example sepsis, malignancy, serious trauma, obstetric complications, or intravascular
hemolysis like you might see with blood type incompatibility, there can be a release of
a procoagulant that tips the scales in favor of clot formation. Procoagulants could be proteins like tissue
factor or bacterial components like lipopolysaccharide, or could even be the presence of enzymes that
help to proteolytically cleave and activate clotting factors. Whatever the cause is, in response the coagulation
pathway goes into overdrive, resulting in widespread clot formation which plugs up medium
and small blood vessels which leads to ischemia, necrosis, and eventually organ damage. The kidneys, liver, lungs and brain are particularly
susceptible. The massive formation of clots throughout
the body depletes the supply of platelets and clotting factors. To make things worse, as the clots are broken
down through fibrinolysis, fibrin degradation products are released into the circulation
and these interfere with platelet aggregation and clot formation, making hemostasis even
more difficult. And the result is a paradox, right? On one side you have thrombosis, which is
when clots obstruct the vessel, and at the same time you have trouble forming clots,
which leads to bleeding. Laboratory findings in disseminated intravascular
coagulation include decreased platelets and decreased fibrinogen. There is also a prolonged prothrombin (or
PT) time, as well as prolonged partial thromboplastin time (or PTT), both of which reflect having
lower levels of circulating coagulation factors. In addition to lower levels of specific clotting
factors, there are elevated levels of D-dimer, which is a fibrin degradation product that
is produced when fibrin clots are broken down. Now, it’s worth mentioning that in some
cases, disseminated intravascular coagulation can be a more chronic process, like in individuals
with certain solid tumors and large aortic aneurysms, and in those situations, there
may be physiologic compensation making the lab results look relatively normal. In either acute or chronic DIC, the treatment
focuses on treating the underlying cause, because that’s what drives the activation
of the coagulation cascade. In addition, the goals are to support the
various organs using supportive measures like ventilator support, hemodynamic support, and
transfusions if they’re needed. Alright, as a quick recap, DIC happens when
the balance between forming new clots and breaking down clots is tipped in favor of
clots, which leads to widespread clotting and organ ischemia, while at the same time
depletes clotting factors, paradoxically leading to bleeding. Thanks for watching, you can help support
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