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.
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