Disseminated intravascular coagulation: why clotting and bleeding coexist
DIC (disseminated intravascular coagulation) is clotting switched on throughout the circulation, forming tiny clots and using up the supplies needed to stop bleeding.
Remember
DIC is overactive clotting that runs out of its own supplies: it forms microthrombi (tiny clots in small vessels), while platelets (the small blood cells that plug a damaged vessel) and clotting factors (the proteins that build a clot) are used up, so the patient bleeds too. Treat the underlying cause first.
Memory aid
DIC is like a shop that sells out of stock; clotting everywhere empties the shelves, so nothing remains when it is truly needed.
Picture the clotting supplies as shop stock that is sold off on tiny clots everywhere, leaving none for a real bleed.
In disseminated intravascular coagulation (DIC), a trigger such as infection, cancer or major trauma (burns, for example) sets off the clotting cascade (the chain of enzyme steps that builds a fibrin clot) throughout the circulation, not just at a site of injury.
Many microthrombi (tiny clots in small vessels) then form. They block blood flow and starve organs of oxygen, so the kidneys, lungs and brain can begin to fail.
At the same time, platelets and clotting factors are consumed, meaning they are used up faster than the body can replace them. When the supply runs low, the blood cannot clot properly where it is needed, so the patient bleeds, classically from venepuncture sites (places where a needle has been put into a vein).
Fibrinolysis (the system that breaks clots down) is switched on as well. It makes plasmin, an enzyme that cuts fibrin into fibrin degradation products. These fragments bind to platelets and interfere with their function, which adds to the bleeding.
So clotting and bleeding come from one process. How fast DIC evolves matters, though: slowly evolving DIC mainly causes venous clots (clots in the veins), while rapidly evolving DIC mainly causes bleeding. Treatment starts by treating the underlying cause, and platelets and clotting factors are replaced if bleeding is severe.
Key facts
- Triggers
- infection, cancer and major trauma such as burns can set off DIC.
- Clotting side
- blocked small vessels can contribute to organ failure.
- Bleeding side
- bleeding occurs once platelets and clotting factors are used up faster than they can be replaced.
- Typical results
- in severe, rapidly evolving DIC the platelets fall, PT and APTT (the tests that measure how quickly clotting factors work) are prolonged, fibrinogen falls and D-dimer (a fragment released when fibrin is broken down) rises.
- Red cells
- red blood cells are often damaged as they flow past the microthrombi, and fragmented cells (schistocytes) may be seen.
- Treatment
- the underlying cause is treated first, while platelets and clotting factors can be given in the short term.
Exam traps
- Antibodies that destroy platelets lower the platelet count and cause bleeding, but the clotting cascade is not driven into overactivity, so there are no widespread microthrombi and clotting factors are not consumed.
- Hyperfibrinolysis means clots are broken down too readily. Fibrinolysis is activated in DIC, but as a response to fibrin that has already formed, so an isolated excess of clot breakdown does not explain the widespread thrombosis.
- A clot on an atherosclerotic plaque (a fatty deposit in an artery wall) blocks one artery and causes ischaemia in its territory, but it does not use up clotting factors and platelets throughout the body, so it does not explain widespread bruising.
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