Last updated on May 25, 2019 at 12:14
We’ve heard a lot about DIC up until now, but who really understood what it is, right? I hope we do by the end of this topic.
The definition of DIC is an acute, widespread (not local) activation of the clotting cascade that leads to the formation of microthrombi everywhere in the body. This massive clotting leads to depletion of clotting factors, so excessive bleeding occurs simultaneously. Simultaneously will the fibrinolytic system be activated. Let’s look at the details.
It has three phases:
- The thrombotic phase is characterised by widespread microthrombi formation, which impairs the tissue circulation by creating sludge-like circulation in the capillaries. This also consumes all the platelets and clotting factors.
- The consumption coagulopathy phase is characterised by widespread bleeding similar to a bleeding disorder, because the platelets and clotting factors are depleted.
- The fibrinolytic phase occurs simultaneously as the previous phases. The fibrinolytic system is activated by the formation of microthrombi. Plasmin cleaves fibrin and fibrin degradation products into other products like D-dimers. These D-dimers impair further clotting.
DIC can occur due to three different pathways:
- The intrinsic pathway – due to widespread endothelial damage or toxins
- The extrinsic pathway – due to massive tissue damage which releases thromboplastin
- By primary activation of the fibrinolytic pathway, which doesn’t really cause DIC but the consequences of both are similar.
Intrinsic pathway of DIC
The intrinsic pathway can be activated due to:
- Endothelial damage
- Circulatory shock
- Extreme cold or heat
- Aortic aneurysm
- Acute glomerulonephritis
- Rocky Mountain spotted fever
- Haemolytic-uraemic syndrome
Endothelial damage or toxins activate factor XII, which in turn activates:
- The intrinsic pathway of coagulation
- The kallikrein-kinin system, especially bradykinin, which causes vasodilation and hypotension
- Fibrinolysis by activating plasminogen and plasmin.
In the intrinsic pathway will hypotension and fibrinolysis occur early.
Extrinsic pathway of DIC
The extrinsic pathway can be activated due to:
- Tissue damage
- Burns, frost-bite
- Head trauma
- Polytrauma (like in car crash)
- Pregnancy complications
- Heat stroke
- Acute pancreatitis
The widespread tissue damage releases thromboplastin, a protein stored in tissues. Thromboplastin is released into the circulation, which activates factor VII, the first factor in the extrinsic pathway of coagulation.
In the extrinsic pathway will hypotension and fibrinolysis appear late.
Primary activation of fibrinolytic system
The job of the fibrinolytic system is to break down clots when they’re no longer needed and to prevent clots from growing too large. The most important components are urokinase and plasmin. Urokinase converts plasminogen into plasmin, which will then lyse fibrin clots.
It can be caused by:
- Prostate tumors (they can secrete urokinase)
- Urogenital inflammation
- Liver cirrhosis
- Heat stroke
- Snake venom
Overactivation of the fibrinolytic system means that no clots will be formed because fibrin is immediately degraded into fibrin degradation products. These degradations products (like D-dimer) suppress further blood clotting as well. The consequence is than any small bleeding, such as a venepuncture or catheter can cause severe bleeding and hypovolaemic shock.
Yes, DIC can be chronic in certain cases, especially in cancer patients. The formation of microthrombi isn’t fulminant and fast but slow and moderate. Spontaneous bleeding and fever doesn’t occur, but the impaired capillary flow still causes cyanosis of the distal parts of the body (fingers, nose, genitalia), a condition called acrocyanosis.
Consequences and treatment
- Widespread tissue damage due to impaired capillary flow
- Circulatory shock (or aggravation of the shock if already present)
- Lactic acidosis
- Multi organ dysfunction syndrome (MODS)
- Fresh frozen plasma
- Platelet replacement if it dips below 50 G/L
60. Thrombosis. Causes and consequences
62. Granulocytes in inflammatory processes