Disseminated intravascular coagulation

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Introduction0:00–0:49

In disseminated intravascular coagulation or DIC, disseminated means that something is spread out. Intravascular means it's happening within the blood vessels, and coagulation refers to the process of blood clotting.
In other words, disseminated intravascular coagulation describes the widespread formation of blood clots within the blood vessels.
When a blood vessel gets injured, the body immediately triggers primary hemostasis to stop the bleeding. Let's say you're trying to thread a needle, but the needle stabs you instead and damages the blood vessels in your fingertip.
This injury exposes the collagen in the blood vessel wall, which is rich in von Willebrand factor, and triggers local endothelial cells to release more von Willebrand factor into circulation.

Physiology0:49–2:31

Once released into the bloodstream, von Willebrand factor sticks to the damaged area and acts like a glue. Circulating platelets bind this glue-like substance using their glycoprotein 1B receptors, eventually adhering to the site of injury.
At this point, platelets become active, so they change their shape and form tentacle-like arms to grab onto other platelets.
Activated platelets release more von Willebrand factor along with serotonin and calcium. Platelets also release adenosine diphosphate and thromboxane A2, which together activate nearby unbound platelets and recruit them to the site.
In addition, these two substances spark platelets to express a new surface protein called GP2B3A, which enables them to catch the circulating blood protein fibrinogen.
Fibrinogen acts like a pair of handcuffs that links two platelets together. This process results in a snowball effect with more platelets piling up, eventually sealing the damaged area and stopping the bleeding.
Once the body creates the platelet plug, it triggers secondary hemostasis to reinforce the clot with a strong fibrine mesh.
This process involves the extrinsic and intrinsic coagulation pathways, both of which eventually spark the common pathway.
With the extrinsic pathway, injury to the blood vessel exposes factor 3, also known as tissue factor, which activates factor 7.
Together, the tissue factor, activated factor 7, and calcium activate factor 10 and initiate the common pathway. Activated factor 10, activated factor 5, and calcium form the prothrombinase complex, which converts factor 2 called prothrombin.

Pathology2:31–3:56

Into activated factor 2 called thrombin. Next, thrombin cleaves factor 1 or fibrinogen into activated factor 1 called fibrin.
Thrombin also activates factor 13, which binds calcium to create fibrin crosslinks to stabilize the clot. On the flip side, the intrinsic pathway starts when collagen of the blood vessel wall activates factor 12, also known as the Hageman factor.
Activated factor 12 then triggers factor 11, which, with the help of calcium, activates factor 9. Next, let's focus on factor 8, which travels through the circulation in its inactive form bound to the von Willebrand factor.
During secondary hemostasis, thrombin releases factor 8 from the von Willebrand factor and activates it. Finally, activated factor 8, activated factor 9, and calcium form a complex that activates factor 10, eventually pushing things toward the common pathway.
Now, as soon as the body creates a clot and stops the bleeding, it initiates pathways to break it down. This is important because uncontrolled piling up of platelets can result in complete obstruction of the blood flow.

Diagnosis3:56–4:51

This process is known as fibroanalysis, and the main guy here is plasminogen. When it's time to clean up blood clots, the body converts plasminogen to plasmin, which acts like a sword, cutting the fibrine mesh into smaller pieces called fibrin degradation products such as D-dimer.
As the body destroys the fibrine mesh, the blood clot begins to resolve. Now DIC can happen for two main reasons.
First, the body might release a large amount of tissue factor or other clot promoting substances into the bloodstream, which can trigger uncontrollable blood clot formation.
This can occur during major traumas, obstetric complications like placental abruption, and malignancies, especially acute promyelocytic leukemia and adenocarcinomas.

Treatment4:51–5:11

The second reason involves widespread damage to the endothelial cells, which exposes subendothelial collagen and sparks hemostasis.
This is common in infections like sepsis and autoimmune conditions such as systemic lupus erythematosis. Moreover, the most common causes are hidden in the pneumonic DIC.

Review5:11–11:14

D stands for delivery or obstetric complications. I stands for infections and immunological conditions, while C refers to cancer.
Regardless of the underlying cause, the outcome is the same widespread microvascular thrombosis. In other words, there's a widespread formation of tiny blood clots called microthrombi throughout the small vessels like arterials and capillaries.
These microthrombi can obstruct blood flow, leading to ischemia and infarction in various organs. But that's not all.
Inside small vessels, they can also act like tiny saws. As red blood cells squeeze past, these microthrombi shred red blood cells into fragments known as helmet cells or schistocytes.
Ultimately, this results in microangiopathic hemolytic anemia. And while all these clots are forming, the body is trying to keep things under control by converting plasminogen into plasmin.
This way, the body breaks down the fibrin, subsequently resolving clots. However, by cutting fibrine, plasmin releases fibrin degradation products into the bloodstream.
Think of these products as day off coupons for platelets, because they block platelets from doing their job. So if there's widespread damage to the endothelial cells, platelets will take a break and ignore the issue, which can eventually result in bleeding.
To make things worse, plasmin also reduces the activity of factors 5 and 8, further impairing the whole clotting process.
Moving on to clinical manifestations, which can be subdivided into two categories. First, thrombotic manifestations occur when blood clots obstruct small blood vessels in various organs.
In the kidneys, this can result in small infarctions of the renal cortex, which can potentially lead to acute renal failure.
In the heart, it can result in myocardial infarction, while in the brain, it can lead to stroke. Finally, in the lungs, microthrombi can obstruct pulmonary capillaries and impair gas exchange, eventually causing acute respiratory distress syndrome.
Next, hemorrhagic manifestations arise from the depletion of platelets and clotting factors, which is why DIC is known as consumptive coagulopathy.
Bleeding typically affects small blood vessels in the skin, causing petechia and ecchymoses, and the mucous membranes, resulting in gum and nose bleeding.
In more severe cases, it can affect the intestinal mucosal lining and result in gastrointestinal hemorrhage. And remember, bleeding can happen anywhere in the body.
For example, bleeding in the adrenal glands can lead to adrenal insufficiency and adrenal crisis. One dramatic example of bilateral adrenal bleeding is known as Waterhouse-Fredriksson syndrome, which is common in meningococcal sepsis.
When the adrenal glands fail, the body runs low on key hormones like cortisol and aldosterone, which help keep BP stable.
Without them, BP drops, leading to cardiovascular shock. Diagnosis primarily relies on clinical features and lab findings.
Due to widespread clot formation and rapid platelet consumption, labs will reveal a low platelet count. Additionally, if there is microangiopathic hemolytic anemia, you will notice anemia.
However, to confirm this, be sure to order a peripheral blood smear to look for schistocytes. Next, use the coagulation profile to assess 3 main blood tests.
Prothrombin time evaluates clotting factors of the extrinsic and common pathways, while activated partial thromboplastin time reflects the intrinsic and common pathways.
On top of that, thrombin time measures how long it takes for fibrinogen to turn into fibrin in the presence of thrombin.
In DIC widespread clot formation depletes not only platelets, but also clotting factors, which results in prolonged prothrombin time and activated partial thromboplastin time.
And since widespread clot formation reduces fibrinogen levels, there's nothing that thrombin can convert to fibrin, so thrombin time will also be prolonged.
However, despite falling fibrinogen levels, D-dimer will be elevated due to the ongoing breakdown of previously formed fibrin clots.
Finally, treatment begins with addressing the underlying cause, such as managing obstetric complications, treating infections, or controlling malignancy.
At the same time, supportive care is necessary to manage bleeding and coagulation abnormalities. This may include blood product transfusions, such as platelets to replenish low counts, or fresh frozen plasma to replace depleted clotting factors.
All right, as a quick recap, disseminated intravascular coagulation refers to the widespread formation of blood clots, which is typically triggered by obstetric complications, infections, and autoimmune conditions.
Widespread clot formation results in the obstruction of small blood vessels in thrombotic manifestations such as ischemia and infarctions.
At the same time, bleeding issues can result in hemorrhagic manifestations, which can affect any organ, but most commonly affect the skin and mucosa.