Disseminated intravascular coagulation

A 76-year-old male is transferred to the intensive care unit (ICU) after developing acute shortness of breath and cough. He was undergoing chemotherapy when the symptoms emerged. Past medical history is notable for alcohol use disorder and multiple myeloma. Temperature is 39.0°C (102.2°F), pulse is 110/min, respirations are 26/min, blood pressure is 90/70 mmHg, and oxygen saturation is 87% on room air. The patient is oriented to self but not place or time. Rales are heard at the right lung base. The patient is subsequently intubated for airway protection, has a central line placed, and initiated on vasopressors. On the second day of ICU stay, the patient is noted to have blood in the foley catheter and diffuse bruising. Coagulation studies are demonstrated below:

Laboratory value	Result	Reference Range
Prothrombin time	25 seconds	11-15 seconds
Partial thromboplastin time	67 seconds	25-40 seconds
Fibrinogen	90 mg/dL	100-150 mg/dL
Factor VIII	24%	60-100%

Which of the following best describes the etiology of this patient’s disease process?

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.

Sources

"Robbins Basic Pathology" Elsevier (2017)

"Harrison's Principles of Internal Medicine, Twentieth Edition (Vol.1 & Vol.2)" McGraw-Hill Education / Medical (2018)

"Pathophysiology of Disease: An Introduction to Clinical Medicine 8E" McGraw-Hill Education / Medical (2018)

"How I treat disseminated intravascular coagulation" Blood (2018)

"Diagnosis and management of sepsis‐induced coagulopathy and disseminated intravascular coagulation" Journal of Thrombosis and Haemostasis (2019)

"Disseminated Intravascular Coagulation: An Update on Pathogenesis, Diagnosis, and Therapeutic Strategies" Clinical and Applied Thrombosis/Hemostasis (2018)

Disseminated intravascular coagulation

Videos

Notes