Disseminated Intravascular Coagulation

Disseminated intravascular coagulation (DIC)
Illustrations
Blood clot
formation
Meningococcemia Meningococcemia Meningococcemia Blood clots

on the calves
on the leg
associated
purpura
Alternative Names
Consumption coagulopathy
Definition
Disseminated intravascular coagulation (DIC) is a serious disorder in which the proteins that control blood
clotting are abnormally active.
Causes
Normally, when you are injured, certain proteins are turned on and travel to the injury site to help stop
bleeding. However, in persons with DIC, these proteins are abnormally active. Small blood clots form
throughout the body. Overtime, the clotting proteins become "used up" and are unavailable during times of
real injury.
This disorder can result in clots or, more often, bleeding. Bleeding can be severe.
Risk factors for DIC include:
Blood transfusion reaction

Cancer, including leukemia
Infection in the blood by bacteria or fungus
Pregnancy complications (such as retained placenta after delivery)
Recent surgery or anesthesia
Sepsis
Severe liver disease
Severe tissue injury (as in burns and head injury)
Symptoms
Bleeding, possibly from multiple sites in the body

Blood clots
Sudden bruising
Exams and Tests

The following tests may be done:
Serum fibrinogen - low
Prothrombin time (PT) - high
Partial thromboplastin time (PTT) - high
Platelet count
Treatment
The goal is to determine and treat the underlying cause of DIC.
Blood clotting factors will be replaced with plasma transfusions. Heparin, a medication used to prevent
thrombosis, is sometimes used in combination with replacement therapy.
Outlook (Prognosis)
The underlying disease that causes the disorder will usually predict the probable outcome.
Possible Complications
Severe bleeding
Stroke
Lack of blood flow to arms, legs, or organs
When to Contact a Medical Professional

Go to the emergency room or call 911 if you have continued bleeding of unknown cause.
Prevention
Get prompt treatment for conditions known to bring on this disorder.
Disseminated intravascular coagulation

Disseminated intravascular coagulation (DIC), also called consumptive coagulopathy,
is a pathological process in the body where the blood starts to coagulate throughout the
whole body. This depletes the body of its platelets and coagulation factors, and there is a
paradoxically increased risk of hemorrhage. It occurs in critically ill patients, especially
those with Gram-negative sepsis (particularly meningococcal sepsis) and acute
promyelocytic leukemia.
Etiology
There are a variety of causes of DIC, all usually causing the release of chemicals into the
blood that instigates the coagulation.
Sepsis, particularly with gram-negative bacteria.

Obstetric complications (most common cause), with chemicals from the uterus
being released into the blood, or from amniotic fluid embolisms, and eclampsia can
be causes. Another obstetric condition which can cause DIC is abruptio placentae.
Tissue trauma such as burns, accidents, surgery or shock.
Liver disease
Incompatible blood transfusion reactions or massive blood transfusion (more than
the total circulatory volume)
Cancers, or widespread tissue damage (e.g. burns), or hypersensitivity reactions all
can produce the chemicals leading to a DIC.
Acute promyelocytic leukemia
Viral hemorrhagic fevers bring about their frank effects, paradoxically, by causing
DIC.
Envenomation by some species of venomous snakes, such as those belonging to the
genus Echis (saw-scaled vipers).
Diagnosis
Although numerous blood tests are often performed on patients prone to DIC, the important
measures are: full blood count (especially the platelet count), fibrin degradation products or
D-dimer tests (markers of fibrinolysis), bleeding time and fibrinogen levels. Decreased
platelets, elevated FDPs or D-dimers, prolonged bleeding time and decreased fibrinogen are
markers of DIC.
Pathophysiology
Under homeostatic conditions, the body is maintained in a finely tuned balance of

coagulation and fibrinolysis. The activation of the coagulation cascade yields thrombin that
converts fibrinogen to fibrin; the stable fibrin clot being the final product of hemostasis.
The fibrinolytic system then functions to break down fibrinogen and fibrin. Activation of
the fibrinolytic system generates plasmin (in the presence of thrombin), which is
responsible for the lysis of fibrin clots. The breakdown of fibrinogen and fibrin results in
polypeptides called fibrin degradation products (FDPs) or fibrin split products (FSPs). In a
state of homeostasis, the presence of thrombin is critical, as it is the central proteolytic
enzyme of coagulation and is also necessary for the breakdown of clots, or fibrinolysis.
In DIC, the processes of coagulation and fibrinolysis lose control, and the result is
widespread clotting with resultant bleeding. Regardless of the triggering event of DIC, once
initiated, the pathophysiology of DIC is similar in all conditions. One critical mediator of
DIC is the release of a transmembrane glycoprotein called tissue factor(TF). TF is present
on the surface of many cell types (including endothelial cells, macrophages, and
monocytes) and is not normally in contact with the general circulation, but is exposed to the
circulation after vascular damage. For example, TF is released in response to exposure to
cytokines (particularly interleukin), tumor necrosis factor, and endotoxin. This plays a
major role in the development of DIC in septic conditions. TF is also abundant in tissues of
the lungs, brain, and placenta. This helps to explain why DIC readily develops in patients
with extensive trauma. Upon activation, TF binds with coagulation factors that then trigger
both the intrinsic and the extrinsic pathways of coagulation.
Excess circulating thrombin results from the excess activation of the coagulation cascade.
The excess thrombin cleaves fibrinogen, which ultimately leaves behind multiple fibrin
clots in the circulation. These excess clots trap platelets to become larger clots, which leads
to microvascular and macrovascular thrombosis. This lodging of clots in the
microcirculation, in the large vessels, and in the organs is what leads to the ischemia,
impaired organ perfusion, and end-organ damage that occurs with DIC.
Coagulation inhibitors are also consumed in this process. Decreased inhibitor levels will
permit more clotting so that a feedback system develops in which increased clotting leads
to more clotting. At the same time, thrombocytopenia occurs because of the entrapment of
platelets. Clotting factors are consumed in the development of multiple clots, which
contributes to the bleeding seen with DIC.
Simultaneously, excess circulating thrombin assists in the conversion of plasminogen to
plasmin, resulting in fibrinolysis. The breakdown of clots results in excess amounts of
FDPs, which have powerful anticoagulant properties, contributing to hemorrhage. The
excess plasmin also activates the complement and kinin systems. Activation of these
systems leads to many of the clinical symptoms that patients experiencing DIC exhibit,
such as shock, hypotension, and increased vascular permeability. The acute form of DIC is
considered an extreme expression of the intravascular coagulation process with a complete
breakdown of the normal homeostatic boundaries. DIC is associated with a poor prognosis
and a high mortality rate.
Treatment
The underlying cause must be treated initially. Anticoagulants are only given when
indicated (development of thrombotic renal complications) as patients with DIC are prone
to bleeding. Platelets may be transfused if counts are very low, and fresh frozen plasma
may be administered.
DIC results in lower fibrinogen (as it has all been converted to fibrin), and this can be tested
for in the hospital lab. A more specific test is for "fibrin split products" (FSPs) or "fibrin
degradation products" (FDPs) which are produced when fibrin undergoes degradation when
blood clots are dissolved by fibrinolysis.
In some situations, infusion with antithrombin may be necessary. A new development is
drotrecogin alfa (Xigris), a recombinant activated protein C product. Activated Protein C
(APC) deactivates clotting factors V and VIII, and the presumed mechanism of action of
drotrecogin is the cessation of the intravascular coagulation. Due to its high cost, it is only
used strictly on indication in intensive care patients.[1]
The prognosis for those with DIC, depending on its cause, is often grim, leading the initials
to be known colloquially as "death is coming".[2

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Disseminated Intravascular Coagulation

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Disseminated intravascular coagulation (DIC)

Meningococcemia Meningococcemia Meningococcemia Blood clots

Blood transfusion reaction

Bleeding, possibly from multiple sites in the body

Exams and Tests

When to Contact a Medical Professional

Disseminated intravascular coagulation

Sepsis, particularly with gram-negative bacteria.

Under homeostatic conditions, the body is maintained in a finely tuned balance of

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