Disseminated Intravascular Coagulopathy Disseminated Intravascular Coagulation (DIC) Is A Pathological

DISSEMINATED INTRAVASCULAR COAGULOPATHY
DEFINITION
Disseminated intravascular coagulation (DIC) is a pathological
process characterized by the widespread activation of the clotting cascade that
results in the formation of blood clots in the small blood vessels throughout the
body. This leads to compromised tissue blood flow and can ultimately lead to
multiple organ damage. In addition, as the coagulation process consumes clotting
factors and platelets, normal clotting is disrupted and severe bleeding can occur
from various sites
ETIOLOGY
DIC can occur in the following conditions:
 Solid tumors and blood cancers (particularly acute promyelocytic leukemia)

 Obstetric complications: abruptio placentae, pre-eclampsia or eclampsia,
amniotic fluid embolism, retained intrauterine fetal demise, septic abortion,
post partum haemorrhage
 Massive tissue injury: severe trauma, burns, hyperthermia, rhabdomyolysis,
extensive surgery
 Sepsis or severe infection of any kind (infections by nearly all
microorganisms can cause DIC, though bacterial infections are the most
common): bacterial (Gram-negative and Gram-positive sepsis), viral, fungal,
or protozoan infections
 Transfusion reactions (i.e., ABO incompatibility haemolytic reactions)
 Severe allergic or toxic reactions (i.e. snake venom)
 Giant haemangiomas (Kasabach-Merritt syndrome)
 Large aortic aneurysms
Liver disease, HELLP syndrome, thrombotic thrombocytopenic

purpura/Haemolytic uremic syndrome, and malignant hypertension may mimic
DIC but do not occur via the same pathways
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 haemostasis. 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 plasmin is critical, as it is the central proteolytic
enzyme of coagulation and is also necessary for the breakdown of clots, or
fibrinolysis.[citation needed]
In DIC, the processes of coagulation and fibrinolysis are

dysregulated, 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 1), tumor necrosis factor, and
endotoxin.[7] 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
exposure to blood and platelets, TF binds with activated factor VIIa (normally
present in trace amounts in the blood), forming the extrinsic tenase complex. This
complex further activates factor IX and X to IXa and Xa, respectively, leading to
the common coagulation pathway and the subsequent formation of thrombin and
fibrin.
The release of endotoxin is the mechanism by which Gram-negative

sepsis provokes DIC. In acute promyelocytic leukemia, treatment causes the
destruction of leukemic granulocyte precursors, resulting in the release of large
amounts of proteolytic enzymes from their storage granules, causing microvascular
damage. Other malignancies may enhance the expression of various oncogenes
that result in the release of TF and plasminogen activator inhibitor-1 (PAI-1),
which prevents fibrinolysis.
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 positive feedback loop develops
in which increased clotting leads to more clotting. At the same time,
thrombocytopenia occurs and this has been attributed to the entrapment and
consumption 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 an excess 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.
There has been a recent challenge however to the basic assumptions

and interpretations of the pathophysiology of DIC. A study of sepsis and DIC in
animal models has shown that a highly expressed receptor on the surface of
hepatocytes, termed the Ashwell-Morell receptor, is responsible for
thrombocytopenia in bacteremia and sepsis due to Streptococcus pneumoniae
(SPN) and possibly other pathogens. The thrombocytopenia observed in SPN
sepsis was not due to increased consumption of coagulation factors such as
platelets, but instead was the result of this receptor's activity enabling hepatocytes
to ingest and rapidly clear platelets from circulation.[9] By removing pro-
thrombotic components before they participate in the coagulopathy of DIC, the
Ashwell-Morell receptor lessens the severity of DIC, reducing thrombosis and
tissue necrosis, and promoting survival. The hemorrhage observed in DIC and
among some tissues lacking this receptor may thereby be secondary to increased
thrombosis with loss of the mechanical vascular barrier. This discovery has
possible significant clinical implications in devising new approaches to reducing
the morbidity and mortality of DIC
CLINICAL MANIFESTATION
 clot formation (with resultant ischemia to all or part of the organ) or, less
often, bleeding.
• Patient may bleed from mucous membranes, venipuncture sites, and
gastrointestinal and urinary tracts.
• Bleeding can range from minimal occult internal bleeding to profuse hemorrhage
from all orifices.
• Patients typically develop multiple organ dysfunction syndrome (MODS), and
they may exhibit renal failure as well as pulmonary and multifocal central nervous
system infarctions as a result of microthromboses, macrothromboses, or
hemorrhages.
• Initially, the only manifestation is a progressive decrease in the platelet count;
then, progressively, the patient exhibits signs and symptoms of thrombosis in the
organs involved.
Eventually bleeding occurs (at first subtle, advancing to frank hemorrhage). Signs
depend on the organs involved.
DIAGNOSTIC EVALUATION
• Clinically, the diagnosis of DIC is often established by adrop in platelet count, an

increase in PT and activated partial thromboplastin time (aPTT), an elevation in
fibrin degradation products, and measurement of one or more clotting
factors and inhibitors (eg, antithrombin [AT]).
• The International Society on Thrombosis and Haemostasis has developed a
highly sensitive and specific scoring system using the platelet count, fibrin
degradation products, PT, and fibrinogen level to diagnose DIC. This system is
also useful in predicting the severity of the disease and subsequent
mortality.
MANAGEMENT
MEDICAL MANAGEMENT
The most important management issue is treating the underlying
cause of DIC. A second goal is to correct the secondary effects of tissue ischemia
by improving oxygenation, replacing fluids, correcting electrolyte imbalances, and
administering vasopressor medications. If serious hemorrhage occurs, the
depleted coagulation factors and platelets may be replaced (cryoprecipitate to
replace fibrinogen and factors V and VII; fresh-frozen plasma to replace other
coagulation factors).
A heparin infusion, which is a controversial management method,
may be used to interrupt the thrombosis process. Other therapies include
recombinant activated protein C and AT infusions.
NURSING MANAGEMENT
Maintaining Hemodynamic Status
•Avoid procedures and activities that can increase intracranial pressure, such as
coughing and straining.
• Closely monitor vital signs, including neurologic checks, and assess for the
amount of external bleeding.
•Avoid medications that interfere with platelet function, if possible (eg, beta-
lactam antibiotics, acetylsalicylic acid, nonsteroidal anti-inflammatory drugs).
•Avoid rectal probes and rectal or intramuscular injection medications.
• Use low pressure with any suctioning.
•Administer oral hygiene carefully: use sponge-tipped swabs, salt or soda mouth
rinses; avoid lemon-glycerine swabs, hydrogen peroxide, commercial
mouthwashes.
•Avoid dislodging any clots, including those around IV sites, injection sites, and so
forth.
Maintaining Skin Integrity

• Assess skin, with particular attention to bony prominences and skin folds.
• Reposition carefully; use pressure-reducing mattress and lamb’s wool between
digits and around ears and soft absorbent material in skin folds, as needed.
• Perform skin care every 2 hours; administer oral hygiene carefully.
•Use prolonged pressure (5 minutes minimum) after essential injections.
Monitoring for Imbalanced Fluid Volume
•Auscultate breath sounds every 2 to 4 hours.
• Monitor extent of edema.
• Monitor volume of IV medications and blood products; decrease volume of IV
medications if possible.
•Administer diuretics as prescribed.
Assessing for Ineffective Tissue Perfusion Related to Microthrombi

• Assess neurologic, pulmonary, and skin systems.
• Monitor response to heparin therapy; monitor fibrinogen levels.
• Assess extent of bleeding.
• Stop epsilon-aminocaproic acid if symptoms of thrombosis occur.
Reducing Fear and Anxiety
• Identify previous coping mechanisms, if possible; encourage patient to use them
as appropriate.
• Explain all procedures and rationale in terms that the patient and family can
understand.
•Assist family in supporting patient.
• Use services from behavioral medicine and clergy, if desired.

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DISSEMINATED INTRAVASCULAR COAGULOPATHY

DIC can occur in the following conditions:

 Solid tumors and blood cancers (particularly acute promyelocytic leukemia)

Liver disease, HELLP syndrome, thrombotic thrombocytopenic

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

In DIC, the processes of coagulation and fibrinolysis are

The release of endotoxin is the mechanism by which Gram-negative

Excess circulating thrombin results from the excess activation of the

Coagulation inhibitors are also consumed in this process. Decreased

Simultaneously, excess circulating thrombin assists in the conversion

There has been a recent challenge however to the basic assumptions

• Clinically, the diagnosis of DIC is often established by adrop in platelet count, an

Maintaining Hemodynamic Status

Maintaining Skin Integrity

Assessing for Ineffective Tissue Perfusion Related to Microthrombi

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