Disseminated Intravascular Coagulation
Disseminated Intravascular Coagulation (DIC)
is a syndrome characterized by massive activation and consumption
of coagulation proteins, fibrinolytic proteins and platelets.
It is not a primary disease, but a disorder secondary to numerous
triggering events such as bacterial, viral, rickettsial, protozoal,
parasitic diseases, heat stroke, burns, neoplasia and severe
trauma. In 41 cases of disseminated intravascular coagulation,
39% were secondary to malignancy, 30% from pancreatitis, 4%
from sepsis, 14% from chronic active hepatitis and 12% secondary
to heat stroke. Disseminated intravascular coagulation can
be traced to platelet activation and/or the release of thromboplastins
into the circulation from tissue damage from various conditions
listed above. It can be acute, subacute or chronic and can
be localized or generalized. Its severity is related to the
rate of release of thromboplastin, the duration of exposure
to the causative agent, the ability of the liver to replace
consumed coagulation factors, and the ability of the bone
marrow to restore platelets.
Tissue necrosis, inflammation, red cell or platelet
damage, or endothelial damage induced by antigen-antibody
or endotoxin initiates the coagulation process which ultimately
forms a clot. Simultaneously, the fibrinolytic system is
also activated. Plasmin, the active protease in fibrinolysis,
degrades fibrinogen and fibrin, producing fibrin degradation
products which in turn prevent fibrin polymerization. Plasmin
can also degrade coagulation factors. Thus, the bleeding
tendency in disseminated intravascular coagulation patients
is a consequence of the depletion of coagulation factors and
platelets and the anticoagulant properties of fibrin degradation
Coagulation disorders are characterized by spontaneous
hemorrhage and/or excessive bleeding after surgery or trauma.
Hemorrhage into the central nervous system may cause acute
onset of neurological dysfunction or sudden death. Bleeding
in association with disseminated intravascular coagulation
is usually severe and occurs from mucosal surfaces and into
body cavities. In addition, signs of the underlying disease
are usually present. Other signs include shock, petechiae
and ecchymoses of the skin and mucous membranes. The organ
or organs involved with their accompanying signs and clinical
effects must also be taken into consideration.
Laboratory diagnosis is usually based on the
triad of prolonged prothrombin time (PT), thrombocytopenia,
and hypofibrino-genemia. The finding of fibrin-fibrinogenemia
degradation products (FDP's), schistocytes (fragmented erythrocytes)
in blood smears, and decreased concentrations of coagulation
factors (factors V and VIII and antithrombin III) aid in the
diagnosis. Also APTT and thrombin clotting time (TCT) are
Therapy should be approached in a logical and
sequential fashion. The most important measure involves removal
of the inciting cause. When this is not possible, specific
treatment may be indicated. Fluid therapy is used to correct
hypovolemia; prevent or alleviate vascular stasis; and dilution
of thrombin, FDP's and activators of fibrinolysis. Drugs
for inhibiting coagulation are indicated if the patient manifests
direct evidence of bleeding, thrombosis, or organ dysfunction.
Heparin potentiates the action of plasma antithrombin III.
When patients with DIC bleed, replacement of some or all blood
constituents is indicated to replenish depleted coagulation
factors and platelets. Plasma infusion is preferred, but
whole blood may be given if red cell infusion is necessary.
The infusion of red cells carries the risk of hemolysis and
exacerbation of DIC.
Normalization of the screening coagulogram (PT,
APTT, and FDP's) usually denotes successful therapy. The
return of the normal fibrinogen concentration is a reliable
long-term indicator of heparin therapy.
- by Arthur Newman, ECFVG
- edited by VictoriaOwiredu-Laast,