Disseminated Intravascular
Coagulation (DIC)
General
Hemorrhagic forms of smallpox and in some cases, progressive
vaccinia may engender consumption of coagulation factors.
Fibrinolytic activity increases, pro-coagulants are
activated, hematologic inhibitors are consumed, platelets
decrease, often dramatically, and ultimately end-organ
failure supervenes. Both acute DIC and chronic forms
have been described. Tissue injury, probably directly
by virus, or by viral antigens, results in endothelial
damage, releasing procoagulant materials that start
the cascade into DIC.
Clinical
Generalized bleeding is the first sign of established
DIC. Petechiae, skin hemorrhages, and massive bleeding
may be observed. Thrombosis of small and large vessels
follows with hypoperfusion of organs or frank infarction
that result in end-organ damage in the kidneys, liver
and other vital organs. Shock, as described above, occurs
rapidly. In the chronic forms, a slower process is observed,
characterized mainly by subacute bleeding and diffuse
evidence for microthrombosis.
Laboratory
Fibrin split products may be detected; elevated levels
are present in almost all patients. The presence of
D-dimer is the most definitive test for DIC. Antithrombin
III, platelets and fibrinogen are all decreased. The
coagulation profile may be disordered, but consistent
findings are not always present. Anemia, azotemia, elevated
liver enzymes, decrease in specific coagulation factors,
hemoglobinuria, hematuria, and hematochezia may be detected.
Clinical symptoms and signs should guide imaging studies.
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