Care for Patients in Septic Shock and/or Disseminated Intravascular Coagulation (DIC)

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.

Treatment

All life-threatening symptoms or signs should be counteracted by appropriate life-support measures as described for septic shock. Specific measures for DIC include:

Immediate consultation with a hematologist and intensivist is mandatory to ensure that modern methods of diagnosis and treatment are provided to the patient.