| Abstrakt: |
Disseminated intravasuclar coagulation (DIC) or consumption coagulopathy has been well documented in children with bacterial septicemia but infrequently reported in viral disease. Fibrin thrombi have been noted with the malignant form of varicellazoster virus infections and there is laboratory evidence that DIC may be present in hemorrhagic smallpox. It is the purpose of this report to describe the changes in the coagulation mechanism in 4 children with severe varicella infection, 3 of whom had hemorrhagic chickenpox. All cases had a malignant disease at the time of their viral infection; 2 with acute leukemia in remission, I acute leukemia in relapse, and I with metastatic retinoblastoma. All were receiving an antineoplastic drug but none were on corticosteroids. None had bacterial sepsis or shock at the time of their chickenpox. Hemorrhagic varicella only occurred in the 3 leukemic patients, and all 3 died. The non-hemorrhagic case survived. The coagulation data revealed that the patients with the hemorrhagic form demonstrated thrombocytopenia, reduced levels of coagulation factors II, V, and VIII, hypofibrinogenemia, positive fibrin split products, and normal euglobulin lysis. In the non-hemorrhagic patient all studies were normal. Heparin therapy was given to one patient with questionable improvement only noted in the fibrinogen level. Although hepatic necrosis may be found in fatal cases of varicella the coagulation data suggest that the multiple defects were due to DIC. In addition, the data furhter suggest that the mechanism by which this virus elicits DIC is different from bacterial sepsis since the DIC was clearly present in the absence of hypotension or shock. |
