Hepatosplanchnic circulatory dysfunction in acute hepatic infection: the case of dengue hemorrhagic fever.

The mechanism of shock in patients with dengue hemorrhagic fever (DHF) has not yet been fully understood. In this study, we investigated the possibility of splanchnic venous pooling as a contributor for circulatory dysfunction in these patients. Ultrasonographic studies of portal vein and inferior vena cava were done in 45 patients with serologically or PCR-confirmed diagnosis of dengue virus infection. The size of portal vein and inferior vena cava, mean blood flow velocity in the right portal vein, and modified portal vein congestion index were compared between patients with dengue fever (DF, n = 20), DHF without shock (n = 14), and dengue shock syndrome (DSS, n = 11) during the toxic stage, convalescent stage, and at follow-up. The portal vein was significantly more dilated in patients with shock (DSS) than DHF without shock and than DF during the toxic and convalescent stages (P < 0.05), but not at follow-up. The change in the size of inferior vena cava followed the opposite trend (not statistically significant). Portal vein blood flow velocity was lower and congestion index was higher in shock cases (DSS) than DHF without shock and than DF at toxic and convalescent stages (P < 0.01). The differences disappeared at follow-up. Hepatosplanchnic venous pooling and/or dysfunction occur and correlate with the severity of circulatory derangement and shock in patients with DHF. The cause(s) and significance of hepatosplanchnic circulatory dysfunction in DHF and possibly other viral hepatic diseases deserve further study.