Table of Contents
ISRN Infectious Diseases
Volume 2013 (2013), Article ID 571646, 6 pages
http://dx.doi.org/10.5402/2013/571646
Review Article

Pathogenesis of Dengue Haemorrhagic Fever and Its Impact on Case Management

Department of Medicine, Melaka Manipal Medical College, Jalan Batu Hampar, Bukit Baru, 75150 Melaka, Malaysia

Received 5 September 2012; Accepted 30 September 2012

Academic Editors: R. Bologna, R. Favory, and K. Sawanyawisuth

Copyright © 2013 Kolitha H. Sellahewa. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Plasma leakage and intrinsic coagulopathy are the pathological hall marks in dengue haemorrhagic fever (DHF). Viral virulence, infection enhancing antibodies, cytokines and chemical mediators in the setting of intense immune activation are the key players implicated in the pathogenesis of DHF; the exact nature of which is yet to be fully understood. The pathophysiological changes the attended clinical features of plasma leakage necessitate recognition of changing physiological parameters for the early recognition of plasma leakage and appropriate fluid therapy. On the other hand, the changes in the haematological indices resulting from coagulopathy can tempt the clinician to initiate other modalities of therapy. A clearer understanding of the pathogenesis of DHF and the appreciation that both of these fundamental pathological changes share common pathogenic mechanisms would facilitate the appropriateness of management decisions and the early recognition of severe disease. Thus, thrombocytopaenia, reduced fibrinogen, and prolonged partial thromboplastin time early in the disease course connoted severe disease and attended plasma leakage rather than clinical bleeding. The detection of plasma cytokine profile by a multiple bead immunoassay could also complement clinical parameters in predicting severe disease early in the disease course. Thus, MIP-β indicates good prognosis while IFN-γ portends severe disease.