Content area
Full Text
Intensive Care Med (2014) 40:19361939DOI 10.1007/s00134-014-3515-1 UNDERSTANDING THE DISEASE
Tom E. Fletcher Robert A. Fowler Nicholas J. Beeching
Understanding organ dysfunction in Ebola virus disease
Received: 19 September 2014 Accepted: 6 October 2014Published online: 1 November 2014 Springer-Verlag Berlin Heidelberg and
ESICM 2014
T. E. FletcherWellcomeTraining Fellow and Lecturer, Liverpool School of Tropical Medicine, Pembroke Place, Liverpool L3 5QA, UK e-mail: [email protected]
R. A. FowlerAssociate Professor of Medicine, Sunnybrook Hospital, University of Toronto, 2075 Bayview Avenue, Room D478, Toronto, ON M4N 3M5, Canada e-mail: [email protected]
N. J. Beeching ())
Senior Lecturer in Infectious Diseases, Liverpool School of Tropical Medicine, Pembroke Place, Liverpool L3 5QA, UK e-mail: [email protected].: ?441517063835
Ebola viruses are single-stranded RNA loviruses which are maintained in nature in fruit bats [1]. The genus includes ve strains that are clinically distinguished by their usual geographic location and severity of disease in humans. The Reston strain does not appear to cause human disease, and asymptomatic human infections can also occur with other strains. The current West African outbreak is caused by the Zaire strain,which is typically associated with mortality rates of 5090 % [2, 3]. This short review summarises knowledge about the pathogenesis of organ dysfunction in Ebola virus disease (EVD).
Clinical disease commences after an incubation period ranging from 2 to 21 days, and is initially non-specic, with fever, headache, lethargy and myalgia. This progresses to a gastrointestinal stage characterised by diarrhoea, vomiting and abdominal pain. Hypovolemia, systemic hypoperfusion and shock are the most obvious clinical syndromes in inadequately resuscitated patients. Haemorrhage and haemorrhagic shock occur in a minority of patients, most commonly due to profound and frequently pre-terminal gastrointestinal haemorrhage. Many patients have features of systemic inammatory response syndrome [46], such as fever, tachycardia and
hyperventilation with less frequent leukopenia. Organ dysfunction (severe sepsis) and shock are also common; however, the capillary leak syndrome and subsequent secondary lung injury and hypoxia are much less apparent than with typical bacterial sepsis [2, 7], possibly due to difculties in achieving adequate replacement for uid loss in endemic treatment settings. Hyperventilation usually occurs in compensation for metabolic acidosis, rather than primary lung involvement with pneumonitis or pneumonia. C-reactive protein levels are often normal, but ferritin levels are raised, especially in those with bleeding and/or a fatal...