What intensivist need to know about hantavirus cardiopulmonary syndrome

Hantavirus infection is a zoonosis caused by Orthohantaviruses, typically acquired in rural settings through inhalation of aerosolized rodent excreta.Two major clinical syndromes are recognized.Hemorrhagic fever with renal syndrome (HFRS) is the predominant Old-World presentation and is mainly caused by Hantaan, Puumala, Dobrava, and Seoul viruses in Europe and Asia.Hantavirus cardiopulmonary syndrome (HCPS), by contrast, is the New World presentation and is caused by Sin Nombre virus, Andes virus, Araraquara virus, Juquitiba virus, Choclo virus, and Laguna Negra virus in the Americas.Andes virus remains distinctive because person-toperson transmission has been documented [1,2].HCPS carries a case fatality rate of approximately 30-45%, whereas mortality in HFRS is lower, generally 1-12% [1].In a globalized world, imported cases may present to ICUs far from endemic regions, making HCPS an important travel-associated critical illness [3].For intensivists, HCPS is defined by speed.Patients may deteriorate from a nonspecific febrile illness to severe hypoxemic respiratory failure and shock over a matter of hours to a few days [4].The accompanying Fig. 1 summarizes seven practical concepts that are particularly relevant for intensivists involved in the early recognition and management of this syndrome.The biological hallmark of HCPS is endothelial dysfunction with increased vascular permeability.Thrombocytopenia is an early and characteristic feature.The downstream consequences are capillary leak, non-hydrostatic pulmonary edema, hemoconcentration, relative intravascular hypovolemia, and progressive circulatory