Close correlation between development of MODS during the initial 72 h of hospitalization and hospital mortality in severe fever with thrombocytopenia syndrome

Abstract

An emerging infectious disease was identified as severe fever with thrombocytopenia syndrome (SFTS) in central China since late March 2009. We found the patients with SFTS had severe clinical symptoms, and progressed rapidly to multiple organ dysfunction syndrome (MODS) with high fatality rate of 25%–30%. The aim of this study was to assess the significance of risk factors predicting the development of MODS and death in SFTS patients. Consecutive SFTS admissions between May 2009 and September 2011 were analyzed for parameters of organ function during hospitalization using Marshall scoring system for MODS, and platelet counts were recorded on admission and at 24, 48, 72 h and one week after admission. We investigated the kinetics of organ failures and analyzed the association between age, platelet count and development of MODS or death. A total of 92 SFTS patients were enrolled in this study. Among them, 32 patients with dysfunction of over 4 organs were identified, 45% of them died within 72 h, 72% died within 5 days, and 76% died within 7 days after admission. We also found cumulative Marshall score was significantly higher in death patients (11.76±2.05) than in survival patients (4.22±1.98) (P<0.001). In addition, SFTS patients had older age and lower platelet counts in MODS and death groups. Furthermore, we also observed that there was a close correlation between platelet count on admission and Marshall score (P<0.001). High Marshall score, advanced age and lower platelet counts were the main risk factors for the development of MODS, and those factors could predict mortality in SFTS patients, suggesting prompt treatment and close monitoring of severe complications, especially MODS, are of great importance in saving patients’ lives.

Keywords

severe fever with thrombocytopenia syndrome / Marshall score / multiple organ dysfunction syndrome / advanced age / lower platelet count

References

[1] FeldmannH.. Truly emerging—a new disease caused by a novel virus. N Engl J Med, 2011, 364(16): 1561-1563

[2] ZhangL., LiuY., NiD., et al.. Nosocomial transmission of human granulocytic anaplasmosis in China. JAMA, 2008, 300(19): 2263-2270

[3] DhandA., NadelmanR.B., Aguero-RosenfeldM., et al.. Human granulocytic anaplasmosis during pregnancy: case series and literature review. Clin J Infect Dis, 2007, 45(5): 589-593

[4] BakkenJ.S., KruethJ.K., LundT., et al.. Exposure to deer blood may be a cause of human granulocytic ehrlichiosis. Clin Infect Dis, 1996, 23: 198

[5] GaiZ., LiangM., ZhangS., et al.. Person-to-person transmission of severe fever with thrombocytopenia syndrome bunyavirus through blood contact. Clin Infect Dis, 2012, 54(2): 249-252

[6] DumlerJ.S., ChoiK.S., Garcia-GarciaJ.C., et al.. Human granulocytic anaplasmosis and anaplasma phagocytophilum. Emerg Infect Dis, 2005, 11(12): 1828-1834

[7] PetersC.J., SimpsonG.L., LevyH.. Spectrum of hantavirus infection: hemorrhagic fever with renal syndrome and hantavirus pulmonary syndrome. Annu Rev Med, 1999, 50: 531-545

[8] LevettP.N.. Leptospirosis. Clin Microbiol Rev, 2001, 14(2): 296-326

[9] YuX.J., LiangM.F., ZhangS.Y., et al.. Fever with thrombocytopenia associated with a novel bunyavirus in China. N Engl J Med, 2011, 364(16): 1523-1532

[10] ZhangY.Z., HeY.W., DaiY.A., et al.. Hemorrhagic fever caused by a novel bunyavirus in China: pathogenesis and correlates of fatal outcome. Clin Infect Dis, 2012, 54(4): 527-533

[11] MarshallJ.C., CookD.J., ChristouN.V., et al.. Multiple organ dysfunction score: a reliable descriptor of a complex clinical outcome. Crit Care Med, 1995, 23(10): 1638-1652

[12] PepinM., BouloyM., BirdB.H., et al.. Rift Valley fever virus (Bunyaviridae: Phlebovirus): an update on pathogenesis, molecular epidemiology, vectors, diagnostics and prevention. Vet Res, 2010, 41(6): 61

[13] ErgonulO.. Crimean-Congo haemorrhagic fever. Lancet Infect Dis, 2006, 6(4): 203-214

[14] VinhD.C., EmbilJ.M.. Hantavirus pulmonary syndrome: a concise clinical review. South Med J, 2009, 102(6): 620-625

[15] MackowE.R., GavrilovskayaI.N.. Hantavirus regulation of endothelial cell functions. Thromb Haemost, 2009, 102(6): 1030-1041

[16] GaiZ.T., ZhangY., LiangM.F., et al.. Clinical progress and risk factors for death in severe fever with thrombocytopenia syndrome patients. J Infect Dis, 2012, 206(7): 1095-1102

[17] SidwellR.W., SmeeD.F.. Viruses of the Bunya- and Togaviridae families: potential as bioterrorism agents and means of control. Antiviral Res, 2003, 57(1–2): 101-111

[18] MardaniM., JahromiM.K., NaieniK.H., et al.. The efficacy of oral ribavirin in the treatment of crimean-congo hemorrhagic fever in Iran. Clin Infect Dis, 2003, 36(12): 1613-1618

[19] HugginsJ.W., HsiangC.M., CosgriffT.M., et al.. Prospective, double-blind, concurrent, placebo-controlled clinical trial of intravenous ribavirin therapy of hemorrhagic fever with renal syndrome. J Infect Dis, 1991, 164(6): 1119-1127

[20] ZhangY.Z., ZhouD.J., XiongY.W., et al.. Hemorrhagic fever caused by a novel tick-borne Bunyavirus in Huaiyangshan, China. Chin J Epidemiol, 2011, 32(3): 209-220