Noninvasive Ventilation in Patients with Severe Acute Respiratory Syndrome
Severe acute respiratory syndrome first emerged in Guangdong, China in November 2002 and then spread rapidly to many countries through Hong Kong in 2003 [1–4]. A 64-year-old physician from southern China, who had visited Hong Kong on February 21, 2003 and
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David S.C. Hui
Keywords
NIV • SARS • Emerging respiratory infections
13.1
Introduction
Severe acute respiratory syndrome first emerged in Guangdong, China in November 2002 and then spread rapidly to many countries through Hong Kong in 2003 [1–4]. A 64-year-old physician from southern China, who had visited Hong Kong on February 21, 2003 and died 10 days later of severe pneumonia, is believed to have been the source of infection causing subsequent outbreaks of severe acute respiratory syndrome (SARS) in Hong Kong, Vietnam, Singapore, and Canada [1–4]. By the end of the epidemic in July 2003, there had been 8,096 cases reported in 29 countries and regions, with a mortality incidence of 774 (9.6 %) [5]. Among the 8,096 cases, 1,706 were health care workers (HCWs). A novel coronavirus (CoV) was responsible for SARS [6]. Bats are likely the natural reservoirs of SARS-like CoV [7, 8]. The clinical course of SARS generally follows a typical pattern [9]. Phase 1 (viral replication) is associated with an increasing viral load during the first week of the illness and is clinically characterized by fever, myalgia, and other systemic symptoms that generally diminish after a few days. Phase 2 (immunopathological injury) is characterized by recurrence of fever, hypoxemia, and radiological progression of pneumonia with falls in viral load during the second week of illness. D.S.C. Hui, MD Department of Medicine & Therapeutics, The Chinese University of Hong Kong, Prince of Wales Hospital, 30-32 Ngan Shing St., Shatin, N.T., Hong Kong Stanley Ho Center for Emerging Infectious Diseases, The Chinese University of Hong Kong, Shatin, N.T., Hong Kong e-mail: [email protected] A.M. Esquinas (ed.), Noninvasive Ventilation in High-Risk Infections and Mass Casualty Events, 129 DOI 10.1007/978-3-7091-1496-4_13, © Springer-Verlag Wien 2014
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D.S.C. Hui
The high morbidity associated with SARS was highlighted by the observation that even when only 12 % of the total lung field is involved by consolidation on chest radiographs, 50 % of patients require supplemental oxygen to maintain satisfactory oxygenation above 90 % [10]. Peiris et al. [9] showed peaking of the nasopharyngeal viral load on day 10 of illness followed by a progressive decrease in rates of viral shedding from the nasopharynx, in stool, and in urine from day 10 to day 21 after symptom onset in 20 patients who had serial measurements with reverse transcription-polymerase chain reaction. Thus, clinical worsening of patients with SARS during phase 2 (second week of illness) is most likely the result of immunemediated lung injury due to an overexuberant host response rather than uncontrolled viral replication [9]. SARS spreads mainly by close person-to-person contact via droplet transmission or fomite [11]. During the global outbreak of SARS, about 20 % of patients progressed into acute respiratory distress syndrome (ARDS), necessitating invasive ventilatory support while reaching a very high viral load at the nasopharynx with the peak on day 10 of illness [9]. Thus, H
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