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Severe Acute Respiratory Syndrome (SARS) Treatment & Management

  • Author: Faustine Ong, MD; Chief Editor: Michael R Pinsky, MD, CM, Dr(HC), FCCP, MCCM  more...
 
Updated: Jun 23, 2016
 

Approach Considerations

Currently, no definitive medication protocol specific to SARS has been developed, although various treatment regimens have been tried without proven success.[11, 12] The CDC recommends that patients suspected of or confirmed as having SARS receive the same treatment that would be administered if they had any serious, community-acquired pneumonia.

Isolate confirmed or suspected patients and provide aggressive treatment in a hospital setting. Mechanical ventilation and critical care treatment may be necessary during the illness.[11, 12] No benefit has been shown with prone ventilation.[57] An infectious disease specialist, a pulmonary specialist, and/or a critical care specialist should direct the medical care team. Communication with local and state health agencies, the CDC, and WHO is critical.

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Pharmacotherapy

Corticosteroids

Various steroid regimens have been used around the world as part of the initial SARS treatment cocktail. In the initial Hong Kong cohort of patients, corticosteroids were first given (with ribavirin) because of the similarity of the clinical and radiographic findings of SARS to those of bronchiolitis obliterans-organizing pneumonia. Despite anecdotal reports of success, the efficacy of steroids has not been confirmed in a clinical trial.[58, 59]

During phase 2 of the clinical course, intravenous (IV) administration of steroids has been shown to suppress cytokine-induced lung injury. It was also associated with favorable clinical improvement, with resolution of fever and lung opacities within 2 weeks.[59, 60]

However, a retrospective analysis showed an increased risk of 30-day mortality. Carefully designed studies will be needed to clarify the optimal role systemic steroids in the treatment SARS. Findings show that local pulmonary inflammation may be reduced with systemic glucocorticoid therapy.

Antiviral agents

The most widely used of these to date is ribavirin (usually in conjunction with steroids). Despite early anecdotal reports of patients with SARS improving with a combination of ribavirin and steroids, ribavirin does not have proven activity against Coronaviridae. It does have significant adverse effects, including hemolysis. It is unlikely that ribavirin is of any clinical benefit in SARS.

Protease inhibitors

Lopinavir/ritonavir was shown to have in vitro effects against the SARS-CoV. Some synergistic benefits with ribavirin were also demonstrated.[61, 62] However, the outcome of the subgroup that received lopinavir/ritonavir as rescue therapy after receiving pulsed methylprednisolone treatment for worsening respiratory symptoms was not better than that for the matched cohort.[63]

Interferon

Type 1 IFNs inhibit a wide range of RNA and DNA viruses, including SARS-CoV, and these effects have been demonstrated in vitro, as well as in some human and animal cell lines.[64] In experimentally infected cynomolgus macaques, prophylactic treatment with pegylated IFN-alfa significantly reduced viral replication and excretion, viral antigen expression by type 1 pneumocytes, and pulmonary damage.[65] However, the results of post exposure treatment with pegylated IFN-alfa were not as impressive.

In patients, use of IFN-alfacon1 plus corticosteroids was associated with improved oxygenation, more rapid resolution of radiographic lung opacities, and lower levels of creatine phosphokinase (CPK). These findings, although encouraging, need to be supported by further studies.[66]

Monoclonal antibodies

A high-affinity human monoclonal antibody (huMab) to the SARS-CoV S protein, known as 80 R, has potent neutralizing activity in vitro and in vivo. This antibody was shown to neutralize SARS-CoV and inhibit syncytia formation between cells expressing the S protein and those expressing the SARS-CoV receptor ACE2.[67] It reduced replication of SARS-CoV in the lungs of infected ferrets, decreased viral secretion, and prevented macroscopic lung pathology.[68] This may be a useful viral entry inhibitor for the emergency prophylaxis and treatment of SARS.

Intravenous immunoglobulin

Intravenous immunoglobulin (IVIG) was used in particular in Singapore during the SARS outbreak. However, its use was associated with a hypercoagulable state, and as many as one third of the patients who received IVIG were diagnosed with venous thromboembolism, including some cases of pulmonary embolism.

Pentaglobulin (immunoglobulin-M [IgM]-enriched immunoglobulin) was also used in a small study, with encouraging results, but its use was also complicated by embolic events.[69] The use of convalescent plasma was also attempted in some centers.[70]

Nitric oxide (NO)

Nitric oxide use was associated with improved oxygenation and weaning from ventilator support in a small study.[71]

Glycyrrhizin

In vitro replication of the virus was shown to be inhibited by glycyrrhizin. A study showed that the use of traditional Chinese medicine was more effective than Western medicine in reducing hypoxemia in patients with phase 1 SARS, although it was unclear what components of the traditional medicine contributed to this effect.[72]

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Vaccine

Chinese researchers began testing a SARS vaccine in humans in May 2004. The Chinese vaccine trial used an inactivated SARS virus vaccine developed through conventional vaccine technology.

The first US SARS vaccine trial began at the NIH in December 2004. The NIH vaccine is composed of a small, circular piece of deoxyribonucleic acid (DNA) that encodes the viral spike protein.

Vaccine containing recombinant surface Spike (S) protein of SARS-CoV nucleocapsid has been shown to induce high levels of SARS-neutralizing antibody in animal models.[73, 74] However, there was a concern about the safety of these vaccines. Several studies reported that SARS vaccine exacerbated lung eosinophilic immunopathology and paradoxically manifested as a severe disease upon subsequent exposure to SARS-CoV infection.[75, 76] To solve this problem, Honda-Okubo et al proposed a new vaccine design that used recombinant S protein with Delta inulin adjuvants. This design was shown to achieve long-lived immunity and prevented lung eosinophilic immunopathology upon SARS-CoV reexposure.[77]

Currently, SARS DNA vaccine encoding S glycoprotein has been investigated in a phase I clinical trial. Although it was shown to be well tolerated in that study, further studies need to be performed before an optimal yet safe vaccine can be implemented clinically.[78]

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Activity and Isolation

The CDC has issued guidelines governing the activity and isolation of patients with SARS, their immediate contacts, and the healthcare professionals who treat SARS.[3, 52]

Patients with SARS pose a risk of transmission to close household contacts and healthcare personnel.[79] In household or residential settings, infection control measures, as described below, are recommended.[80]

Patients with SARS should limit interactions outside the home and should not go to work, school, out-of-home child-care facilities, or other public areas until 10 days after the fever resolves, provided that respiratory symptoms are absent or improving. During this time, infection control precautions should be used to minimize the potential for transmission.

All members of a household of a patient with SARS should carefully follow recommendations for hand hygiene (eg, frequent hand washing, use of alcohol-based hand rubs), particularly after contact with body fluids (eg, respiratory secretions, urine, feces).

Disposable gloves should be used for any direct contact with the body fluids of a patient with SARS. However, gloves are not intended to replace proper hand hygiene. Immediately after activities involving contact with body fluids, gloves should be removed and discarded, and hands should be cleaned. Gloves must never be washed or reused.

Each patient with SARS should be advised to cover his or her mouth and nose with a facial tissue when coughing or sneezing. If possible, patients with SARS should wear surgical masks during close contact with uninfected persons in order to prevent the spread of infectious droplets. If a patient with SARS cannot wear a surgical mask, his or her household members should wear surgical masks when in close contact.

Sharing of eating utensils, towels, and bedding between patients with SARS and others should be avoided, although such items can be used by others after routine cleaning (eg, washing with soap and hot water). Environmental surfaces soiled by body fluids should be cleaned with a household disinfectant according to the manufacturer's instructions; gloves should be worn during this activity.

Household waste soiled with body fluids of patients with SARS, including facial tissues and surgical masks, may be discarded as normal waste.

Precautions by close patient contacts

Household members and other close contacts of patients with SARS should be actively monitored by local health departments.

Household members or other close contacts of patients with SARS should be vigilant for the development of fever or respiratory symptoms and, if these develop, should seek a healthcare evaluation. Prior to the evaluation, healthcare providers should be informed that the individual is a close contact of a patient with SARS so that necessary arrangements can be made to prevent transmission of the disease in the healthcare setting. Household members or other close contacts who have symptoms of SARS should follow the precautions recommended for patients with SARS.

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Contributor Information and Disclosures
Author

Faustine Ong, MD Resident Physician, Department of Internal Medicine, Einstein Medical Center

Faustine Ong, MD is a member of the following medical societies: American College of Physicians

Disclosure: Nothing to disclose.

Coauthor(s)

Sarah Perloff, DO, FACP Director, Antibiotic Stewardship Program, Associate Program Director, Internal Medicine Residency, Program Director, Infectious Diseases Fellowship, Einstein Medical Center

Sarah Perloff, DO, FACP is a member of the following medical societies: American College of Physicians, American Osteopathic Association, Infectious Diseases Society of America, HIV Medicine Association

Disclosure: Nothing to disclose.

Chief Editor

Michael R Pinsky, MD, CM, Dr(HC), FCCP, MCCM Professor of Critical Care Medicine, Bioengineering, Cardiovascular Disease, Clinical and Translational Science and Anesthesiology, Vice-Chair of Academic Affairs, Department of Critical Care Medicine, University of Pittsburgh Medical Center, University of Pittsburgh School of Medicine

Michael R Pinsky, MD, CM, Dr(HC), FCCP, MCCM is a member of the following medical societies: American College of Chest Physicians, Association of University Anesthetists, European Society of Intensive Care Medicine, American College of Critical Care Medicine, American Heart Association, American Thoracic Society, Shock Society, Society of Critical Care Medicine

Disclosure: Received income in an amount equal to or greater than $250 from: Masimo<br/>Received honoraria from LiDCO Ltd for consulting; Received intellectual property rights from iNTELOMED for board membership; Received honoraria from Edwards Lifesciences for consulting; Received honoraria from Masimo, Inc for board membership.

Additional Contributors

Prashant Malhotra, MBBS, FACP, FIDSA Assistant Professor of Medicine, Division of Infectious Diseases, Department of Medicine, LIJ School of Medicine at Hofstra University; Attending Physician, Division of Infectious Diseases, Department of Internal Medicine, North Shore-Long Island Jewish Health System

Prashant Malhotra, MBBS, FACP, FIDSA is a member of the following medical societies: American College of Physicians, Infectious Diseases Society of America, Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Manish N Trivedi, MD Fellow in Infectious Diseases, North Shore-Long Island Jewish Hospital

Disclosure: Nothing to disclose.

Acknowledgements

Burke A Cunha, MD Professor of Medicine, State University of New York School of Medicine at Stony Brook; Chief, Infectious Disease Division, Winthrop-University Hospital

Burke A Cunha, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, and Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Asim A Jani, MD, MPH, FACP Clinician-Educator and Epidemiologist, Consultant and Senior Physician, Florida Department of Health; Diplomate, Infectious Diseases, Internal Medicine and Preventive Medicine

Asim A Jani, MD, MPH, FACP is a member of the following medical societies: American Association of Public Health Physicians, American College of Physicians, American College of Preventive Medicine, American Medical Association, American Public Health Association, and Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Richard Oehler, MD Associate Professor, Department of Internal Medicine, Division of Infectious Diseases and International Medicine, University of South Florida College of Medicine; Director of Clinical Education, Division of Infectious Diseases, Tampa Veterans Affairs Medical Center

Richard Oehler, MD is a member of the following medical societies: American College of Physicians, American Medical Association, Infectious Diseases Society of America, and Society for Healthcare Epidemiology of America

Disclosure: Nothing to disclose.

Charles V Sanders, MD Edgar Hull Professor and Chairman, Department of Internal Medicine, Professor of Microbiology, Immunology and Parasitology, Louisiana State University School of Medicine at New Orleans; Medical Director, Medicine Hospital Center, Charity Hospital and Medical Center of Louisiana at New Orleans; Consulting Staff, Ochsner Medical Center

Charles V Sanders, MD is a member of the following medical societies: Alliance for the Prudent Use of Antibiotics, Alpha Omega Alpha, American Association for the Advancement of Science, American Association of University Professors, American Clinical and Climatological Association, American College of Physician Executives, American College of Physicians, American Federation for Medical Research, American Foundation for AIDS Research, American GeriatricsSociety, American Lung Association, American Medical Association, American Society for Microbiology, American Thoracic Society, American Venereal Disease Association, Association for Professionals in Infection Control and Epidemiology, Association of American Medical Colleges, Association of American Physicians, Association of Professors of Medicine, Infectious Disease Society for Obstetrics and Gynecology, Infectious Diseases Societyof America, Louisiana State Medical Society, Orleans Parish Medical Society, Royal Society of Medicine, Sigma Xi, Society of General Internal Medicine, Southeastern Clinical Club, Southern Medical Association, Southern Society for Clinical Investigation, and Southwestern Association of Clinical Microbiology

Disclosure: Nothing to disclose.

Sat Sharma, MD, FRCPC Professor and Head, Division of Pulmonary Medicine, Department of Internal Medicine, University of Manitoba; Site Director, Respiratory Medicine, St Boniface General Hospital

Sat Sharma, MD, FRCPC is a member of the following medical societies: American Academy of Sleep Medicine, American College of Chest Physicians, American College of Physicians-American Society of Internal Medicine, American Thoracic Society, Canadian Medical Association, Royal College of Physicians and Surgeons of Canada, Royal Society of Medicine, Society of Critical Care Medicine, and World Medical Association

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Reference Salary Employment

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Thin-section electron micrograph of the severe acute respiratory syndrome–associated coronavirus isolated in FRhK-4 cells. Courtesy of the Government Virus Unit, Department of Health, Hong Kong SAR, China.
World map of severe acute respiratory syndrome (SARS) distribution from the 2002-2003 outbreak infection. The greatest number of past and new cases of SARS are in mainland China, Hong Kong, Taiwan, and Singapore (red). Canada, more specifically Toronto, Ontario (yellow), is the fifth-ranked area, although community transmission of SARS now appears to be contained, according to the US Centers for Disease Control and Prevention. Green represents the other countries reporting SARS cases.
Pathologic slide of pulmonary tissue infected with severe acute respiratory syndrome–associated coronavirus. Diffuse alveolar damage is seen along with a multinucleated giant cell with no conspicuous viral inclusions. Courtesy of the US Centers for Disease Control and Prevention.
Severe acute respiratory syndrome case definition put forth by the US Centers for Disease Control and Prevention (CDC) on April 29, 2003. Courtesy of the CDC.
Clinical and laboratory criteria for severe acute respiratory syndrome cases and infection per the US Centers for Disease Control and Prevention (CDC) on April 29, 2003. Courtesy of the CDC.
Chest radiograph of a 52-year-old symptomatic woman with severe acute respiratory syndrome (March 20, 2003) taken 5 days after presentation. Moderately severe-to-severe ground-glass and consolidative bilateral changes are noted in the lung fields and are somewhat worse on the left side. Courtesy of Michael E. Katz, MD.
 
 
 
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