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Infection control
Mechanical ventilation
Specimens for RT-PCR
Steroids in SARS

Severe acute respiratory syndrome (SARS)

Charles Gomersall and Gavin Joynt

Note that due to the  recent emergence of this condition much of the information given on this page is based on, as yet, unpublished data collected in Hong Kong.

This page is updated regularly. Last update January 13th 2004.

A lecture on the ICU management of SARS is available for download.

Epidemiology

  • In 2003 large outbreaks of SARS occurred in
    • Mainland China
    • Hong Kong
      • large proportion of those infected are health care workers and medical students
    • Singapore
    • Hanoi
    • Taiwan
    • Toronto
  • In 2004
    • four confirmed cases of SARS, unrelated to laboratory exposure, have been diagnosed in Guangzhou, China

Updated information on epidemiology

Aetiology

  • infection with SARS coronavirus (SARS-CoV)

Infection control

  • respiratory droplet
  • possibly airborne
  • faecal droplets
  • SARS CoV may be able to survive on inert surfaces for days at 20ºC but fomite spread is probably not a major route of spread
  • early data suggests that the illness is highly, although selectively contagious:
    • evidence of transmission of the disease between patients without very close contact (eg guests in the same hotel)
    • absence of transmission between family members with very close contact (eg husband and wife sharing a bed)
    • reasons for selectivity are unclear
    • appear to be super-spreading events where certain patients and certain times infect a large number of events. Also occurs in other diseases
  • infection with SARS CoV is not invariably associated with severe respiratory disease but asymptomatic infection probably does not occur or is rare. Similarly transmission from patients with mild illness is unusual.
  • patients thought to remain infectious for up to 10 days after resolution of fever (but little data

Nosocomial infection

  • transmission to healthcare workers, other patients and visitors documented
  • increased risk with increased proximity to the patient
  • evidence of temporal association between use of nebulizer and infection of medical students taking clinical examination in close proximity to index case

Infection control measures in PWH ICU

Click here for details

Clinical features

Suspect SARS in patients with a history of contact with SARS patient or travel to Far East

Incubation period

  • mean 6 days
  • range 2-16 days

Prodrome/early phase

  • viral replication is probably most active during this phase
  • fever (>38°C), which is often high
    • may be absent, particularly in the elderly
    • ~10% of patients are afebrile throughout their illness
  • chills and rigors common
  • headache, malaise, or myalgia frequent
  • ± mild respiratory symptoms
  • ± nausea, vomiting and diarrhoea
  • rash, neurologic findings usually absent

Later/Lower respiratory phase

  • usually occurs in second week of illness and may be due to immunological response to infection

  • clinical and radiological changes consistent with bronchiolities obliterans organizing pneumonia (BOOP) with acute lung injury/ARDS

  • dry, non-productive cough

  • dyspnoea

  • ± hypoxemia

  • ± inspiratory crackles. Wheezing is not a feature of the syndrome. Auscultation of chest often normal.

  • 20-25% require ICU admission, usually with single organ failure (respiratory)

  • ~90% of those admitted to ICU develop ARDS and ~50% require intubation and ventilation

    • Approx. 25-35% of ventilated patients develop pneumomediastinum or pneumothorax despite use of low tidal volumes and low inspiratory pressures

  • some patients respond to prone ventilation

  • other organ failure, apart from mild cardiovascular failure, is unusual but gastrointestinal and haematological manifestations are common.

    • bleeding tendency in some, thrombosis in others

    • 38-73% of patients have diarrhoea at some time in disease

      • large volume

      • watery

      • no blood

      • no mucus

      • usually early feature

      • SARS-CoV found in stool of very high proportion of patients

  • does not cause a marked clinically detectable inflammatory response

Investigations

  • CXR (Click here for examples of Radiological Imaging)

    • features non-specific

    • ± normal in up to 20% at presentation. CT thorax more sensitive

    • respiratory phase is characterized by focal infiltrates progressing to more generalized, patchy, interstitial infiltrates. Peripheral zone involvement predominant.

    • ± areas of consolidation in late stages

    • pleural effusions, cavitation and hilar lymphadenopathy do not appear to be features of the syndrome

  • CT thorax

    • non-specific

    • ill defined peripheral ground glass opacities, usually in a subpleural location. Similar in appearance to those of BOOP

    • traction bronchiectasis

    • thickened interlobular septa

    • no obvious bronchial dilatation

  • Full blood count

    • absolute lymphocytopaenia common (~70%).Due to reduction in T cells. B cell counts appear to be normal.

    • total WCC normal or decreased

    • thrombocytopenia or low-normal platelet counts (50,000 – 150,000 / μl)

    • significant coagulopathy does not appear to be a feature except in patients with bacterial superinfection

    • D-dimer often raised

  • Biochemistry

    • ± raised creatine phosphokinase levels (up to 3000 IU / L)

    • ± hepatic transaminases (2-6 x upper limit of normal)

    • raised LDH common

    • hyponatraemia and hypokalaemia both occur in about 20-25%

  • Reverse transcription-polymerase chain reaction (RT-PCR)

    • Conventional

      • low sensitivity in first few days of illness. Improves after day 6. Overall ~64% sensitivity

      • Overall specificity 76.7-100%

    • Real-time

      • nasopharyngeal aspirates - 80% sensitivity in first 3 days of illness

      • stool - sensitivity lower

      • serum - 78-87% at day 2-3. Sensitivity falls after day 7.

      • specificity unclear

    • Specimens

  • Serology

    • paired samples on day 7 and day 21 of illness ~90% sensitivity

    • seroconversion can only be detected around day 10 of illness and is common by the 3rd week. May be later in patients treated with steroids

The diagnosis is less likely if there is no history of exposure and the patient has one of the following:

  • leucocytosis on admission
  • lobar consolidation on CXR
  • a known pathogen

Treatment

  • Broad spectrum antibiotics to cover usual causes of severe community acquired pneumonia
  • Corticosteroids appear to control fever in 1-2 days and improve general well being. There is no controlled data demonstrating a beneficial effect of steroids. Use is controversial.
    • hydrocortisone 2 mg/kg 6 hourly IV or 4 mg/kg 8 hourly IV. Tail off over 1 week when there is clear clinical improvement
    • severe cases: methylprednisolone 10 mg/kg daily IV for 2 days followed by hydrocortisone as above
      • give repeated doses of methylprednisolone 10 mg/kg  or 20 mg/kg daily if fever or CXR changes persist in the absence of obvious secondary bacterial infection. Up to a maximum of approximately 5g total dose
    • probably should not be used in early phase when active viral replication is taking place
    • significant long term adverse effects eg avascular necrosis of femoral head
  • Ribavirin has been routinely used in Hong Kong but not recommended for use by by Health Canada.
    • dose: 8 mg/kg 8 hourly IV for 7-10 days followed by 4mg/kg PO/NG for another 11-14 days
    • adverse effects include:
      • haemolytic anaemia. High incidence in Canadian series but higher doses used
      • bone marrow suppression
    • contraindicated in pregnancy
    • in vitro tests on SARS Co-V suggest that the concentrations required to inhibit reproduction of the virus are unlikely to be achieved in vivo
    • preliminary data suggest combination with Kaletra may result in better outcome
  • Fluids. Avoid fluid overload and aim for low cardiac filling pressures.
  • Low pressure low volume ventilation with permissive hypercapnia using algorithms based on the ARDSnet study. Pneumomediastinum (both spontaneous and associated with ventilation) and pneumothoraces are common

Prognosis

Worse outcome appears to be associated with:

  • increasing age
  • initial high LDH
  • high absolute neutrophil count on presentation
  • male sex
  • hypoxia

ICU mortality ~25-50%

There are insufficient data to reliably identify prognostic factors in critically ill patients with SARS but on univariate analysis advanced age, more severe illness, shorter delay between symptom onset and ICU admission, chronic disease or immunosuppression, lower steroid dose, higher lymphocyte count, nosocomial sepsis and positive fluid balance were associated with poor outcome (click here for details).

Lung function tests 3 months after presentation are suggestive of a restrictive lung defect but in most the gas transfer factor is normal and in some cases the changes are explicable on the basis of respiratory muscle weakness.

Acknowledgement

We would like to thank all the staff of the Prince of Wales Hospital ICU for their courage and commitment to patient care, particularly in the early stages of the outbreak when little was known about this disease other than that it was highly contagious and could cause severe life-threatening illness.

Further reading

World Health Organization. Severe acute respiratory syndrome

CDC SARS website

N. Lee et al. A major outbreak of Severe Acute Respiratory Syndrome in Hong Kong

K.W. Tsang et al. A Cluster of Cases of Severe Acute Respiratory Syndrome in Hong Kong 

S.M. Poutanen et al. Identification of Severe Acute Respiratory Syndrome in Canada

J.M. Drazen. Case Clusters of the Severe Acute Respiratory Syndrome

T.G. Ksiazek et al. A novel coronavirus associated with Severe Acute Respiratory Syndrome

C. Drosten et al. Identification of a novel coronavirus in patients with Severe Acute Respiratory Syndrome

Beijing Medical University SARS website

Mount Sinai Hospital, Toronto website

R. A. Fowler, et al. Critically ill patients with severe acute respiratory syndrome. JAMA 290 (3):367-373, 2003.

T. W. K. Lew, et al. Acute respiratory distress syndrome in critically ill patients with severe acute respiratory syndrome. JAMA 290 (3):374-380, 2003.

C.D. Gomersall, et al. Short term outcome of critically ill patients with severe acute respiratory syndrome. 


© Gavin Joynt & Charles Gomersall March, 2003; April, 2003; May 2003; June 2003; July 2003; September 2003; January 2004


©Charles Gomersall, April, 2014 unless otherwise stated. The author, editor and The Chinese University of Hong Kong take no responsibility for any adverse event resulting from the use of this webpage.
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