Background

Severe acute respiratory syndrome (SARS) is a newly emerged disease and the epidemic in Hong Kong came as a crisis. The clinical course of SARS appears to follow a triphasic pattern: phase I is clinically characterized by fever, myalgia and other systemic symptoms that generally improve after a few days. This is the phase when active viral replication occurs. Phase II is characterized by recurrence of fever, oxygen desaturation and radiological progression of pneumonia. The clinical progression during phase II appears to be related to immuno-pathological damage. The majority of patients recovered spontaneously but in some the disease progressed into phase III, characterized by acute respiratory distress syndrome (ARDS) necessitating ventilatory support (Figure 9.1). Reports show that with the development of respiratory failure and ARDS, 15–30% of patients will require intensive care admission.

Histological examination shows the presence of coronavirus particles in the alveoli of the infected lungs. Histopathology of post-mortem cases also reveal diffuse alveolar damage, pulmonary oedema, hyaline membrane formation and highly activated macrophages with haemophagocytosis. Thus, the treatment modalities should include antivirals, immuno-modulators and respiratory support at the different stages of the diseases.