Editorial: SARS: Facts and considerations for the orthopaedic community

Journal of Orthopaedic Surgery, Jun 2003 by Fang, David

Hong Kong is known as HKSAR (special administrative region) of China. It is ironic that the atypical pneumonia emanating from, or at least made notorious by Hong Kong, is named the SAR (severe acute respiratory) syndrome.

The outbreak began in November 2002 in the Southern Chinese city of Foshan, where a family of 4 contracted a new and serious atypical pneumonia. By February 2003 clusters of infected patients had been identified in Guangzhou. It was still relatively well contained then, until a professor of nephrology came from there and spread the disease to 12 others at the Hong Kong Metropole Hotel. He later developed the full-blown SARS and died at the Kwong Wah Hospital despite intensive resuscitation. The 12 took the disease to Vietnam, Canada, Singapore, Ireland and US, and various hospitals in Hong Kong. Among these was the Prince of Wales Hospital (PWH), where a nebuliser that was used on an infected patient contaminated the whole ward. 18 staff attending the ward, and 16 medical students who visited the patient came down with SARS. A visitor at the ward caused a massive outbreak at a housing estate, the Amoy Garden. He had diarrhoea, and there was a leak in the sewage pipes. In addition, the drains installed beneath bathroom floors were emitting gas from the sewage pipes, because water could not be retained in the U-traps. This gas was sucked up from the pipes by powerful exhaust fans which residents had installed in their bathrooms. Massive infection ensued. Daily updates of the pandemic are available from the WHO website (http://www.who.int/csr/sars/en/).

Symptoms of SARS1,2 include a body temperature of more than 38[degrees] C (observed in 99-100% of cases), chills and rigors (73%), myalgia (49-61%), cough (51-69%), sputum production (29%), dyspnoea (42%), headache (56%), dizziness (43%), and diarrhoea (20%). Blood tests show leukopenia (34%), lymphopenia (70%), thrombocytopenia (45%), prolonged activated partial thromboplastin time (43%), and elevated creatine phosphokinase (CPK; 32%), lactic dehydrogenase (LDH; 71-87%), and hyponatraemia (20%).

The incubation period from initial contact with the virus now appears to be no more than 10 days. There are 3 clinical phases, each lasting roughly a week. In the first week, infected individuals are still relatively well but febrile. The virus replicates rapidly during this phase and peaks at 7-10 days. Fever may diminish in the second week. This is the immune reaction phase. If the immune system is overcome, lung parenchymal damage occurs in the third week and heralds acute respiratory distress. Post-mortem studies have shown a range of lung pathology suggesting a role for cytokine-invoked tissue destruction.3

The chest X-ray may be normal or show a single area of consolidation in a lower peripheral zone. By the end of the first week lesions increase. Still, 54% of lesions remain unifocal, while a third become multiple and bilateral. High-resolution computer tomography of the lungs has given the best correlation with lung infection where plain radiographs are negative or doubtful.

A novel coronavirus was first identified by cell culture by K Y Yuen and his team in Hong Kong and reported by Peiris et al.4 in Lancet. Soon afterwards, Ksiazek et al.5 in Atlanta, US, and then Drosten et al.6 from Hamburg, Germany reported the same. It is now widely believed that the novel coronavirus (SARS-CoV) is the causative agent of SARS. Specific laboratory tests depend on isolating the causative virus from specimens of blood, respiratory secretions, stool, urine, and tissue biopsies. Cell culture is technically demanding, but a polymerase chain reaction (PCR) test for genetic material of the SARS-CoV is available from WHO collaboration laboratories. The currently available PCR has a high specificity but low sensitivity (a negative result gives poor value for excluding SARS). Antibody tests, on the other hand, by either enzyme linked immunosorbent assay (ELISA) or immunofluorescent assay (IFA) can detect if a patient has been or is recently infected by the virus. A repeatedly negative result excludes infection.

Treatment remains controversial. One regimen gives broad spectrum antibiotic and antiviral coverage early on. Antiviral agents used include ribavirin and Kaletra (combination of lopinavir and ritonavir). Convalescent serum should logically work best during the initial viral replication phase, but has also been used effectively in late unresponsive cases.1 The use of steroids is based on the finding of cytokine-mediated tissue damage. High-dose pulsed steroids are reserved for cases that progress to lung damage. Respiratory support is necessary for hypoxaemia, but cases that require intubation and mechanical ventilation carry an increased fatality rate.

Mortality from SARS, originally thought to mimic that of most community-acquired pneumonia is around 5%, has been steadily climbing. While the final mortality rate remains to be seen, at the time of writing 623 fatalities have been reported out of 7761 cases worldwide (8%).7 In Hong Kong 243 of 1710 patients have died, whereas 1191 have been discharged from hospital. Singapore reported 28 deaths from 205 cases and 157 recoveries. The respective figures are 35, 274, 46 for Taiwan; 23, 140, 106 for Canada; 5, 63, 58 for Vietnam, and 282, 5209, and 2009 for mainland China.7