The worldwide outbreak of severe acute respiratory syndrome (SARS) has had its epicenter in Asia. Lee and colleagues from the Prince of Wales Hospital in Hong Kong described pooled data on clinical presentations and outcomes from their cluster of patients with SARS.
In early March, an outbreak of atypical, severe pneumonia was recognized, and a special multidisciplinary team was mobilized. Before the causative agent (a novel coronavirus) was identified, the team used the SARS case criteria established by the Centers for Disease Control and Prevention: temperature greater than 38°C (100.4°F), chest radiography with consolidation, and contact with a previously identified patient with SARS. The authors derived their information from a group of 138 infected persons, 50 percent of whom were health care workers secondarily infected by index patients with SARS.
Initial treatment included empiric antibiotics, followed by corticosteroids and ribavirin when fever persisted for more than 48 hours and patients had a low white blood cell or platelet count. Intravenous therapy was instituted if lung opacities worsened (ribavirin in a dosage of 1.2 g three times daily and methylprednisolone in a dosage of 500 mg two to three times daily). Patients were admitted to the intensive care unit (ICU) if respiratory failure ensued.
The incubation period between exposure and onset of fever ranged from two to 16 days (mean: six days). SARS appeared to be highly infectious, with 19 percent of cases occurring in tertiary exposures (i.e., no contact with an index patient, but rather contact with an infected health care worker with secondary exposure).
The most common presenting symptoms were fever, chills or rigors, myalgias, cough, headache, and dizziness. Chest radiography results were abnormal in about three fourths of patients at presentation, with most radiographs showing peripheral lung areas with patchy consolidation. Computed tomography of the chest was performed in many patients with suspected SARS and unremarkable plain chest radiography and often revealed peripheral “ground-glass” opacifications near the outer edges of the lungs. Progression to ICU admission occurred in 23.2 percent of patients about 6.5 days after initial hospitalization, on average. Mechanical ventilation was necessary in 13.8 percent of patients. Five patients (3.6 percent), all of whom had other major comorbidities (e.g., myelodysplasia, heart failure, alcoholic cirrhosis, or active hepatitis B infection), died.
|Variable||No ICU care||ICU care or death||Pvalue|
|Age (years)||36.1 14.6||50.2 18.4||.007|
|Male gender (%)||41.9||66.7||.01|
|Peakd-dimer (ng per mL)||951.0 1,197.9||1,686.9 2,132.3||.31|
|Platelets, 3 103 per mm3 (3 109 per L)||156.8 61.2 (156.8 61.2)||131.7 64.9 (131.7 64.9)||.06|
|Neutrophils per L (3 109 per L)||3.7 1.9||4.6 2.1||.02|
|Lymphocytes per L (3 109 per L)||0.9 0.7||0.8 0.5||.49|
|Activated partial thromboplastin time (seconds)||41.0 7.5||43.6 11.7||.23|
|Sodium, mEq per L (mmol per L)||136.1 2.7 (136.1 2.7)||134.0 4.6 (134.0 4.6)||.02|
|Urea, mg per dL (mmol per L)||10.64 3.08 (3.8 1.1)||20.45 26.89 (7.3 9.6)||.05|
|Creatinine, mg per dL (mol per L)||0.97 0.22 (86.1 19.4)||1.53 2.47 (135.5 218.0)||.21|
|Alanine transaminase, U per L||46.5 81.4 (46.5 81.4)||99.4 262.0 (99.4 262.0)||.27|
|Creatine kinase, U per L|
|On presentation||268.5 434.8 (268.5 434.8)||609.3 973.2 (609.3 973.2)||.06|
|Peak||352.7 544.0 (352.7 544.0)||697.4 971.1 (697.4 971.1)||.04|
|Lactate dehydrogenase, U per L|
|On presentation||287.7 143.3 (287.7 143.3)||558.0 258.0 (558.0 258.0)||<.001|
|Peak||310.0 153.8 (310.0 153.8)||629.7 283.5 (629.7 283.5)||<.001|
A number of clinical factors were associated with ICU admission or death (see accompanying table). The only factors that were independently predictive in multivariate analysis were advanced age, increased lactate dehydrogenase level, or elevated blood neutrophil count.