OBJECTIVE: To study the pathological characteristics of severe acute respiratory syndrome (SARS) and its relationship to clinical manifestation. METHODS: Tissue specimens from 3 autopsies of probable SARS cases were studied by microscope, and the clinical data was reviewed. RESULTS: The typical pathological changes of lungs were diffuse hemorrhaging on the surface. A combination of serous, fibrinous and hemorrhagic inflammation was seen in most of the pulmonary alveoli with the engorgement of capillaries and detection of micro-thrombosis in some of these capillaries. Pulmonary alveoli thickened with interstitial mononuclear inflammatory infiltrates, suffered diffuse alveolar damage, experienced desquamation of pneumocytes and had hyaline-membrane formation, fibrinoid materials, and erythrocytes in alveolar spaces. There were thromboembolisms in some bronchial arteries. Furthermore, hemorrhagic necrosis was also evident in lymph nodes and spleen with the attenuation of lymphocytes. Other atypical pathological changes, such as hydropic degeneration, fatty degeneration, interstitial cell proliferation and lesions having existed before hospitalization were observed in the liver, heart, kidney and pancreas. CONCLUSION: Severe damage to the pulmonary and immunological systems is responsible for the clinical features of SARS and may lead to the death of patients.
OBJECTIVE: To study the pathological characteristics of severe acute respiratory syndrome (SARS) and its relationship to clinical manifestation. METHODS: Tissue specimens from 3 autopsies of probable SARS cases were studied by microscope, and the clinical data was reviewed. RESULTS: The typical pathological changes of lungs were diffuse hemorrhaging on the surface. A combination of serous, fibrinous and hemorrhagic inflammation was seen in most of the pulmonary alveoli with the engorgement of capillaries and detection of micro-thrombosis in some of these capillaries. Pulmonary alveoli thickened with interstitial mononuclear inflammatory infiltrates, suffered diffuse alveolar damage, experienced desquamation of pneumocytes and had hyaline-membrane formation, fibrinoid materials, and erythrocytes in alveolar spaces. There were thromboembolisms in some bronchial arteries. Furthermore, hemorrhagic necrosis was also evident in lymph nodes and spleen with the attenuation of lymphocytes. Other atypical pathological changes, such as hydropic degeneration, fatty degeneration, interstitial cell proliferation and lesions having existed before hospitalization were observed in the liver, heart, kidney and pancreas. CONCLUSION: Severe damage to the pulmonary and immunological systems is responsible for the clinical features of SARS and may lead to the death of patients.
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