[Morphological study of severe acute respiratory syndrome (SARS)].
OBJECTIVE
Seven cases of autopsy from SARS patients are studied to investigate the pathogenesis and the pathologic changes of the major organs.


METHODS
Detailed gross and microscopic examination of the autopsy specimen is performed, including lung, heart, liver, kidney, spleen and lymph nodes.


RESULTS
All of the lungs are markedly enlarged and consolidated. Microscopically, pulmonary edema is a prominent finding, especially at the early stage of the disease (5 days after the onset). The alveolar spaces are filled with fibrinous exudates and lined with hyaline membrane. In 5 cases that undergo over 3 weeks of the course, the main pattern is organization of intra-alveolar deposit, along with fibroblastic proliferation in the alveolar septa, which leads to obliteration of alveolar space and pulmonary fibrosis. All of the lungs show bronchopneumonia, scattered hemorrhage, and proliferation of alveolar epithelial cells with desquamation. Microthrombi are seen in 6 cases. Fungal infection is noted in 2 cases. One of them is disseminative, involving bilateral lungs, heart, and kidney; the other one is diagnosed in hilar lymph nodes. In immune system, hilar and abdominal lymph nodes are usually congested and hemorrhagic, with depletion of lymphocytes, and accompanied with subcapsular sinus histiocytosis. One of the cases shows enlargement of abdominal lymph nodes, which have reduced number of germinal centers. Spleen exhibits atrophy of white pulps, and even lost of white pulps in some areas. The red pulp is markedly congested and hemorrhagic. In 5 cases, cardiomegale is prominent. Thrombosis (2 cases), focal myocarditis (1 case), and fungal myocarditis (1 case) are observed. In addition, liver shows massive necrosis (1 case) and nodular cirrhosis (1 case).


CONCLUSIONS
Lung is the major organ affected by SARS, demonstrated as diffuse alveolar damage. It is postulated that viral infection induces severe damage of alveolar epithelial and capillary endothelial cells, leads to pulmonary edema, intra-alveolar fibrin deposit, and hyaline membrane formation. Consequently, intra-alveolar organization and alveolar septal fibrosis causes loss of alveolar spaces, eventually, pulmonary fibrosis and atelectasis. The immune system is often affected, and presented as depletion of lymphoid tissue in lymph nodes and spleen. Secondary infection is a common complication, which should be paid close attention in the management of SARS patients.
Chen
Jie
J
Department of Pathology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100730, China. chenj@csc.pumch.ac.cn
Zhang
Hong-tu
HT
Xie
Yong-qiang
YQ
Wan
Jian-wei
JW
Lu
Zhao-hui
ZH
Wang
De-tian
DT
Wang
Qing-zhi
QZ
Xue
Xin-hua
XH
Si
Wen-xue
WX
Luo
Yu-feng
YF
Qiu
Hong-mei
HM
D000311:Adrenal Glands / Q000473:pathology; D000328:Adult; D001344:Autopsy; D001853:Bone Marrow / Q000473:pathology; D005260:Female; D006801:Humans; D007668:Kidney / Q000473:pathology; D008099:Liver / Q000473:pathology; D008168:Lung / Q000473:pathology; D008297:Male; D008875:Middle Aged; D009206:Myocardium / Q000473:pathology; D045169:Severe Acute Respiratory Syndrome / Q000473:pathology*; D013154:Spleen / Q000473:pathology