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. 2020 Jun;33(6):1007-1014.
doi: 10.1038/s41379-020-0536-x. Epub 2020 Apr 14.

Pathological study of the 2019 novel coronavirus disease (COVID-19) through postmortem core biopsies

Sufang Tian  1 , Yong Xiong  2 , Huan Liu  1 , Li Niu  1 , Jianchun Guo  1 , Meiyan Liao  3 , Shu-Yuan Xiao  4   5
Affiliations

Pathological study of the 2019 novel coronavirus disease (COVID-19) through postmortem core biopsies

Sufang Tian et al. Mod Pathol. 2020 Jun.

Abstract

Data on pathologic changes of the 2019 novel coronavirus disease (COVID-19) are scarce. To gain knowledge about the pathology that may contribute to disease progression and fatality, we performed postmortem needle core biopsies of lung, liver, and heart in four patients who died of COVID-19 pneumonia. The patients' ages ranged from 59 to 81, including three males and one female. Each patient had at least one underlying disease, including immunocompromised status (chronic lymphocytic leukemia and renal transplantation) or other conditions (cirrhosis, hypertension, and diabetes). Time from disease onset to death ranged from 15 to 52 days. All patients had elevated white blood cell counts, with significant rise toward the end, and all had lymphocytopenia except for the patient with leukemia. Histologically, the main findings are in the lungs, including injury to the alveolar epithelial cells, hyaline membrane formation, and hyperplasia of type II pneumocytes, all components of diffuse alveolar damage. Consolidation by fibroblastic proliferation with extracellular matrix and fibrin forming clusters in airspaces is evident. In one patient, the consolidation consists of abundant intra-alveolar neutrophilic infiltration, consistent with superimposed bacterial bronchopneumonia. The liver exhibits mild lobular infiltration by small lymphocytes, and centrilobular sinusoidal dilation. Patchy necrosis is also seen. The heart shows only focal mild fibrosis and mild myocardial hypertrophy, changes likely related to the underlying conditions. In conclusion, the postmortem examinations show advanced diffuse alveolar damage, as well as superimposed bacterial pneumonia in some patients. Changes in the liver and heart are likely secondary or related to the underlying diseases.

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Figures

Fig. 1
Fig. 1
Timeline charts of CBC including WBC, neutrophil, and lymphocyte counts for four cases. The solid flat-line demarcates the lower normal limit of lymphocyte count (1.1 × 109/L). In Case 1 (a) the elevated lymphocyte count is consistent with her history of chronic lymphocytic leukemia (CLL). Marked lymphocytopenia is seen in Cases 2, 3, and 4 (b, c, d).
Fig. 2
Fig. 2
Radiographic images of chest CT scan and X-ray from the four patients. For each patient, the left and right images represent an earlier and latter time-point, respectively. Chest CT from Case 1 showed multiple patchy GGO in the bilateral upper lobes of the lungs and appeared more prominent in the right upper lobe (RUL) (A1). Repeat CT showed similar changes as A1 but with thickened fascicles of vasculatures and bronchi (A2). In Case 2, patchy GGO, consolidation, and air bronchogram can be seen in RUL; scattered GGO can be identified in the left upper lobe (LUL) (B1). Repeat CT showed additional consolidation in LUL (B2). In Case 3, X-ray showed patchy high-density shadows in both lungs, which were more prominent in the lower lobes (C1) and worsened during the couple of days before death (C2). In Case 4, diffuse GGO is seen in both lungs as well as consolidation in the posterior segment (D1), and additional air bronchogram can be detected in the later radiography (D2).
Fig. 3
Fig. 3
Histologic changes in the lungs. a Case 1: thick hyaline membrane mixed with desquamative pneumocytes and mononuclear inflammatory cells. b Case 2: more delicate hyaline membranes without evident inflammatory infiltration. c Case 3: focal hyaline membrane, type II pneumocyte hyperplasia, and mild interstitial thickening. d Case 4: alveolar spaces were filled with red blood cell exudation, and small fibrin plugs seen in adjacent alveoli. e Organization with intra-alveolar fibroblasts mixed with fibrin and inflammatory cellular infiltration. Diffuse type II pneumocyte hyperplasia in the background (inset: fibrinoid vascular necrosis, arrow heads). f Changes of bronchopneumonia with prominent neutrophilic infiltration filling up alveolar spaces.
Fig. 4
Fig. 4
Pathological findings in liver from all four cases. a Dense portal infiltration by atypical small lymphocytes (insert: CD20 immunostaining), and focal glycogenated nuclei in hepatocyte in Case 1. b Cirrhotic nodules with thick fibrosis in Case 2. c Mild sinusoidal dilatation with increased lymphocytic infiltration. d Higher power view showing sinusoidal lymphocytes. e Focal hepatic necrosis in periportal zone. f Focal centrilobular hepatic necrosis in Case 4.
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