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    Case Report: Lancet Respir Med 2020

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    1. A 50-year-old man was admitted to the hospital in Beijing with fever, cough, fatigue, and shortness of breath after traveling to Wuhan where the COVID-19 outbreak began. 2. Tests confirmed he had COVID-19 and he received antiviral and antibiotic treatment, but his condition deteriorated with progressive lung infiltrates seen on chest x-rays. 3. He died on the 14th day of illness and post-mortem biopsies found pathological changes in the lungs associated with acute respiratory distress syndrome caused by COVID-19.

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    Case Report: Lancet Respir Med 2020

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    mizraim
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    1. A 50-year-old man was admitted to the hospital in Beijing with fever, cough, fatigue, and shortness of breath after traveling to Wuhan where the COVID-19 outbreak began. 2. Tests confirmed he had COVID-19 and he received antiviral and antibiotic treatment, but his condition deteriorated with progressive lung infiltrates seen on chest x-rays. 3. He died on the 14th day of illness and post-mortem biopsies found pathological changes in the lungs associated with acute respiratory distress syndrome caused by COVID-19.

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    1. A 50-year-old man was admitted to the hospital in Beijing with fever, cough, fatigue, and shortness of breath after traveling to Wuhan where the COVID-19 outbreak began. 2. Tests confirmed he had COVID-19 and he received antiviral and antibiotic treatment, but his condition deteriorated with progressive lung infiltrates seen on chest x-rays. 3. He died on the 14th day of illness and post-mortem biopsies found pathological changes in the lungs associated with acute respiratory distress syndrome caused by COVID-19.

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    © All Rights Reserved
    Download as PDF, TXT or read online from Scribd
    Download as pdf or txt
    24 views3 pages

    Case Report: Lancet Respir Med 2020

    Uploaded by

    mizraim
    1. A 50-year-old man was admitted to the hospital in Beijing with fever, cough, fatigue, and shortness of breath after traveling to Wuhan where the COVID-19 outbreak began. 2. Tests confirmed he had COVID-19 and he received antiviral and antibiotic treatment, but his condition deteriorated with progressive lung infiltrates seen on chest x-rays. 3. He died on the 14th day of illness and post-mortem biopsies found pathological changes in the lungs associated with acute respiratory distress syndrome caused by COVID-19.

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    © All Rights Reserved
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    of 3

    Case Report

    Pathological findings of COVID-19 associated with acute


    respiratory distress syndrome
    Zhe Xu*, Lei Shi*, Yijin Wang*, Jiyuan Zhang, Lei Huang, Chao Zhang, Shuhong Liu, Peng Zhao, Hongxia Liu, Li Zhu, Yanhong Tai, Changqing Bai,
    Tingting Gao, Jinwen Song, Peng Xia, Jinghui Dong, Jingmin Zhao, Fu-Sheng Wang

    Lancet Respir Med 2020; Since late December, 2019, an outbreak of a novel A 50-year-old man was admitted to a fever clinic on
    8: 420–22 coronavirus disease (COVID-19; previously known as Jan 21, 2020, with symptoms of fever, chills, cough,
    Published Online 2019-nCoV)1,2 was reported in Wuhan, China,2 which fatigue and shortness of breath. He reported a travel
    February 17, 2020
    has subsequently affected 26 countries worldwide. In history to Wuhan Jan 8–12, and that he had initial
    https://doi.org/10.1016/
    S2213-2600(20)30076-X general, COVID-19 is an acute resolved disease but it can symptoms of mild chills and dry cough on Jan 14 (day 1
    This online publication has also be deadly, with a 2% case fatality rate. Severe disease of illness) but did not see a doctor and kept working
    been corrected. onset might result in death due to massive alveolar until Jan 21 (figure 1). Chest x-ray showed multiple
    The corrected version first damage and progressive respiratory failure.2,3 As of Feb 15, patchy shadows in both lungs (appendix p 2), and a
    appeared at thelancet.com/
    about 66  580 cases have been confirmed and over throat swab sample was taken. On Jan 22 (day 9 of
    respiratory on February 25,
    2020 1524 deaths. However, no pathology has been reported illness), the Beijing Centers for Disease Control (CDC)
    *Contributed equally
    due to barely accessible autopsy or biopsy.2,3 Here, we confirmed by reverse real-time PCR assay that the
    Treatment and Research Center
    investigated the pathological characteristics of a patient patient had COVID-19.
    for Infectious Diseases who died from severe infection with severe acute He was immediately admitted to the isolation ward and
    (Z Xu MD, L Shi MD, J Zhang PhD, respiratory syndrome coronavirus 2 (SARS-CoV-2) by received supplemental oxygen through a face mask. He
    L Huang MD, C Zhang PhD, postmortem biopsies. This study is in accordance with was given interferon alfa-2b (5 million units twice daily,
    P Zhao MSc, H Liu BSc,
    J Song PhD, P Xia MSc,
    regulations issued by the National Health Commission of atomisation inhalation) and lopinavir plus ritonavir
    Prof F-S Wang MD), Department China and the Helsinki Declaration. Our findings (500 mg twice daily, orally) as antiviral therapy, and
    of Pathology and Hepatology will facilitate understanding of the pathogenesis of moxifloxacin (0·4 g once daily, intravenously) to prevent
    (Y Wang PhD, S Liu MSc, COVID-19 and improve clinical strategies against secondary infection. Given the serious short­ ness of
    L Zhu MSc, Prof Y Tai MD,
    T Gao BSc, Prof J Zhao MD),
    the disease. breath and hypoxaemia, methylprednisolone (80 mg twice
    Department of Respiration
    (Prof C Bai MD), and
    Hospital
    Department of Radiology Symptoms
    (J Dong MD), The Fifth Medical Medications Travel in
    Wuhan Work Work Work Fever clinic Day 1 Day 2 Day 3 Day 4 Day 5 Day 6
    Center of PLA General Hospital,
    National Clinical Research Day of illness 1–6 7 8 9 10 11 12 13 14
    Center for Infectious Diseases,
    Beijing 100039, China Cough

    Correspondence to:
    Dr Fu-Sheng Wang, Treatment Chills
    and Research Center for
    Infectious Diseases, The Fifth Fever (°C) Subjective 39 37·4 36·4 37·1 37·2 36·4 36·6
    Medical Center of PLA General
    Hospital, National Clinical Fatigue
    Research Center for Infectious
    Diseases, Beijing 100039, China
    Shortness of breath
    [email protected]
    or
    Methylprednisolone
    Dr Jingmin Zhao, Department of
    Pathology and Hepatology,
    Moxifloxacin
    The Fifth Medical Center of PLA
    General Hospital, National
    Clinical Research Center for Lopinavir plus ritonavir tablets
    Infectious Diseases,
    Beijing 100039, China Interferon alfa-2b physicochemical inhalation
    [email protected]
    See Online for appendix Meropenem

    SARS-CoV-2
    Chest Chest Chest Death Post-
    RNA
    x-ray x-ray x-ray at 18:31 mortem
    positive
    biopsy
    Jan 8–12 Jan 13 Jan 14–19 Jan 20 Jan 21 Jan 22 Jan 23 Jan 24 Jan 25 Jan 26 Jan 27

    Figure 1: Timeline of disease course according to days from initial presentation of illness and days from hospital admission, from Jan 8–27, 2020
    SARS-CoV-2=severe acute respiratory syndrome coronavirus 2.

    420 www.thelancet.com/respiratory Vol 8 April 2020


    Case Report

    daily, intravenously) was administered to attenuate lung


    A B
    inflammation. Laboratory tests results are listed in the
    appendix (p 4). After receiving medication, his body
    temperature reduced from 39·0 to 36·4 °C. However, his
    cough, dyspnoea, and fatigue did not improve. On day 12
    of illness, after initial presentation, chest x-ray showed
    progressive infiltrate and diffuse gridding shadow in
    both lungs. He refused ventilator support in the intensive
    care unit repeatedly because he suffered from claustro­
    phobia; there­fore, he received high-flow nasal cannula
    (HFNC) oxygen therapy (60% concentration, flow rate C D
    40 L/min). On day 13 of illness, the patient’s symptoms
    had still not improved, but oxygen saturation remained
    above 95%. In the afternoon of day 14 of illness, his
    hypoxaemia and shortness of breath worsened. Despite
    receiving HFNC oxygen therapy (100% concentration,
    flow rate 40 L/min), oxygen saturation values decreased
    to 60%, and the patient had sudden cardiac arrest. He
    was immediately given invasive ventilation, chest com­
    pression, and adrenaline injection. Unfortunately, the Figure 2: Pathological manifestations of right (A) and left (B) lung tissue, liver tissue (C), and heart tissue (D)
    rescue was not successful, and he died at 18:31 (Beijing in a patient with severe pneumonia caused by SARS-CoV-2
    SARS-CoV-2=severe acute respiratory syndrome coronavirus 2.
    time).
    Biopsy samples were taken from lung, liver, and heart
    tissue of the patient. Histological examination showed (appendix p 3). Additionally, CD8 T cells were found to
    bilateral diffuse alveolar damage with cellular fibromyxoid harbour high concentrations of cytotoxic granules, in
    exudates (figure 2A, B). The right lung showed evident which 31·6% cells were perforin positive, 64·2% cells
    desquamation of pneumocytes and hyaline mem­brane were granulysin positive, and 30·5% cells were
    formation, indicating acute respiratory distress syndrome granulysin and perforin double-positive (appendix p 3).
    (ARDS; figure 2A). The left lung tissue displayed Our results imply that overactivation of T cells,
    pulmonary oedema with hyaline membrane formation, manifested by increase of Th17 and high cytotoxicity of
    suggestive of early-phase ARDS (figure 2B). Inter­stitial CD8 T cells, accounts for, in part, the severe immune
    mononuclear inflammatory infiltrates, dominated by injury in this patient.
    lymphocytes, were seen in both lungs. Multi­nucleated X-ray images showed rapid progression of pneumonia
    syncytial cells with atypical enlarged pneumocytes and some differences between the left and right lung. In
    character­ised by large nuclei, amphophilic granular cyto­ addition, the liver tissue showed moderate microvesicular
    plasm, and prominent nucleoli were identified in the intra- steatosis and mild lobular activity, but there was no
    alveolar spaces, showing viral cytopathic-like changes. No conclusive evidence to support SARS-CoV-2 infection
    obvious intranuclear or intracytoplasmic viral inclusions or drug-induced liver injury as the cause. There were
    were identified. no obvious histological changes seen in heart tissue,
    The pathological features of COVID-19 greatly suggesting that SARS-CoV-2 infection might not directly
    resemble those seen in SARS and Middle Eastern impair the heart.
    respiratory syndrome (MERS) coronavirus infection.4,5 In Although corticosteroid treatment is not routinely
    addition, the liver biopsy specimens of the patient with recommended to be used for SARS-CoV-2 pneumonia,1
    COVID-19 showed moderate microvesicular steatosis according to our pathological findings of pulmonary
    and mild lobular and portal activity (figure 2C), indicating oedema and hyaline membrane formation, timely and
    the injury could have been caused by either SARS-CoV-2 appropriate use of corticosteroids together with ventilator
    infection or drug-induced liver injury. There were a few support should be considered for the severe patients to
    interstitial mononuclear inflammatory infil­trates, but no prevent ARDS development.
    other substantial damage in the heart tissue (figure 2D). Lymphopenia is a common feature in the patients with
    Peripheral blood was prepared for flow cytometric COVID-19 and might be a critical factor associated with
    analysis. We found that the counts of peripheral CD4 disease severity and mortality.3
    and CD8 T cells were substantially reduced, while Our clinical and pathological findings in this severe
    their status was hyperactivated, as evidenced by the case of COVID-19 can not only help to identify a cause
    high proportions of HLA-DR (CD4 3·47%) and CD38 of death, but also provide new insights into the
    (CD8 39·4%) double-positive fractions (appendix p 3). pathogenesis of SARS-CoV-2-related pneumonia, which
    Moreover, there was an increased concentration of might help physicians to formulate a timely therapeutic
    highly proinflammatory CCR6+ Th17 in CD4 T cells strategy for similar severe patients and reduce mortality.

    www.thelancet.com/respiratory Vol 8 April 2020 421


    Case Report

    Contributors 2 Huang C, Wang Y, Li X, et al. Clinical features of patients infected


    F-SW and JZhao conceived the study. ZX and LS designed the study. with 2019 novel coronavirus in Wuhan, China. Lancet 2020;
    F-SW and JZhao supervised the overall study. ZX and LS collected 395: 497–506.
    specimens. LH, PZ, and HL collected clinical data. SL collected 3 Chan JF, Yuan S, Kok KH, et al. A familial cluster of pneumonia
    pathological images. LZ and TG disposed of tissues and H&E staining. associated with the 2019 novel coronavirus indicating person-to-
    LS and YW analysed and interpreted the data. YT analysed the person transmission: a study of a family cluster. Lancet 2020;
    pathological data. CB and JD formulated the treatment regimen and 395: 514–23.
    analysed the x-ray images. JZhang, JS, PX, and CZ did the flow 4 Ding Y, Wang H, Shen H, et al. The clinical pathology of severe
    cytometric analysis. LS and YW made the tables and figures. LS and YW acute respiratory syndrome (SARS): a report from China. J Pathol
    searched the literature. LS and YW wrote the manuscript. CZ, F-SW, 2003; 200: 282–89.
    and JZhao critically revised the manuscript. 5 Ng DL, Al Hosani F, Keating MK, et al. Clinicopathologic,
    immunohistochemical, and ultrastructural findings of a fatal case
    Declaration of interests of Middle East respiratory syndrome coronavirus infection in the
    We declare no competing interests. United Arab Emirates, April 2014. Am J Pathol 2016; 186: 652–58.
    References
    1 Wu F, Zhao S, Yu B, et al. A new coronavirus associated with
    human respiratory disease in China. Nature 2020; published online
    Feb 3. DOI:10.1038/s41586-020-2008-3.

    422 www.thelancet.com/respiratory Vol 8 April 2020

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