tetano
Editor, Senior Moderator
Am J Clin Pathol. 2020 Apr 10. pii: aqaa062. doi: 10.1093/ajcp/aqaa062. [Epub ahead of print]
COVID-19 Autopsies, Oklahoma, USA.
Barton LM[SUP]1[/SUP], Duval EJ[SUP]1[/SUP], Stroberg E[SUP]1[/SUP], Ghosh S[SUP]2[/SUP], Mukhopadhyay S[SUP]2[/SUP].
Author information
Abstract
OBJECTIVES:
To report the methods and findings of two complete autopsies of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) positive individuals who died in Oklahoma (United States) in March 2020.
METHODS:
Complete postmortem examinations were performed according to standard procedures in a negative-pressure autopsy suite/isolation room using personal protective equipment, including N95 masks, eye protection, and gowns. The diagnosis of coronavirus disease 2019 (COVID-19) was confirmed by real-time reverse transcriptase polymerase chain reaction testing on postmortem swabs.
RESULTS:
A 77-year-old obese man with a history of hypertension, splenectomy, and 6 days of fever and chills died while being transported for medical care. He tested positive for SARS-CoV-2 on postmortem nasopharyngeal and lung parenchymal swabs. Autopsy revealed diffuse alveolar damage and chronic inflammation and edema in the bronchial mucosa. A 42-year-old obese man with a history of myotonic dystrophy developed abdominal pain followed by fever, shortness of breath, and cough. Postmortem nasopharyngeal swab was positive for SARS-CoV-2; lung parenchymal swabs were negative. Autopsy showed acute bronchopneumonia with evidence of aspiration. Neither autopsy revealed viral inclusions, mucus plugging in airways, eosinophils, or myocarditis.
CONCLUSIONS:
SARS-CoV-2 testing can be performed at autopsy. Autopsy findings such as diffuse alveolar damage and airway inflammation reflect true virus-related pathology; other findings represent superimposed or unrelated processes.
? American Society for Clinical Pathology, 2020. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.
KEYWORDS:
Acute lung injury; Autopsy; COVID-19; Coronavirus; Diffuse alveolar damage; Pulmonary pathology; SARS-CoV-2
PMID:32275742DOI:10.1093/ajcp/aqaa062
COVID-19 Autopsies, Oklahoma, USA.
Barton LM[SUP]1[/SUP], Duval EJ[SUP]1[/SUP], Stroberg E[SUP]1[/SUP], Ghosh S[SUP]2[/SUP], Mukhopadhyay S[SUP]2[/SUP].
Author information
Abstract
OBJECTIVES:
To report the methods and findings of two complete autopsies of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) positive individuals who died in Oklahoma (United States) in March 2020.
METHODS:
Complete postmortem examinations were performed according to standard procedures in a negative-pressure autopsy suite/isolation room using personal protective equipment, including N95 masks, eye protection, and gowns. The diagnosis of coronavirus disease 2019 (COVID-19) was confirmed by real-time reverse transcriptase polymerase chain reaction testing on postmortem swabs.
RESULTS:
A 77-year-old obese man with a history of hypertension, splenectomy, and 6 days of fever and chills died while being transported for medical care. He tested positive for SARS-CoV-2 on postmortem nasopharyngeal and lung parenchymal swabs. Autopsy revealed diffuse alveolar damage and chronic inflammation and edema in the bronchial mucosa. A 42-year-old obese man with a history of myotonic dystrophy developed abdominal pain followed by fever, shortness of breath, and cough. Postmortem nasopharyngeal swab was positive for SARS-CoV-2; lung parenchymal swabs were negative. Autopsy showed acute bronchopneumonia with evidence of aspiration. Neither autopsy revealed viral inclusions, mucus plugging in airways, eosinophils, or myocarditis.
CONCLUSIONS:
SARS-CoV-2 testing can be performed at autopsy. Autopsy findings such as diffuse alveolar damage and airway inflammation reflect true virus-related pathology; other findings represent superimposed or unrelated processes.
? American Society for Clinical Pathology, 2020. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.
KEYWORDS:
Acute lung injury; Autopsy; COVID-19; Coronavirus; Diffuse alveolar damage; Pulmonary pathology; SARS-CoV-2
PMID:32275742DOI:10.1093/ajcp/aqaa062