ABSTRACT
Objectives
To study the histopathology of patients dying of COVID-19 using post-mortem minimally invasive sampling techniques.
Methods
This was a single-center observational study conducted at JPNATC, AIIMS. Thirty-seven patients who died of COVID-19 were enrolled. Post-mortem percutaneous biopsies were taken from lung, heart, liver, kidney and stained with hematoxylin and eosin. Immunohistochemistry was performed using CD61 and CD163. SARS-CoV-2 virus was detected using IHC with primary antibodies.
Results
The mean age was 48.7 years and 59.5% were males. Lung histopathology showed diffuse alveolar damage in 78% patients. Associated bronchopneumonia was seen in 37.5% and scattered microthrombi in 21% patients. Immunopositivity for SARS-CoV-2 was observed in Type II pneumocytes. Acute tubular injury with epithelial vacuolization was seen in 46% of renal biopsies. Seventy-one percent of liver biopsies showed Kupffer cell hyperplasia and 27.5% showed submassive hepatic necrosis.
Conclusions
Predominant finding was diffuse alveolar damage with demonstration of SARS-CoV-2 protein in the acute phase. Microvascular thrombi were rarely identified in any organ. Substantial hepatocyte necrosis, Kupffer cell hypertrophy, microvesicular, and macrovesicular steatosis unrelated to microvascular thrombi suggested that liver might be a primary target of COVID-19.
Reviewer disclosures
Peer reviewers on this manuscript have no relevant financial or other relationships to disclose.
Article Highlights
Post-mortem minimally invasive tissue sampling (MITS) was performed in 37 patients who died with COVID-19.
Samples were obtained from lung, liver, kidney, heart and was stained with hematoxylin & eosin and SARS-CoV-2 viral antigens were detected using IHC.
Diffuse alveolar damage was seen in 78% of the lung specimens.
SARS-CoV-2 nucleoprotein was detected in Type 2 pneumocytes in the acute exudative phase.
Twenty-seven percent of the liver biopsies showed submassive hepatic necrosis and 72% showed Kupffer cell hyperplasia.
Forty-six percent of the kidney specimens showed evidence of acute tubular injury.
Changes of myocarditis were seen in only one sample.
Author contributions
A Ray, D Jain, R Guleria, N Wig, A Trikha contributed to conceptualization of the study. S Kumar, S Sahni, J Nehra, Nazneen, M BM, N Rastogi, S Mahato, C Gupta, S Bharadhan, G Dhital, P Goel, P Pandey, S KN, S Chaudhary, V C Keri, V S Chauhan, N Mahishi, A Shahi, R R, BK Gupta contributed to acquisition of samples and data collection. P Das, SK Arava, AR Mridha, A Nambirajan, G Singh, S Arulselvi, P Mathur contributed to interpretation of the histopathology samples. A Goel, S Agarwal, S Swaroop, R Aggarwal, KD Soni, N Nischal, M Soneja, S Lalwani, C Sarkar contributed to analysis of the data. A Ray, D Jain, A Goel, S Agarwal, P Das, SK Arava, G Singh contributed to drafting the initial manuscript.
All authors contributed to the final approval of the manuscript and have agreed to be accountable for the same.
Declaration of interest
The authors have no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.