Coronavirus (COVID-19) Autopsy Report is analyzed in this video by Dr. Mike Hansen.
Coronavirus or more appropriately its new name SARS-CoV-2 is the virus responsible for the Covid-19 outbreak. Wuhan, China has been the epicenter of this epidemic, but some experts, like Dr. Anthony Fauci, are now saying that we are on the verge of a pandemic.
Before I get to the autopsy results of a patient with Covid-19, its important to understand the context of the numbers of total people infected, total people with coronavirus pneumonia, number of people who developed ARDS, and the total number of deaths. When looking at the numbers, we should realize that they are almost certainly being underreported in China, and there are multiple reasons for that, which I won’t get into right now.
Although these are not concrete numbers, its what we have to go by at this point. The percentage of people. Also, up to this point, there has not been any pathology reported on this disease because of limited access to autopsy and biopsy results.
But finally, we now have a new case report study in Lancet Respir Med, published Feb 17, that has autopsy results for a patient who died from Covid-19.
Pathological findings of COVID-19 associated with acute respiratory distress syndrome The patient is a 50-year-old man from China, who visited Wuhan Jan 8–12.
On Jan 14, he developed a dry cough and some mild chills, so this is day 1 of illness). However, he did not initially seek medical attention and kept working until Jan 21.
He then went to a medical clinic on Jan 21, because by that time, he had developed worsening symptoms. He had fever, chills, fatigue, cough, and shortness of breath.
On Jan 22 (day 9 of illness), the Beijing Centers for Disease Control (CDC) confirmed by reverse real-time PCR assay that the patient had COVID-19. He was immediately admitted to the isolation ward and received supplemental oxygen through a face mask.
He was given several different medications, which included the inhaled version of interferon alfa-2b, lopinavir plus ritonavir as antiviral therapy, and Moxifloxacin, to prevent secondary bacterial infection. He was also given a steroid, methylprednisolone, to attenuate lung inflammation.
On day 12 of illness, after the initial presentation, his symptoms did not improve, other than his fever, which he received medication for. His chest x-ray on day 12 showed progressive bilateral infiltrates. He repeatedly refused ventilator support in the intensive care unit repeatedly, apparently because he suffered from claustrophobia.
His oxygen saturation values decreased to 60%, and the patient had a cardiac arrest. At that point he was intubated with mechanical ventilation, he had chest compressions and epinephrine. Unfortunately, they are unable to revive him.
An autopsy is done, and biopsy samples were taken from the lung, liver, and heart. The heart tissue was essentially normal. The liver biopsy of this patient showed moderate microvascular steatosis and mild lobular and portal activity, indicating the injury could have been caused by either SARS-CoV-2 infection or as a result drug-induced liver injury.
Histological examination of lung tissue showed diffuse alveolar damage with cellular fibromyxoid exudates, along with the desquamation of pneumocytes and hyaline membrane formation.
These findings are consistent with acute respiratory distress syndrome. Interstitial mononuclear inflammatory infiltrates, dominated by lymphocytes, were seen in both lungs.
There were multinucleated syncytial cells with atypical large alveoli characterized with prominent nucleoli, consistent with viral cytopathic-like changes.
These pathological features of COVID-19 greatly resemble those seen in SARS and Middle Eastern respiratory syndrome (MERS) coronavirus infection.