They are in the apartments now
Did the last occupants leave the technological devices and other things they were given? Or does everything have to be new due to possible infection?
They are in the apartments now
I was wondering this also. I was also thinking of the toys given to the children, I was hoping they might be able to keep them.Did the last occupants leave the technological devices and other things they were given? Or does everything have to be new due to possible infection?
Liver: Collateral damage
When a zoonotic coronavirus spreads from the respiratory system, your liver is often one downstream organ that suffers. Doctors have seen indications of liver injury with SARS, MERS, and COVID-19—often mild, though more severe cases have led to severe liver damage and even liver failure. So what’s happening?
“Once a virus gets into your bloodstream, they can swim to any part of your body,” Lok says. “The liver is a very vascular organ so [a coronavirus] can very easily get into your liver.”
Your liver works pretty hard to make sure your body can function properly. Its main job is to process your blood after it leaves the stomach, filtering out the toxins and creating nutrients your body can use. It also makes the bile that helps your small intestine break down fats. Your liver also contains enzymes, which speed up chemical reactions in the body.
In a normal body, Lok explains, liver cells are constantly dying off and releasing enzymes into your bloodstream. This resourceful organ then quickly regenerates new cells and carries on with its day. Because of that regeneration process, the liver can withstand a lot of injury.
When you have abnormally high levels of enzymes in your blood, though—as has been a common characteristic of patients suffering from SARS and MERS—it’s a warning sign. It might be a mild injury that the liver will quickly bounce back from or it could be something more severe—even liver failure.
Lok says scientists don’t completely understand how these respiratory viruses behave in the liver. The virus might be directly infecting the liver, replicating and killing off the cells itself. Or those cells might be collateral damage as your body’s immune response to the virus sets off a severe inflammatory reaction in the liver.
Either way, she notes that liver failure was never the sole cause of death for SARS patients. “By the time the liver fails,” she says, “oftentimes you’ll find that the patient not only has lung problems and liver problems but they may also have kidney problems. By then it becomes a systemic infection.”
The pathological features of COVID-19 greatly resemble those seen in SARS and Middle Eastern respiratory syndrome (MERS) coronavirus infection.
In addition, the liver biopsy specimens of the patient with COVID-19 showed moderate microvascular steatosis and mild lobular and portal activity (figure 2C), indicating the injury could have been caused by either SARS-CoV-2 infection or drug-induced liver injury.
Regarding tylenol use discussed upthread, and liver involvement in the acute phase of disease-- elevated liver enzymes are one of the first indicators that the disease course will be severe. Most drugs (including ibuprofen) are metabolized by the liver, but acetominophen is a known "stressor" in regular or high doses.
ttps://www.thelancet.com/journals/lanres/article/PIIS2213-2600(20)30076-X/fulltext
This is a very interesting article.
The graphic clinical record is very helpful.
https://www.thelancet.com/journals/lanres/article/PIIS2213-2600(20)30076-X/fulltext#fig2
This 50 year old male died of cardio/respiratory failure 14 days after the onset of cough and only 7 days after the onset of fever (although he had self-reported chills during the time he had a cough).
He also refused to go on a ventilator when he developed AARDS. The clinicians had to resort to HighFlowNasal Canula 02 therapy, which is not at all as effective in ventilation and oxygenation as intubation and mechanical ventilation.
Ventilators in these cases are a response to the "work of breathing", more than "increasing oxygen diffusion at the cellular level". A ventilator alone can't fix or reverse what's going on at the cellular level in the alveoli in the disease process. The progression to respiratory failure and multi organ system dysfunction seems to happen pretty rapidly once the cytokine storm effects are clinically evident. (You can see these effects in Covid-19 patients in online pictures of vented patients with ventilator tubing full of secretions from the endotracheal tube all the way back to the ventilator machines.) It's likely he would not have survived even with ventilator care. Additionally, they tried steroids in his care, which I understand are agreed by most experts to be avoided in SARS type ARDS-- but I think it was all they had to try. He was already on the antiviral agents, among other meds for concomitant (opportunistic) bacterial pneumonia (the moxifloxacin).
For those with severe disease, who recover, most of them have a type of lung damage that is similar to emphysema. Sadly, if they are re-infected, the disease progression is often quite rapid and fatal.
Live chat now
Of note, his autopsy liver core samples show some inflammation, but at least in those samples, there is not apparent necrosis or cytolysis of hepatic tissue proper. The findings are pretty non-specific and don't imply fatal hepatocyte injury.
The lungs show hyaline membrane formation which is the hallmark of ARDS, along with the inflammation and edema, and the typical viral cytopathic effects. None of those features are at all specific for COVID-19 and this would be seen in many kinds of fatal viral pneumonias, including influenza, CMV, measles, etc.
(Hyaline membrane formation is also characteristic of Neonatal Respiratory Distress Syndrome seen in premature birth)
Biopsy samples from a 50-year-old Beijing man who died from his infection found that lung, liver, and heart tissue showed pathologic features similar to severe acute respiratory syndrome (SARS) and Middle East respiratory syndrome coronavirus (MERS-CoV) infection, a team from China reported today in The Lancet Respiratory Medicine. It wasn't clear if the changes in liver tissue were drug-induced or from the COVID-19 virus. Overactivation of T cells may have accounted for severe immune injury, the authors noted. And they didn't observe any obvious histologic changes in heart tissue.
Agree. Unfortunately, there are not a lot of post mortem exams being done (or results shared with world experts) on the largest cohort of patients who have died, in China. We are still in the "gaining info" phase of this pathogen. Most of the severe cases in China were not autopsied, nor specimens preserved, prior to cremation, from what is in the news.
China COVID-19 cases rise, as do worries over Diamond Princess risk
Yes, good point, but nasal cannula is just not going to be anywhere as efficient as a mechanical ventilator to present high levels of O2 to the alveoli.
And agree, they were aggressive in use of antivirals, antibiotics, and steroids, but the cytokine reaction storm is the difference between a simple bacterial pneumonia and this overwhelming and rapid respiratory failure.
Crazy? thought about how coronavirus might travel to Iran from China or anywhere- without direct person to person contact...
Could the virus droplets be rising into the atmosphere, "riding" in the smog, moving along and released?
Obviously complete speculation, imo.
Neat real-time pollution map..
AirVisual Earth - 3D Real-time Air pollution map
Watch air pollution flow across the planet in real time | Science | AAAS
''China’s air is notoriously toxic: Each year, it contributes to the premature deaths of some 1.6 million people. Concerned about how such pollution was affecting his family, Beijing-based data scientist Yann Boquillod founded AirVisual Earth, an online air pollution map that uses data from satellites and more than 8000 monitoring stations to display global air pollution in real time. The AirVisual Earth interactive maps prevailing wind patterns and shows color-coded concentrations of PM2.5—airborne particulate matter less than 2.5 microns in diameter that can penetrate deep into the lungs. Users can zoom in, tilt, and spin the globe for better viewing''
rbbm
I see the use of postmortem "biopsies" being used in a more widespread fashion to avoid the risk of a full open autopsy. Presumable pre-morbid CT or other imaging has defined the organs most affected, and systems that don't need extensive examination. Very simple to get large core samples of most all organs.
I was wondering this also. I was also thinking of the toys given to the children, I was hoping they might be able to keep them.