https://www.nytimes.com/2020/02/06/world/asia/coronavirus-china.html
The fatality rate in Wuhan is 4.1 percent and 2.8 percent in Hubei, compared to 0.17 percent elsewhere in mainland China.
see also my post #30 here:
http://www.freerepublic.com/focus/f-chat/3814339/posts?page=30#30
“First of all, new coronary pneumonia is not the same as SARS or avian influenza. In many cases, SARS is very severe when the patient comes up. However, the early onset of new crown patients is not very dangerous, but in the later period, there will be an acceleration, and the patient will soon enter a state of multiple organ failure, which will be a storm of inflammation. Once in this state, it is difficult for our treatment to pull it back. This is completely different from the past. Many patients do not die from the lungs. Because the hospital has ECMO (Extracorporeal Cardiopulmonary Support), a ventilator, and various treatment strategies, which can replace the patient’s lung function. But many patients die of multiple organ failure outside the lungs, which is very different from the past.
Why is there such a sudden acceleration?
Zhong Ming said that the patient’s body may have initiated an inflammatory storm, which caused the failure of various organs. What they observed is that many patients have elevated markers of myocardial damage, so the virus is likely to damage the heart muscle itself, similar to myocarditis, and may damage many other organs....
However, this disease has a characteristic that some patients may be relatively mild in the first two days, and suddenly worsen on the third day or later. If it is not treated in time, it may die. This may be related to patient infection and the resulting “inflammatory storm”.
“Inflammation storm” is that the patient’s infection activates the body’s immune cells, causing excessive damage to the immune cells. Normal immunity is protection, and excessive immunity is damage, which not only causes damage to the lungs, but also causes damage to the kidneys, liver, and heart muscle.
For example, after our body is infected, the body’s white blood cells and lymphocytes will start secreting a cytokine. The cytokine acts like a correspondent or herald, attracting these spare white blood cells and lymphocytes distributed in other parts of the muscle to the lesion site, killing the microbial virus and bacteria. In the middle, it will release an inflammatory mediator. Moderate release is normal. Excessive release will not only kill viruses and bacteria, but also cause damage to normal cells.
Zhou Zheng said that after the “inflammatory storm”, the patient’s condition tends to turn sharply, and soon he will have unconsciousness, rapid breathing, and then there will be decreased blood oxygen saturation, even coagulation dysfunction, oliguria and anuria, and elevated transaminase . Various organs fail, not just the lungs, which is the reason for the high mortality and mortality of many patients with new coronary pneumonia, especially the elderly.
...Zhou Zheng said that in a certain period of time, a small amount of hormones can be used to suppress this inflammatory response, but this varies from person to person..”
The reporters at the NYT have no idea how fatality rates are calculated. Those are not fatality rates. They are just confirmed dead divided by confirmed cases, which is a number that really only has relevance once the virus has stopped spreading (clearly not the case here).
The calculations of fatality rates are very complicated, when dealing with incomplete, inaccurate information. The best guestimates, though, have to at least take into account the median time between diagnosis and death (it takes far more than this to get anywhere useful, but it is at least a starting point). Then, you can take confirmed deaths and divide by the number of deaths “that many” days ago. It is by no means perfect, but at least gets you closer to an accurate, meaningful number. (And don’t forget that the time between diagnosis and death changes drastically from area to area, and over time).
As far as the discrepancy between the areas, it can be explained by a huge number of factors. In all likelihood, though, it is because the gap from confirmation to death is wildly different. For example, in an area like a foreign country where the virus hasn’t taken hold yet, people tend to get tested much earlier (no backlog of cases, many people caught by screening, no testing backlog, etc.), and also tend to live longer, even if they eventually die (access to more doctors, ICUs, equipment, etc.). These factors can dramatically effect the time from diagnosis to death (by quite a number of days), and this increased gap can cause a wildly different deaths/confirmed ratio, even if nothing else is different.
The fatality rate in Wuhan is 4.1 percent and 2.8 percent in Hubei, compared to 0.17 percent elsewhere in mainland China.
The DR that died was infected 3 weeks ago...so there will be a lag time from “new cases” to any deaths...but I’m sure that the areas outside Hubei are catching more of the overall cases including the mild cases too