That woman is dying. Mount Sinai Hospital in New York is about to call her husband and tell him there is nothing he can try. Later Dr. Human Poole took a bet.
Faced with high-stress, high-risk decisions, doctors around the world are crazy, trying to find out how COVID-19 killed their patients so that they can try new methods to fight back.
An evolving theory is that in the most severely ill patients, there are very few blood clots blocking the lungs.
Poole couldn’t prove it. The required testing will further endanger his staff, who are already at risk of contracting the virus. But lung experts found some “surprising blood clots”. So Poole took out a medicine for stroke and held his breath.
“I said,” What are we actually losing? “Poole told The Associated Press. “It was then that I decided not only to use blood thinners for patients, but also to use clot scavengers for them.”
At least in some patients with COVID-19, what happened to the blood clot is a mystery.
Chinese doctors first issued an alarm. In March this year, Chinese cardiologists recommended that the American College of Cardiology pay attention to blood clots, and said that certain blood tests showed an increased risk of blood clots, which may prompt which patients are in the most dangerous state. Other reports indicate that blood clots will appear throughout the body. But will they cause deterioration or just influence?
Many hospitals are already trying prophylactic doses of blood thinners to prevent the formation of blood clots. There is a huge controversy about which drugs to try, what doses are safe-these drugs may cause dangerous bleeding-and when to start treatment.
In New York, Poole did a further study on a drug called tPA, which does not prevent blood clots—it breaks down blood clots.
In the absence of a vaccine or approval to treat coronavirus, many overwhelmed doctors are following clues to find out what to do next. This is an example.
After the 55-year-old patient received an extreme ventilation technique called “prone position”, even if the doctor turned her to her abdomen, she did not get enough oxygen. She was shocked, and other organs also quickly failed. Twenty minutes after the injection of tPA, her oxygen level rose. Poole was full of joy. But the good times are not long.
“Her condition improved, but then it started to deteriorate again,” Poole said. “We are probably breaking down the blood clot, but she is immediately forming a blood clot in the blood vessel.” Therefore, Poole next tried some novel methods to make this woman receive a low-dose tPA injection with blood thinner for about 24 Hours, hoping to block new blood clots while removing existing ones.
What disappointed Poole was that this experimental treatment would only allow her to live a few more days. On Friday, April 10, she suddenly died of a different complication. But on April 3 last weekend, Poole’s team tested this new anticoagulant method on four other critically ill patients. One of them did not survive and died of cardiac arrest because of a large blood clot in his heart.
The remaining patients had improved oxygen content and shock symptoms. As of Friday, April 10, there are still three people using the ventilator, but the situation has improved, especially one of them received treatment shortly after lung failure. In a new report, Poole called for an urgent study on whether abnormal blood coagulation will cause some people’s condition to deteriorate, although his hospital has updated treatment recommendations for the most severely ill patients.
Other people have the same idea. Experts from the University of Colorado and Harvard recently published a similar tPA research report and listed three other cases.
Dr. Steven Pugliese, a lung specialist at the University of Pennsylvania, said, “We are taking care of those patients who are about to leave us and we cannot take any diagnostic tests,” but still must Make treatment decisions.
Pulis called Poole’s tPA report “very attractive” and concluded: “These doctors are making a judgment about these dying patients who are about to die. This is the right thing.
However, due to the risk of bleeding, research must be conducted on carefully selected patients, especially when there is no good way to determine in advance who actually has these small blood clots, Price said.
For the first time, Poole noticed the strange thing that his intensive care unit (ICU) was packed with patients and they did not respond to the treatments expected by the doctor.
After acute respiratory distress syndrome (ARDS), they used a ventilator. This is an inflammatory form of lung failure that can cause the lungs to harden when caused by other infections.
At least early, Poole did not see this.
“For every patient, this is like” Groundhog Day “,” he said. Their oxygen and carbon dioxide levels are severely abnormal, but “surprisingly, their lungs are not stiff.”
Poole recalled that Italian doctors discovered the same situation and wrote in a journal of the American Thoracic Society that COVID-19 caused atypical acute respiratory distress syndrome (ARDS).
Back at Pripps Hospital, when a patient with a good respiratory system looks a little awake, the alarm will sound when the patient’s blood oxygen level drops immediately.
“The resident doctor will yell at me,” Poole recalled. “In acute respiratory distress syndrome, we think the typical cause is lung failure.” But the new coronavirus is not.
Poole often treats an emergency called pulmonary embolism. A large blood clot in the lung can quickly kill. The COVID-19 patient does not look very similar. Their heart pumps blood into the lungs effortlessly.
Then Poole remembered a rare disease when he was washing his clothes at 2am. Some people had abnormal pulmonary vasodilation, while others had blocked blood vessels. Poole believes that if this can explain the contradiction of blood clots in COVID-19 patients, it may be helpful.
“I did five series of cases. This does not prove anything,” Poole said. “Maybe this brings some possibilities, in which further research can explore what happened to the blood clot.”