WASHINGTON (AP) – The woman was dying. Mount Sinai Hospital in New York was about to call her husband and announce that there was nothing left to try. Then Dr. Hooman Poor took a bet.
With very stressful and high-stakes decisions, doctors around the world are frantically trying to figure out how COVID-19 is killing their patients so they can try new ways to fight back. A growing theory: in the sickest of the sick, small blood clots clog the lungs.
The poor couldn’t prove it. The required tests would endanger its staff, who were already at risk of contracting the virus. But the lung specialist saw evidence that “cries of blood clots.” Poor therefore withdrew a drug known to treat stroke and held his breath.
“I said, ‘What do we really have to lose? “” Poor told The Associated Press. “It was then that I decided to give not only an anticoagulant but also an anti-blood clot. “
Exactly what happens with blood clots in at least some COVID-19 patients is a mystery.
Chinese doctors were the first to sound the alarm. In March, Chinese heart specialists advised the American College of Cardiology to watch for clots and said certain blood tests showing an increased risk of a clot may indicate which patients were most at risk. Other reports suggest that clots may appear all over the body. But were they a cause of deterioration or an effect?
Many hospitals are already trying to administer blood thinners to prevent clots. There’s a huge debate over what type to try, the safe dose – drugs can cause dangerous bleeding – and when to start.
In New York, Poor went even further with a drug called tPA that doesn’t stop clots – it breaks them.
This is an example of how, without a vaccine or approved treatment for the coronavirus, many overwhelmed doctors are following clues to what to try next.
Poor’s 55-year-old patient didn’t get enough oxygen even after doctors rolled her over her stomach for an extreme ventilation technique called “lying down.” She was in shock. Other organs quickly failed.
Twenty minutes after injecting tPA, her oxygen levels increased. The poor man was delighted. But not for long.
“She’s getting better, but she’s starting to get worse,” he said. “Most likely, we are breaking the clot, but she is forming the clot again. “
He then tried something new, putting the woman on a low-dose tPA for about 24 hours on an anticoagulant, hoping to reduce existing clots while blocking new ones.
To Poor’s dismay, the experimental treatment only allowed the woman to live a few more days. A sudden and different complication killed her on Friday.
But last weekend, the Poor’s team tested the new clot approach in four other critically ill patients. One did not survive, dying from cardiac arrest due to a massive blood clot in his heart.
The rest saw improved oxygen levels and shock. As of Friday, three were still on ventilation but were doing better, particularly one who had been treated soon after a lung failure. In a new report, Poor called for an urgent study to find out whether the abnormal coagulation is causing at least some people to deteriorate, even though his own hospital has updated treatment advice for his sickest patients.
Others are on the same wavelength. Experts from the University of Colorado and Harvard recently released a similar research call for tPA and cited three other cases where he was tried while hospitals in Colorado and Massachusetts were preparing for a study.
“We are taking care of extremely sick patients who are dying before us, and we cannot get any diagnostic tests,” but have yet to make treatment decisions, said Dr. Steven Pugliese, a pulmonologist at the University of Pennsylvania.
Pugliese called Poor’s TPA report “very intriguing” and concluded, “What these doctors did for these very sick patients who died was judgment, and it was the right thing to do.”
But with the risk of bleeding, it should be studied in carefully selected patients, said Pugliese, especially with no way of knowing in advance who really has these tiny clots.
The poor man first noticed oddities as his intensive care unit was filled with patients who simply did not respond to care as doctors expected. They were on respirators after developing ARDS, acute respiratory distress syndrome. It is an inflammatory form of lung failure which, when caused by other infections, stiffens the lungs.
At least at first, Poor didn’t see this.
“It was like” Groundhog Day “with each patient,” he said, referring to the film where the same events are repeated day after day. They had severe abnormalities in oxygen and carbon dioxide levels, but “shockingly, their lungs weren’t stiff.”
He recalled Italian doctors who spotted the same thing and wrote in an American Thoracic Society journal that COVID-19 was the cause of an atypical ARDS.
Back at Poor’s Hospital, when ventilated patients appeared to be sufficiently improved to let them wake up a bit, alarms sounded as their blood oxygen levels immediately plummeted.
“The residents were shouting at me:” Such and such is desaturating! Remembers Poor. “Conventionally in ARDS, we think it’s because the lung is collapsing. But that was not the case.
Poor people often treat an emergency called pulmonary embolism, a large clot in the lungs that can kill quickly. COVID-19 patients did not really look like that. Their hearts also didn’t struggle to pump blood to the lungs.
Then, while doing laundry at 2 a.m., Poor remembered a rare condition in which some pulmonary blood vessels dilate abnormally while others are blocked. If that explains the contradictions of COVID-19, he thought, an anti-clot could help.
“I made a series of five cases. It doesn’t prove anything, ”he warned. “Perhaps that highlights possibilities where new research can deepen exactly what is going on.”
The Associated Press’s Department of Health and Science is supported by the Department of Science Education at the Howard Hughes Medical Institute. The AP is solely responsible for all content.