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Doctors Puzzle Over COVID-19 Lung Problems

April 7, 2020 — As doctors treat more patients who are severely ill from COVID-19, they’re noticing differences in how their lungs are damaged.

Some patients coming to the hospital have very low oxygen levels in their blood, but you wouldn’t necessarily know it from talking to them. They don’t seem starved of oxygen. They may be a little confused. But they aren’t struggling to breathe.

When doctors take pictures of their lungs — either with a CT scanner or an X-ray machine — those also look fairly healthy. The lungs may have a few areas of cloudiness and crazing, indicating spots of damage from their infection, but most of the lung is black, indicating that it is filled with air.MORE COVERAGEVideo Series: Coronavirus in Context

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One doctor treating COVID-19 patients in New York says it was like altitude sickness. It was “as if tens of thousands of my fellow New Yorkers are stuck on a plane at 30,000 feet and the cabin pressure is slowly being let out. These patients are slowly being starved of oxygen,” said Cameron Kyle-Sidell, MD, an emergency room and critical care doctor at Maimonides Medical Center in Brooklyn who has been posting about his experience on social media.

“A whole bunch of these patients really have low oxygen, but their lungs don’t look all that bad,” says Todd Bull, MD, director for the Center of Lungs and Breathing at the University of Colorado School of Medicine, in Aurora.

Doctors in Italy have noticed the same thing. And in some cases, that might mean patients need to be treated a little differently to ensure the best outcome.

In an editorial in the journal Intensive Care Medicine, Luciano Gattinoni, MD, a guest professor of anesthesia and intensive care at the University of Gottingen in Germany, and one of the world’s experts in mechanical ventilation, says more than half the patients he and his colleagues have treated in Northern Italy have had this unusual symptom. They seem to be able to breathe just fine, but their oxygen is very low.

According to Gattinoni, about 30% of COVID-19 patients who come to the hospital have more classic symptoms of acute respiratory distress syndrome, or ARDS. Their lungs are cloudy on imaging scans, and they’re stiff and inflamed, showing that they aren’t working well. The patients also have low levels of oxygen in their blood, and they are struggling to breathe. They look like patients with severe pneumonia caused by a virus. This is the type of lung trouble doctors are more used to seeing with respiratory diseases like influenza and SARS.PlayCurrent Time0:00/Duration Time0:00MuteFullscreenProgress: 0%

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Gattinoni says doctors need to pay attention to how COVID-19 has affected the lungs and breathing of each patient they’re treating before deciding on treatment. Patients with more classic ARDS-type COVID-19 often need mechanical ventilation right away, which forces air into the lungs to increase oxygen.

Patients with respiratory failure who can still breathe OK, but have still have very low oxygen, may improve on oxygen alone, or on oxygen delivered through a lower pressure setting on a ventilator.

Gattinoni thinks the trouble for these patients may not be swelling and stiffening of their lung tissue, which is what happens when an infection causes pneumonia. Instead, he thinks the problem may lie in the intricate web of blood vessels in the lungs.

Normally, when lungs become damaged, the vessels that carry blood through the lungs so it can be re-oxygenated constrict, or close down, so blood can be shunted away from the area that’s damaged to an area that’s still working properly. This protects the body from a drop in oxygen.

Gattinoni thinks some COVID-19 patients can’t do this anymore. So blood is still flowing to damaged parts of the lungs. People still feel like they’re taking good breaths, but their blood oxygen is dropping all the same.

This problem with the blood vessels is similar to what happens in a condition called high-altitude pulmonary edema, or HAPE, says Bull.

HAPE patients recover when you bring them down from a high altitude and give them oxygen. They are sometimes also placed on ventilators and treated with medicines including diuretics to remove fluid that’s flooded their lungs. More research is needed to know if any of those strategies may help COVID-19 patients. Steroids, in particular, have not been shown to help with ARDS and may make it worse.

“Is it possible that there’s a problem with how the blood vessels regulate blood flow? That is, I guess, a possibility, which would be different than what we usually see in ARDS,” Bull says.

“This is just a hypothesis at this point. It has to be proven,” he says.

It’s also important to note that patients with relatively normal-looking lungs can progress to ARDS as the virus attacks their lung tissue, Gattinoni says.

He says these patients with more normal-looking lungs, but low blood oxygen, may also be especially vulnerable to ventilator-associated lung injury, where pressure from the air that’s being forced into the lungs damages the thin air sacs that exchange oxygen with the blood.

In normal breathing, our lungs expand because of negative pressure. A large thin muscle at the bottom of the lungs, called the diaphragm, pulls down and our lungs expand to fill the increased space. But ventilators work by forcing air into the lungs, which is positive pressure, like what happens when you blow up a balloon. These machines can help people whose lungs have become too weak to work, but they can also cause damage because they force the lung to work in a way it wasn’t designed to.

“When those pressures get too high, you can cause trauma to those little air sacs. Those are very fragile,” says Michael Mohning, MD, a pulmonologist and critical care specialist at National Jewish Health in Denver.

Gattinoni says putting a patient like this on a ventilator under too high a pressure may cause lung damage that ultimately looks like ARDS.

So he cautions that doctors need to be aware of the COVID-19 patients’ symptoms  and need to use the ventilator carefully and sparingly.PlayCurrent Time0:00/Duration Time0:00MuteFullscreenProgress: 0%

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In an interview with MDEdge, Gattinoni said one center in central Europe that had begun using different treatments for different types of COVID-19 patients had not seen any deaths among those patients in its intensive care unit. He said a nearby hospital that was treating all COVID-19 patients based on the same set of instructions had a 60% death rate in its ICU.

“This is a kind of disease in which you don’t have to follow the protocol — you have to follow the physiology,” Gattinoni said. “Unfortunately, many, many doctors around the world cannot think outside the protocol.”

Other experts agree.

“If you over-distend somebody’s lung on mechanical ventilation, you essentially generate more ARDS. You make the lung leaky,” Bull says.

He says pulmonologists have gotten much better at using ventilators to make them safer for patients. Doctors work to keep the pressure on the lung as low as possible, to prevent that damage.

Several recent studies have helped to cut the death rate for patients who need to be on a ventilator. The PROSEVA study, published in The New England Journal of Medicine, showed the death rate among ventilated patients could be as low as 16% under optimal care.

So far, death rates for ventilated patients with COVID-19 have been higher than that. That could be because some COVID-19 patients often need to be on ventilators for a long time, sometimes as long as 2 weeks. They also tend to have other conditions, so it’s possible that they are sicker to begin with. More research is needed to understand why, and doctors will continue to share best practices as they see things that need to be addressed.WebMD Health News Reviewed by Neha Pathak, MD on April 07

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COVID-19 will likely be with us forever. Here’s how we’ll live with it.

As COVID-19 continues to run its course, the likeliest long-term outcome is that the virus SARS-CoV-2 becomes endemic in large swaths of the world, constantly circulating among the human population but causing fewer cases of severe disease. Eventually—years or even decades in the future—COVID-19 could transition into a mild childhood illness, like the four endemic human coronaviruses that contribute to the common cold.

“My guess is, enough people will get it and enough people will get the vaccine to reduce person-to-person transmission,” says Paul Duplex, director of the University of Pittsburgh’s Center for Vaccine Research. “There will be pockets of people who won’t take [the vaccines], there will be localized outbreaks, but it will become one of the ‘regular’ coronaviruses.”

But this transition won’t happen overnight. Experts say that SARS-CoV-2’s exact post-pandemic trajectory will depend on three major factors: how long humans retain immunity to the virus, how quickly the virus evolves, and how widely older populations become immune during the pandemic itself.

Depending on how these three factors shake out, the world could be facing several years of a halting post-pandemic transition—one marked by continued viral evolution, localized outbreaks, and possibly multiple rounds of updated vaccinations.

“People have got to realize, this is not going to go away,” says Roy Anderson, an infectious disease epidemiologist at Imperial College London. “We’re going to be able to manage it because of modern medicine and vaccines, but it’s not something that will just vanish out of the window.”

The long road to another common cold

One of the essential factors governing the future of COVID-19 is our immunity to the illness. Immunity to any pathogen, including SARS-CoV-2, isn’t binary like a light switch. Instead, it’s more like a dimmer switch: The human immune system can confer varying degrees of partial protection from a pathogen, which can stave off severe illness without necessarily preventing infection or transmission.

In general, the partial protection effect is one of the reasons why the four known endemic human coronaviruses—the ones that cause a common cold—have such mild symptoms. A 2013 study in BMC Infectious Diseases shows that on average, humans are first exposed to all four of these coronaviruses between the ages of three and five-part of the first wave of infections that young children experience.

These initial infections lay the foundation for the body’s future immune response. As new variants of the endemic coronaviruses naturally evolve, the immune system has a head start in fighting them off—not enough to eradicate the virus instantly, but enough to ensure that symptoms don’t progress much beyond the sniffles.

“The virus is also its own enemy. Every time it infects you, it tops up your immunity,” says Marc Veldhoen, an immunologist at the Portugal’s University of Lisbon.

Past studies make clear that partial immunity can keep people from getting seriously ill, even as coronaviruses successfully enter their systems. Long-term, the same is likely to be true for the new coronavirus. Emory University postdoctoral fellow Jennie Lavine modeled SARS-CoV-2’s post-pandemic trajectory based on the 2013 study’s data, and her results—published in Science on January 12—suggest that if SARS-CoV-2 behaves like other coronaviruses, it will likely morph into mild nuisance years to decades from now.

This transition from pandemic to minor ailment, however, depends on how the immune response to SARS-CoV-2 holds up over time. Researchers are actively examining the body’s “immunological memory” of the virus. A study published in Science on January 6 tracked the immune response of 188 COVID-19 patients for five to eight months post-infection, and while individuals are varied, about 95 percent of patients had measurable levels of immunity.

“Immunity is waning, but certainly not gone, and I think this is key,” says Lavine, who wasn’t involved with the study.

In fact, it’s even possible that one of the cold-causing coronaviruses sparked a serious outbreak in the 1800s before fading into the litany of mild, commonplace human pathogens. Based on the spread of its family tree, researchers estimated in 2005 that the endemic coronavirus OC43 entered humans sometime in the late 19th century, likely the early 1890s. The timing has led some researchers to speculate that the original version of OC43 may have caused the “Russian flu” pandemic of 1890, which was noted for its unusually high rate of neurological symptoms—a noted effect of COVID-19.

“There’s no hard proof, but there are a lot of indications that this wasn’t an influenza pandemic but a corona-pandemic,” Veldhoen says.

The crucible of evolution

Though the carnage of past coronaviruses has faded over time, the road to a relatively painless coexistence between humans and SARS-CoV-2 will likely be bumpy. In the medium-term future, the impact of the virus will depend largely on its evolution.

SARS-CoV-2 is spreading uncontrollably around the world, and with every new replication, there’s a chance for mutations that could help the virus more effectively infect human hosts.

The human immune system, while protecting many of us from a serious illness, is also acting as an evolutionary crucible, putting pressure on the virus that selects for mutations that make it bind more effectively to human cells. The coming months and years will reveal how well our immune systems can keep up with these changes.

New SARS-CoV-2 variants also make widespread vaccination and other transmission-blocking measures, such as face masks and distancing, more crucial than ever. The less the virus spreads, the fewer opportunities it has to evolve.

We’re going to be able to manage it because of modern medicine and vaccines, but it’s not something that will just vanish out of the window.

ROY ANDERSONIMPERIAL COLLEGE LONDON

Current vaccines should still work well enough against emerging variants, such as the B.1.1.7 lineage first found in the United Kingdom, to prevent many cases of serious illness. Vaccines and natural infections create diverse swarms of antibodies that glom onto many different parts of SARS-CoV-2’s spike protein, which means that a single mutation can’t make the virus invisible to the human immune system.

Mutations may produce future variants of SARS-CoV-2 that partially resist current vaccines, however. In a preprint posted on November 19 and updated on January 19, Duplex and his colleagues show that mutations that delete parts of the SARS-CoV-2 genome’s spike protein region prevent certain human antibodies from binding.

“What I’ve learned from our own work is how deviously beautiful evolution is,” Duplex says.

Other labs have found that mutations in 501Y.V2, the variant first found in South Africa, are especially effective at helping the virus elude antibodies. Out of 44 recovered COVID-19 patients in South Africa, blood extracts from 21 of the patients didn’t effectively neutralize the 501Y.V2 variant, according to another preprint published on January 19. Those 21 people had mild to moderate cases of COVID-19, however, so their antibody levels were lower, to begin with, perhaps explaining why their blood did not neutralize the 501Y.V2 variant.

So far, currently authorized vaccines—which spur the production of high levels of antibodies—seem to be effective against the most concerning variants. In a third preprint published on January 19, researchers showed that antibodies from 20 people who had received the Pfizer-BioNTech or Moderna vaccines didn’t bind quite as well to viruses with the new mutations as they did to earlier variants—but they still bound, suggesting the vaccines will still protect against severe illness.

The new variants bring other threats as well. Some, such as B.1.1.7, appear to be more transmissible than earlier forms of SARS-CoV-2, and if left to spread uncontrollably, these variants could make many more people severely ill, which risks overwhelming healthcare systems around the world and even higher death tolls. Veldhoen adds that new variants also may pose a greater risk of reinfection to recovered COVID-19 patients.

Researchers are closely monitoring the new variants. If vaccines need to be updated in the future, Anderson says that it could be done quickly—in roughly six weeks for currently authorized mRNA vaccines, such as those made by Pfizer-BioNTech and Moderna. That timetable, though, doesn’t account for the regulatory approvals that updated vaccines would need to go through.

Anderson adds that depending on how the evolution of the virus progresses, lineages of SARS-CoV-2 may arise that are distinct enough that vaccines will need to be tailored to specific regions akin to vaccines for pneumococcus. To successfully guard against SARS-CoV-2 going forward, we will need a global monitoring network similar to the worldwide reference laboratories used to collect, sequence, and study variants of influenza.

“We’re going to have to live with it, we’re going to have to have constant vaccination, and we’re constantly going to have to have a very sophisticated molecular surveillance program to keep track of how the virus is evolving,” Anderson says.

The promise and challenge of widespread vaccination

Experts agree that transitioning beyond a pandemic depends on the prevalence of immunity, especially among older and more vulnerable populations. Younger people, especially children, will build up immunity to SARS-CoV-2 over a lifetime of exposure to the virus. Today’s adults have had no such luxury, leaving their immune systems naive and exposed.

The exact threshold for achieving population-wide immunity that slows down the virus’s spread will depend on how contagious future variants become. But so far, research of early variants of SARS-CoV-2 suggests at least 60 to 70 percent of the human population will need to become immune to end the pandemic phase.

This immunity can be achieved in one of two ways: large-scale vaccination, or recovery from natural infections. But achieving widespread immunity through uncontrolled spread comes at a terrible cost: hundreds of thousands more deaths and hospitalizations around the world. “If we don’t want to push forward vaccines and champion vaccines, we have to decide collectively how many old people we want to die—and I don’t want to be the one making that decision,” Duplex says.

Jeffrey Shaman, an infectious diseases expert at Columbia University, points out that the global push for vaccines also exposes existing inequities in global health. In a widely shared map from December, The Economist Intelligence Unit estimated that rich countries such as the U.S. will have widely accessible vaccines by early 2022, which may not happen for poorer countries in Africa and Asia until as late as 2023.

Efforts to vaccinate the developing world hinge, in part, on vaccines that can be stored with standard refrigeration, such as the vaccines under development by Oxford/AstraZeneca and Johnson & Johnson. (See the latest on COVID-19 vaccine development around the world.)

As of the week of January 18, according to a World Health Organization estimate, some 40 million COVID-19 vaccine doses have been administered around the world, mostly in high-income countries. In Africa, only two countries, Seychelles and Guinea, have started providing vaccines. And in Guinea, a low-income country, only 25 people have received doses.

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Patients with IBD should receive COVID-19 vaccine, despite concerns

“For patients with IBD we would advocate, based on [International Organization for the Study of Inflammatory Bowel Disease (IOIBD)], that patients get vaccinated, acknowledging that there is a lack of data specifically in IBD patients,” Ryan C. Ungaro, MD, MS, gastroenterologist with Mount Sinai Hospital’s Feinstein IBD Center, told Healio Gastroenterology. “But we think the benefits outweigh the risks and based on prior experience with vaccinations in IBD patients.”

CDC and IOIBD recommend patients with IBD should receive the COVID-19 vaccine.

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According to Ungaro, the CDC recommended immunocompromised patients should get the COVID-19 vaccine. Patients should be counseled that it is not yet known whether the safety and effectiveness of the vaccine in immunocompromised patients are the same compared with the general population.

“The major concern would be certain medications could lead to decreased response to the vaccine,” he said. “That is something that is going to need to be studied but right now the expert consensus is that IBD patients should get vaccinated against COVID-19.”

According to IOIBD recommendations, patients with IBD should receive the COVID-19 vaccine as soon as possible. Messenger RNA vaccines, replication vector vaccines, inactivated vaccines, and recombinant vaccines are safe to be administered in IBD patients, Ungaro said.

Additionally, the IOIBD said vaccines should not be deferred if an IBD patient is receiving immune-modifying therapies.

According to Ungaro, patients with IBD who take corticosteroids and get the vaccine should receive counseling that there may be a decreased systemic response. He said this needs to be studied further.

“Prospective studies are being planned to look at the real-world effectiveness and side effects of the COVID-19 vaccine in IBD patients,” Ungaro said. “This would require cohorts that are vaccinated and followed. Some studies are ongoing for that both in the United States and internationally. [Surveillance Epidemiology of Coronavirus Under Research Exclusion-IBD (SECURE-IBD)] is going to help support some of these efforts as well.”

Ungaro and his team at Mount Sinai in collaboration with the University of North Carolina developed the SECURE-IBD registry early in 2020 to monitor and report outcomes of COVID-19 in patients with IBD.

He said, “Physicians can encourage IBD patients to enroll in the Crohn’s and Colitis Foundation’s IBD Partners, they will be one of the sources for the prospective COVID-19 vaccine studies.”

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Udo’s Choice® Super 8 Microbiotic

People liveing with crohns sisease can have a altered “microbiome” which means that the digestive bacteria thats in ther gut can be unbalanced ,that were takeing

Some experts maintain that using probiotics to restore the microbiome can allow a person with Crohn’s disease to reduce irregular immune responses and experience fewer symptoms.

They believe that adding healthful bacteria to the digestive tract, potentially by incorporating natural probiotic food sources to the diet, can reduce both intestinal inflammation and anomalies of the immune system. This could minimize symptoms of Crohn’s disease, such as gastrointestinal irritation, diarrhea, and stomach upset.

To see whether or not probiotics work for them, people with Crohn’s disease can keep a food diary and slowly incorporate some of these foods into their diet, noting any changes in their symptoms.

Probiotic foods include:

  • yogurt
  • kombucha
  • kefir
  • sauerkraut
  • kimchi
  • tempeh
  • miso

A person may also incorporate prebiotic foods into their diet. These are food sources that feed bacteria in the digestive tract and can promote their growth. These foods include onions, leeks, and asparagus.

Research has not proven that the probiotics in food can help reduce Crohn’s disease symptoms, so some people may wish to try taking a supplement first.

However, as long as someone does not have an allergy to foods that contain probiotics, incorporating them into the diet is a relatively risk-free method to try to improve overall health and help manage the disease.

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