Prayers and Grief Counseling After COVID: Trying to Aid Healing in Long-Term Care

A tidal wave of grief and loss has rolled through long-term care facilities as the coronavirus pandemic has killed more than 91,000 residents and staffers — nearly 40% of recorded COVID-19 deaths in the U.S.

And it’s not over: Facilities are bracing for further shocks as coronavirus cases rise across the country.

Workers are already emotionally drained and exhausted after staffing the front lines — and putting themselves at significant risk — since March, when the pandemic took hold. And residents are suffering deeply from losing people they once saw daily, the disruption of routines and being cut off from friends and family.

In response, nursing homes and assisted living centers are holding memorials for people who’ve died, having chaplains and social workers help residents and staff, and bringing in hospice providers to offer grief counseling, among other strategies. More than 2 million vulnerable older adults live in these facilities.

“Everyone is aware that this is a stressful, traumatic time, with no end in sight, and there needs to be some sort of intervention,” said Barbara Speedling, a long-term care consultant working on these issues with the American Health Care Association and National Center for Assisted Living, an industry organization.

Connie Graham, 65, is corporate chaplain at Community Health Services of Georgia, which operates 56 nursing homes. For months, he’s been holding socially distant prayer services in the homes’ parking lots for residents and staff members.

“People want prayers for friends in the facilities who’ve passed away, for relatives and friends who’ve passed away, for the safety of their families, for the loss of visitation, for healing, for the strength and perseverance to hold on,” Graham said.

Central Baptist Village, a Norridge, Illinois, nursing home, held a socially distanced garden ceremony to honor a beloved nurse who had died of COVID-19. “Our social service director made a wonderful collage of photos and left Post-its so everyone could write a memory” before delivering it to the nurse’s wife, said Dawn Mondschein, the nursing home’s chief executive officer.

“There’s a steady level of anxiety, with spikes of frustration and depression,” Mondschein said of staff members and residents.

Vitas Healthcare, a hospice provider in 14 states and the District of Columbia, has created occasional “virtual blessing services” on Zoom for staffers at nursing homes and assisted living centers. “We thank them for their service and a chaplain gives words of encouragement,” said Robin Fiorelli, Vitas’ senior director of bereavement and volunteers.

Vitas has also been holding virtual memorials via Zoom to recognize residents who’ve died of COVID-19. “A big part of that service is giving other residents an opportunity to share their memories and honor those they’ve lost,” Fiorelli said.

On Dec. 6, Hospice Savannah is going one step further and planning an online broadcast of its annual national “Tree of Light” memorial, with grief counselors who will offer healing strategies. During the service, candles will be lit and a moment of silence observed in remembrance of people who’ve died.

“Grief has become an urgent mental health issue, and we hope this will help begin the healing process for people who haven’t been able to participate in rituals or receive the comfort and support they’d normally have gotten prior to COVID-19,” said Kathleen Benton, Hospice Savannah’s president and chief executive officer.

But these and other attempts are hardly equal to the extent of anguish, which has only grown as the pandemic stretches on, fueling a mental health crisis in long-term care.

“There is a desperate need for psychological services,” said Toni Miles, a professor at the University of Georgia’s College of Public Health and an expert on grief and bereavement in long-term care settings. She’s created two guides to help grieving staffers and residents and is distributing them digitally to more than 400 nursing homes and 1,000 assisted living centers in the state.

A recent survey by Altarum, a nonprofit research and consulting firm, highlights the hopelessness of many nursing home residents. The survey asked 365 people living in nursing homes about their experiences in July and August.

“I am completely isolated. I might as well be buried already,” one resident wrote. “There is no hope,” another said. “I feel like giving up. … No emotional support nor mental health support is available to me,” another complained.

Inadequate mental health services in nursing homes have been a problem for years. Instead of counseling, residents are typically given medications to ease symptoms of distress, said David Grabowski, a professor of health care policy at Harvard Medical School who has published several studies on this topic.

The situation has worsened during the pandemic as psychologists and social workers have been unable to enter facilities that limited outsiders to minimize the risk of viral transmission.

“Several facilities didn’t consider mental health professionals ‘essential’ health care providers, and many of us weren’t able to get in,” said Lisa Lind, president of Psychologists in Long-Term Care. Although some facilities switched to tele-mental health services, staff shortages have made those hard to arrange, she noted.

Fewer than half of nursing home staffers have health insurance, and those who do typically don’t have “minimal” access to mental health services, Grabowski said. That’s a problem because “there’s a real fragility right now on the part of the workforce.”

Colleen Frankenfield, president and chief executive officer of Lutheran Social Ministries of New Jersey, said what staffers need most of all is “the ability to vent and to have someone comfort them.” She recalls a horrible day in April, when four residents died in less than 24 hours at her organization’s continuing care retirement community in northern New Jersey, which includes an assisted living facility and a nursing home.

“The phone rang at 1 a.m. and all I heard on the other end was an administrator, sobbing,” she remembered. “She said she felt she was emotionally falling apart. She felt like she was responsible for the residents who had died, like she had let them down. She just had to talk about what she was experiencing and cry it out.”

Although Lutheran Social Ministries has been free of COVID-19 since the end of April, “our employees are tired — always on edge, always worried,” Frankenfield said. “I think people are afraid and they need time to heal. At the end of the day, all we can really do is stand with them, listen to them and support them in whatever way we can.”

Coming Monday: The Navigating Aging column will look at the grief faced by long-term care workers as COVID-19 cases and deaths mount.

Join Judith Graham for a Facebook Live event on grief and bereavement during the coronavirus pandemic on Monday, Nov. 16, at 1 p.m. ET. You can watch the conversation here and submit questions in advance here.

We’re eager to hear from readers about questions you’d like answered, problems you’ve been having with your care and advice you need in dealing with the health care system. Visit khn.org/columnists to submit your requests or tips.

Kaiser Health News (KHN) is a national health policy news service. It is an editorially independent program of the Henry J. Kaiser Family Foundation which is not affiliated with Kaiser Permanente.

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Black Hair Matters: How Going Natural Made Me Visible

The night before I chopped off my hair, I got nervous.

This decision felt bigger than me, given all the weight that Black women’s hair carries. But after three months of wearing hats and scarves in a pandemic when trips to the hairdresser felt unsafe, I walked into a salon emotionally exhausted but ready to finally see my natural hair.

I thought a few tears would fall, but, as the last of my chemically straightened hair floated to the floor like rain, I felt cleansed. Free. I laughed hysterically as I drove away from the salon.

Friends and family cheered me on virtually, but my father quietly worried about my decision. My dad grew up in the Jim Crow South, where many women straightened their hair to land jobs, husbands and respect. Before my big chop, he never said much about my hair beyond the occasional compliment, which is why I was surprised when he issued a warning.

“Watch it out there. Your hair is cut now,” he blurted when he saw me walking out of the house.

My mother heard him but remained silent. She had her own set of concerns. She was worried about me looking less professional.

I also had to help my now 4-year-old daughter understand why I decided to go natural. We’ve watched the animated “Hair Love” a million times. We’ve read books like “Happy Hair” by Mechal Renee Roe, “I Love My Hair!” by Natasha Anastasia Tarpley and my personal favorite, “Don’t Touch My Hair!” by Sharee Miller.

Still, my daughter had a hard time adjusting to my new haircut, often asking when I planned to get my hair styled again. She preferred my extensions, saying she thought I looked more like a princess that way. I gently explained that my hair is a style — and the one I choose — even if it’s not long and straight.

My family’s emotions about my hair left me tangled.

Of course, the styling of Black hair has been fraught for centuries. The CROWN Act, which passed the U.S. House in September and is now pending in the Senate, is intended to protect Black people from discrimination in schools, housing and employment based on their hairstyle. But such a law, even if passed, cannot stop bigotry, bullets and the emotional battle that comes with being a Black woman in America as seen through something as simple as our hair.

I hadn’t considered talking to my daughter about how hair could affect her personal safety until my father broke his silence. A haircut shouldn’t influence your life expectancy.

On the night of my haircut, I drove to the store more aware of how others would perceive my new look. My father, however, was more worried about my safety because my silhouette could possibly be mistaken for a Black man’s frame.

We live in the Midwest, just outside St. Louis, where natural hair still makes a statement for Black women. If my buzz cut made me look more like a Black man, would the cops in our town treat me differently? In my dad’s eyes, my femininity increased my chances of making it home safely.

His comments also led to a conversation about the intersection between racism and sexism. Without reading the crucial work of scholar Kimberlé Crenshaw and other activists, my father intuitively understood that society has placed Black women in a blind spot, where our gender and our race make us invisible in many ways.

But that space isn’t safe, is it? A Eurocentric feminine hairstyle can’t protect Black women from the many deadly forms of racism.

Police officers can see us. Since 2015, at least 48 Black women have been killed by the police. I’m guessing the style of their hair didn’t matter to the officers pulling the triggers. In the past few years, the #SayHerName campaign has put a spotlight on their killings, but society still pays less attention to the police killings of Black women. While most people have heard of George Floyd, Michael Brown and Breonna Taylor, fewer know about Kathryn Johnston, Korryn Gaines and India Kager.

In death and life, our rights and our achievements don’t seem to hold as much weight compared with those of our male counterparts or our white ones. Yet, many Black women go to great lengths to be accepted in this country.

In the past few weeks, I’ve listened to other Black women in my life vent about their hair and navigating racism. We’ve shared our fears, hair horror stories and moments of victory. I’ve come to realize that my haircut wasn’t just about changing my style. It was also about reclaiming my crown after years of letting society control it.

Kaiser Health News (KHN) is a national health policy news service. It is an editorially independent program of the Henry J. Kaiser Family Foundation which is not affiliated with Kaiser Permanente.

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‘Breakthrough Finding’ Reveals Why Certain COVID Patients Die

Dr. Megan Ranney has learned a lot about COVID-19 since she began treating patients with the disease in the emergency department in February.

But there’s one question she still can’t answer: What makes some patients so much sicker than others?

Advancing age and underlying medical problems explain only part of the phenomenon, said Ranney, who has seen patients of similar age, background and health status follow wildly different trajectories.

“Why does one 40-year-old get really sick and another one not even need to be admitted?” asked Ranney, an associate professor of emergency medicine at Brown University.

In some cases, provocative new research shows, some people — men in particular — succumb because their immune systems are hit by friendly fire. Researchers hope the finding will help them develop targeted therapies for these patients.

In an international study in Science, 10% of nearly 1,000 COVID patients who developed life-threatening pneumonia had antibodies that disable key immune system proteins called interferons. These antibodies — known as autoantibodies because they attack the body itself — were not found at all in 663 people with mild or asymptomatic COVID infections. Only four of 1,227 healthy individuals had the autoantibodies. The study, published on Oct. 23, was led by the COVID Human Genetic Effort, which includes 200 research centers in 40 countries.

“This is one of the most important things we’ve learned about the immune system since the start of the pandemic,” said Dr. Eric Topol, executive vice president for research at Scripps Research in San Diego, who was not involved in the new study. “This is a breakthrough finding.”

In a second Science study by the same team, authors found that an additional 3.5% of critically ill patients had mutations in genes that control the interferons involved in fighting viruses. Given that the body has 500 to 600 of these genes, it’s possible researchers will find more mutations, said Qian Zhang, lead author of the second study.

Interferons serve as the body’s first line of defense against infection, sounding the alarm and activating an army of virus-fighting genes, said virologist Angela Rasmussen, an associate research scientist at the Center of Infection and Immunity at Columbia University’s Mailman School of Public Health.

“Interferons are like a fire alarm and a sprinkler system all in one,” said Rasmussen, who wasn’t involved in the new studies.

Lab studies show interferons are suppressed in some people with COVID-19, perhaps by the virus itself.

Interferons are particularly important for protecting the body against new viruses, such as the coronavirus, which the body has never encountered, said Zhang, a researcher at Rockefeller University’s St. Giles Laboratory of Human Genetics of Infectious Diseases.

When infected with the novel coronavirus, “your body should have alarms ringing everywhere,” said Zhang. “If you don’t get the alarm out, you could have viruses everywhere in large numbers.”

Significantly, patients didn’t make autoantibodies in response to the virus. Instead, they appeared to have had them before the pandemic even began, said Paul Bastard, the antibody study’s lead author, also a researcher at Rockefeller University.

For reasons that researchers don’t understand, the autoantibodies never caused a problem until patients were infected with COVID-19, Bastard said. Somehow, the novel coronavirus, or the immune response it triggered, appears to have set them in motion.

“Before COVID, their condition was silent,” Bastard said. “Most of them hadn’t gotten sick before.”

Bastard said he now wonders whether autoantibodies against interferon also increase the risk from other viruses, such as influenza. Among patients in his study, “some of them had gotten flu in the past, and we’re looking to see if the autoantibodies could have had an effect on flu.”

Scientists have long known that viruses and the immune system compete in a sort of arms race, with viruses evolving ways to evade the immune system and even suppress its response, said Sabra Klein, a professor of molecular microbiology and immunology at the Johns Hopkins Bloomberg School of Public Health.

Antibodies are usually the heroes of the immune system, defending the body against viruses and other threats. But sometimes, in a phenomenon known as autoimmune disease, the immune system appears confused and creates autoantibodies. This occurs in diseases such as rheumatoid arthritis, when antibodies attack the joints, and Type 1 diabetes, in which the immune system attacks insulin-producing cells in the pancreas.

Although doctors don’t know the exact causes of autoimmune disease, they’ve observed that the conditions often occur after a viral infection. Autoimmune diseases are more common as people age.

In yet another unexpected finding, 94% of patients in the study with these autoantibodies were men. About 12.5% of men with life-threatening COVID pneumonia had autoantibodies against interferon, compared with 2.6% of women.

That was unexpected, given that autoimmune disease is far more common in women, Klein said.

“I’ve been studying sex differences in viral infections for 22 years, and I don’t think anybody who studies autoantibodies thought this would be a risk factor for COVID-19,” Klein said.

The study might help explain why men are more likely than women to become critically ill with COVID-19 and die, Klein said.

“You see significantly more men dying in their 30s, not just in their 80s,” she said.

Akiko Iwasaki, a professor of immunobiology at the Yale School of Medicine, noted that several genes involved in the immune system’s response to viruses are on the X chromosome.

Women have two copies of this chromosome — along with two copies of each gene. That gives women a backup in case one copy of a gene becomes defective, Iwasaki said.

Men, however, have only one copy of the X chromosome. So if there is a defect or harmful gene on the X chromosome, they have no other copy of that gene to correct the problem, Iwasaki said.

Bastard noted that one woman in the study who developed autoantibodies has a rare genetic condition in which she has only one X chromosome.

Scientists have struggled to explain why men have a higher risk of hospitalization and death from COVID-19. When the disease first appeared in China, experts speculated that men suffered more from the virus because they are much more likely to smoke than Chinese women.

Researchers quickly noticed that men in Spain were also more likely to die of COVID-19, however, even though men and women there smoke at about the same rate, Klein said.

Experts have hypothesized that men might be put at higher risk by being less likely to wear masks in public than women and more likely to delay seeking medical care, Klein said.

But behavioral differences between men and women provide only part of the answer. Scientists say it’s possible that the hormone estrogen may somehow protect women, while testosterone may put men at greater risk. Interestingly, recent studies have found that obesity poses a much greater risk to men with COVID-19 than to women, Klein said.

Yet women have their own form of suffering from COVID-19.

Studies show women are four times more likely to experience long-term COVID symptoms, lasting weeks or months, including fatigue, weakness and a kind of mental confusion known as “brain fog,” Klein noted.

As women, “maybe we survive it and are less likely to die, but then we have all these long-term complications,” she said.

After reading the studies, Klein said, she would like to learn whether patients who become severely ill from other viruses, such as influenza, also harbor genes or antibodies that disable interferon.

“There’s no evidence for this in flu,” Klein said. “But we haven’t looked. Through COVID-19, we may have uncovered a very novel mechanism of disease, which we could find is present in a number of diseases.”

To be sure, scientists say that the new study solves only part of the mystery of why patient outcomes can vary so greatly.

Researchers say it’s possible that some patients are protected by past exposure to other coronaviruses. Patients who get very sick also may have inhaled higher doses of the virus, such as from repeated exposure to infected co-workers.

Although doctors have looked for links between disease outcomes and blood type, studies have produced conflicting results.

Screening patients for autoantibodies against interferons could help predict which patients are more likely to become very sick, said Bastard, who is also affiliated with the Necker Hospital for Sick Children in Paris. Testing takes about two days. Hospitals in Paris can now screen patients on request from a doctor, he said.

Although only 10% of patients with life-threatening COVID-19 have autoantibodies, “I think we should give the test to everyone who is admitted,” Bastard said. Otherwise, “we wouldn’t know who is at risk for a severe form of the disease.”

Bastard said he hopes his findings will lead to new therapies that save lives. He notes that the body manufactures many types of interferons. Giving these patients a different type of interferon — one not disabled by their genes or autoantibodies — might help them fight off the virus.

In fact, a pilot study of 98 patients published Thursday in the Lancet Respiratory Medicine journal found benefits from an inhaled form of interferon. In the industry-funded British study, hospitalized COVID patients randomly assigned to receive interferon beta-1a were more than twice as likely as others to recover enough to resume their regular activities.

Researchers need to confirm these findings in a much larger study, said Dr. Nathan Peiffer-Smadja, a researcher at Imperial College London who was not involved in the study but wrote an accompanying editorial. Future studies should test patients’ blood for genetic mutations and autoantibodies against interferon, to see if they respond differently than others.

Peiffer-Smadja notes that inhaled interferon may work better than an injected form of the drug because it’s delivered directly to the lungs. While injected versions of interferon have been used for years to treat other diseases, the inhaled version is still experimental and not commercially available.

And doctors should be cautious about interferon for now, because a study led by the World Health Organization found no benefit to an injected form of the drug in COVID patients, Peiffer-Smadja said. In fact, there was a trend toward higher mortality rates in patients given interferon, although this finding could have been due to chance. Giving interferon later in the course of disease could encourage a destructive immune overreaction called a cytokine storm, in which the immune system does more damage than the virus.

Around the world, scientists have launched more than 100 clinical trials of interferons, according to clinicaltrials.gov, a database of research studies from the National Institutes of Health.

Until larger studies are completed, doctors say, Bastard’s findings are unlikely to change how they treat COVID-19.

Dr. Lewis Kaplan, president of the Society of Critical Care Medicine, said he treats patients according to their symptoms, not their risk factors.

“If you are a little sick, you get treated with a little bit of care,” Kaplan said. “You are really sick, you get a lot of care. But if a COVID patient comes in with hypertension, diabetes and obesity, we don’t say, ‘They have risk factors. Let’s put them in the ICU.’”

Kaiser Health News (KHN) is a national health policy news service. It is an editorially independent program of the Henry J. Kaiser Family Foundation which is not affiliated with Kaiser Permanente.

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KHN on the Air This Week

KHN Editor-in-Chief Elisabeth Rosenthal discussed how to manage unexpected health care costs with CBSN on Wednesday.

• Click here to watch Rosenthal on CBSN

KHN chief Washington correspondent Julie Rovner discussed the Affordable Care Act case before the Supreme Court with WBEZ’s “Reset” and WDET’s “Detroit Today” on Tuesday and with WHYY’s “Radio Times” on Wednesday.

• Click here to hear Rovner on WBEZ
• Click here to hear Rovner on WDET
• Click here to hear Rovner on WHYY
• Read Rovner’s “What to Know as ACA Heads to Supreme Court — Again“

KHN partnerships editor and senior correspondent Mary Agnes Carey discussed the ACA Supreme Court case on Newsy’s “Morning Rush” on Tuesday and on Connecticut Public Radio’s “Where We Live” on Nov. 6.

• Click here to watch Carey on Newsy
• Click here to hear Carey on Connecticut Public Radio

On Thursday, KHN correspondent Rachana Pradhan discussed with Newsy the challenges President-elect Joe Biden faces in trying to seat Food and Drug Administration leadership quickly to deal with the pandemic.

• Click here to watch Pradhan on Newsy
• Read Pradhan’s “As Nation Awaits Vaccine, Biden Is Under Pressure to Name New FDA Chief ASAP“

KHN senior correspondent Sarah Jane Tribble discussed KHN’s “Where It Hurts” podcast with Kansas Public Radio’s “KPR Presents” on Nov. 1.

• Click here to hear Tribble on Kansas Public Radio
• Tribble hosts “No Mercy,” the first season of “Where It Hurts.” Click here to listen to Chapter 1.

Kaiser Health News (KHN) is a national health policy news service. It is an editorially independent program of the Henry J. Kaiser Family Foundation which is not affiliated with Kaiser Permanente.

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Stanford vs. Harvard: Two Famous Biz Schools’ Opposing Tactics on COVID

At the Stanford Graduate School of Business in Northern California, the stories got weird almost immediately upon students’ return for the fall semester. Some said they were being followed around campus by people wearing green vests telling them where they could and could not be, go, stop, chat or conduct even a socially distanced gathering. Others said they were threatened with the loss of their campus housing if they didn’t follow the rules.

“They were breaking up picnics. They were breaking up yoga groups,” said one graduate student, who asked not to be identified so as to avoid social media blowback. “Sometimes they’d ask you whether you actually lived in the dorm you were about to go into.”

Across the country in Boston, students at the Harvard Business School gathered for the new semester after being gently advised by the school’s top administrators, via email, that they were part of “a delicate experiment.” The students were given the ground rules for the term, then received updates every few days about how things were going. And that, basically, was that.

In the time of COVID-19, it’s fair to say that no two institutions have come to quite the same conclusions about how to proceed safely. But as Harvard’s and Stanford’s elite MBA-granting programs have proved, those paths can diverge radically, even as they may eventually lead toward the same place.

For months, college and university administrators nationwide have huddled with their own medical experts and with local and county health authorities, trying to determine how best to operate in the midst of the novel coronavirus. Could classes be offered in person? Would students be allowed to live on campus — and, if so, how many? Could they hang out together?

“The complexity of the task and the enormity of the task really can’t be overstated,” said Dr. Sarah Van Orman, head of student health services at the University of Southern California and a past president of the American College Health Association. “Our first concern is making sure our campuses are safe and that we can maintain the health of our students, and each institution goes through that analysis to determine what it can deliver.”

With a campus spread over more than 8,000 acres on the San Francisco Peninsula, Stanford might have seemed like a great candidate to host large numbers of students in the fall. But after sounding hopeful tones earlier in the summer, university officials reversed course as the pandemic worsened, discussing several possibilities before finally deciding to limit on-campus residential status to graduate students and certain undergrads with special circumstances.

The Graduate School of Business sits in the middle of that vast and now mostly deserted campus, so the thought was that Stanford’s MBA hopefuls would have all the physical distance they needed to stay safe. Almost from the students’ arrival in late August, though, Stanford’s approach was wracked by missteps, policy reversals and general confusion over what the COVID rules were and how they were to be applied.

Stanford’s business grad students were asked to sign a campus compact that specified strict safety measures for residents. Students at Harvard Business School signed a similar agreement. In both cases, state and local regulations weighed heavily, especially in limiting the size of gatherings. But Harvard’s compact emerged fully formed and relied largely on the trustworthiness of its students. The process at Stanford was unexpectedly torturous, with serial adjustments and enforcers who sometimes went above and beyond the stated restrictions.

Graduate students there, mobilized by their frustration over not being consulted when the policy was conceived, urged colleagues not to sign the compact even though they wouldn’t be allowed to enroll in classes, receive pay for teaching or live in campus housing until they did. Among their objections: Stanford’s original policy had no clear appeals process, and it did not guarantee amnesty from COVID violation punishments to those who reported a sexual assault “at a party/gathering of multiple individuals” if the gathering broke COVID protocols.

Under heavy pressure, university administrators ultimately altered course, solicited input from the grad student population and produced a revised compact addressing the students’ concerns in early September, including the amnesty they sought for reporting sexual assault. But the Stanford business students were already unsettled by the manners of enforcement, including the specter of vest-wearing staffers roaming campus.

According to the Stanford Daily, nine graduate students were approached in late August by armed campus police officers who said they’d received a call about the group’s outdoor picnic and who — according to the students — threatened eviction from campus housing as an ultimate penalty for flouting safety rules. “For international students, [losing] housing is really threatening,” one of the students told the newspaper.

The people in the vests were Event Services staff working as “Safety Ambassadors,” Stanford spokesperson E.J. Miranda wrote in an email. The staffers were not on campus to enforce the compact, but rather were “emphasizing educational and restorative interventions,” he said. Still, when the university announced the division of its campus into five zones in September, it told students in a health alert email that the program “will be enforced by civilian Stanford representatives” — the safety ambassadors.

The Harvard Business School’s approach was certainly different in style. In July, an email from top administrators reaffirmed the school’s commitment to students living on campus and taking business classes in person in a hybrid learning model. As for COVID protocols, the officials adopted “a parental tone,” as the graduate business education site Poets & Quants put it. “All eyes are on us,” the administrators wrote in an August email.

But the guts of the school’s instructions were similar to those at Stanford. Both Harvard and Stanford severely restricted who could be on campus at any given time, limiting access to students, staff members and preapproved visitors. Both required that anyone living on campus report their health daily through an online portal, checking for any symptoms that could be caused by COVID-19. Both required face coverings when outside on campus — even, a Harvard missive said, in situations “when physical distancing from others can be maintained.”

So far, both Harvard and Stanford have posted low positive test rates overall, and the business schools are part of those reporting totals, with no significant outbreaks reported. Despite their distinct delivery methods, the schools ultimately relied on science to guide their COVID-related decisions.

“I feel like we’ve been treated as adults who know how to stay safe,” said a Harvard second-year MBA candidate who requested anonymity. “It’s worked — at least here.”

But as the experiences at the two campuses show, policies are being written and enforced on the fly, in the midst of a pandemic that has brought challenge after challenge. While the gentler approach at Harvard Business School largely worked, it did so within a larger framework of the health regulations put forth by local and county officials. As skyrocketing COVID-19 rates across the nation suggest, merely writing recommendations does little to slow the spread of disease.

Universities have struggled to strike a balance between the desire to deliver a meaningful college experience and the discipline needed to keep the campus caseload low in hopes of further reopening in 2021. In Stanford’s case, that struggle led to overreach and grad-student blowback that Harvard was able to avoid.

The fall term has seen colleges across the country cycling through a series of fits and stops. Some schools welcomed students for in-person classes but quickly reverted to distance learning only. And large campuses, with little ability to maintain the kind of control of a grad school, have been hit tremendously hard. Major outbreaks have been recorded at Clemson, Arizona State, Wisconsin, Penn State, Texas Tech — locations all over the map that opened their doors with more students and less stringent guidelines.

In May, as campuses mostly shut down to consider their future plans, USC’s Van Orman expressed hope that universities’ past experiences with international students and global outbreaks, such as SARS, would put them in a position to better plan for COVID-19. “In many ways, we’re one of the best-prepared sectors for this test,” she said.

Six months later, colleges are still being tested.

This KHN story first published on California Healthline, a service of the California Health Care Foundation.

Kaiser Health News (KHN) is a national health policy news service. It is an editorially independent program of the Henry J. Kaiser Family Foundation which is not affiliated with Kaiser Permanente.

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Clots, Strokes and Rashes: Is COVID a Disease of the Blood Vessels?

Whether it’s strange rashes on the toes or blood clots in the brain, the widespread ravages of COVID-19 have increasingly led researchers to focus on how the novel coronavirus sabotages blood vessels.

As scientists have come to know the disease better, they have homed in on the vascular system — the body’s network of arteries, veins and capillaries, stretching more than 60,000 miles — to understand this wide-ranging disease and to find treatments that can stymie its most pernicious effects.

Some of the earliest insights into how COVID-19 can act like a vascular disease came from studying the aftermath of the most serious infections. Those reveal that the virus warps a critical piece of our vascular infrastructure: the single layer of cells lining the inside of every blood vessel, known as the endothelial cells or simply the endothelium.

Dr. William Li, a vascular biologist, compares this lining to a freshly resurfaced ice rink before a hockey game on which the players and pucks glide smoothly along.

“When the virus damages the inside of the blood vessel and shreds the lining, that’s like the ice after a hockey game,” said Li, a researcher and founder of the Angiogenesis Foundation. “You wind up with a situation that is really untenable for blood flow.”

In a study published this summer, Li and an international team of researchers compared the lung tissues of people who died of COVID-19 with those of people who died of influenza. They found stark differences: The lung tissues of the COVID victims had nine times as many tiny blood clots (“microthrombi”) as those of the influenza victims, and the coronavirus-infected lungs also exhibited “severe endothelial injury.”

“The surprise was that this respiratory virus makes a beeline for the cells lining blood vessels, filling them up like a gumball machine and shredding the cell from the inside out,” Li said. “We found blood vessels are blocked and blood clots are forming because of that lining damage.”

It’s already known that the coronavirus breaks into cells by way of a specific receptor, called ACE2, which is found all over the body. But scientists are still trying to understand how the virus sets off a cascade of events that cause so much destruction to blood vessels. Li said one theory is that the virus directly attacks endothelial cells. Lab experiments have shown that the coronavirus can infect engineered human endothelial cells.

It’s also possible the problems begin elsewhere, and the endothelial cells sustain collateral damage along the way as the immune system reacts — and sometimes overreacts — to the invading virus.

Endothelial cells have a slew of important jobs; these include preventing clotting, controlling blood pressure, regulating oxidative stress and fending off pathogens. And Li said uncovering how the virus jeopardizes the endothelium may link many of COVID-19’s complications: “the effects in the brain, the blood clots in the lung and elsewhere in the legs, the COVID toe, the problem with the kidneys and even the heart.”

In Spain, skin biopsies of distinctive red lesions on toes, known as chilblains, found viral particles in the endothelial cells, leading the authors to conclude that “endothelial damage induced by the virus could be the key mechanism.”

Is Blood Vessel Damage Behind COVID Complications?

With a surface area larger than a football field, the endothelium helps maintain a delicate balance in the bloodstream. These cells are essentially the gatekeeper to the bloodstream.

“The endothelium has developed a distant early warning system to alert the body to get ready for an invasion if there’s trouble brewing,” said Dr. Peter Libby, a cardiologist and research scientist at Harvard Medical School. When that happens, endothelial cells change the way they function, he said. But that process can go too far.

“The very functions that help us maintain health and fight off invaders, when they run out of control, then it can actually make the disease worse,” Libby said.

In that case, the endothelial cells turn against their host and start to promote clotting and high blood pressure.

“In COVID-19 patients, we have both of these markers of dysfunction,” said Dr. Gaetano Santulli, a cardiologist and researcher at the Albert Einstein College of Medicine in New York City.

The novel coronavirus triggers a condition seen in other cardiovascular diseases called endothelial dysfunction. Santulli, who wrote about this idea in the spring, said that may be the “cornerstone” of organ dysfunction in COVID patients.

“The common denominator in all of these COVID-19 patients is endothelial dysfunction,” he said. “It’s like the virus knows where to go and knows how to attack these cells.”

Runaway Immune Response Adds a Plot Twist

A major source of damage to the vascular system likely also comes from the body’s own runaway immune response to the coronavirus.

“What we see with the SARS-CoV-2 is really an unprecedented level of inflammation in the bloodstream,” said Dr. Yogen Kanthi, a cardiologist and vascular medicine specialist at the National Institutes of Health who’s researching this phase of the illness. “This virus is leveraging its ability to create inflammation, and that has these deleterious, nefarious effects downstream.”

When inflammation spreads through the inner lining of the blood vessels — a condition called endothelialitis — blood clots can form throughout the body, starving tissues of oxygen and promoting even more inflammation.

“We start to get this relentless, self-amplifying cycle of inflammation in the body, which can then lead to more clotting and more inflammation,” Kanthi said.

Another sign of endothelial damage comes from analyzing the blood of COVID patients. A recent study found elevated levels of a protein produced by endothelial cells, called von Willebrand factor, that is involved in clotting.

“They are through the roof in those who are critically ill,” said Dr. Alfred Lee, a hematologist at the Yale Cancer Center who coauthored the study with Hyung Chun, a cardiologist and vascular biologist at Yale.

Lee pointed out that some autoimmune diseases can lead to a similar interplay of clotting and inflammation called immunothrombosis.

Chun said the elevated levels of von Willebrand factor show that vascular injury can be detected in patients while in the hospital — and perhaps even before, which could help predict their likelihood of developing more serious complications.

But he said it’s not yet clear what is the driving force behind the blood vessel damage: “It does seem to be a progression of disease that really brings out this endothelial injury. The key question is, what’s the root cause of this?”

After they presented their data, Lee said, Yale’s hospital system started putting patients who were critically ill with COVID-19 on aspirin, which can prevent clotting. While the best combinations and dosages are still being studied, research indicates blood thinners may improve outcomes in COVID patients.

Chun said treatments are also being studied that may more directly protect endothelial cells from the coronavirus.

“Is that the end-all-be-all to treating COVID-19? I absolutely don’t think so. There’s so many aspects of the disease that we still don’t understand,” he said.

COVID Is Often a Vascular ‘Stress Test’

Early in the pandemic, Dr. Roger Seheult, a critical care and pulmonary physician in Southern California, realized the patients he expected to be most vulnerable to a respiratory virus, those with underlying lung conditions such as chronic obstructive pulmonary disease and asthma, were not the ones ending up disproportionately in his intensive care unit. Seheult, who runs the popular medical education website MedCram, said, “Instead, what we are seeing are patients who are obese, people who have large BMIs, people who have Type 2 diabetes and with high blood pressure.”

Over time, all those conditions can cause inflammation and damage to the lining of blood vessels, he said, including a harmful chemical imbalance known as oxidative stress. Seheult said infection with the coronavirus becomes an added stress for people with those conditions that already tax the blood vessels: “If you’re right on the edge and you get the wind blown from this coronavirus, now you’ve gone over the edge.”

He said the extensive damage to blood vessels could explain why COVID patients with severe respiratory problems don’t necessarily resemble patients who get sick from the flu.

“They are having shortness of breath, but we have to realize the lungs are more than just the airways,” he said. “It’s an issue with the blood vessels themselves.”

This is why COVID patients struggle to fill their blood supply with oxygen, even when air is being pumped into their lungs.

“The endothelial cells get leaky, so instead of being like saran wrap, it turns into a sieve and then it allows fluid from the bloodstream to accumulate in the air spaces,” Harvard’s Libby said.

Doctors who treat COVID-19 are now keenly aware that complications such as strokes and heart problems can appear even after a patient gets better and their breathing improves.

“They are off oxygen, they can be discharged home, but their vasculature is not completely resolved. They still have inflammation,” he said. “What can happen is they develop a blood clot, and they have a massive pulmonary embolism.”

Patients can be closely monitored for these problems, but one of the big unknowns for doctors and patients is the long-term effects of COVID-19 on the circulatory system. The Angiogenesis Foundation’s Li puts it this way: “The virus enters your body and it leaves your body. You might or might not have gotten sick. But is that leaving behind a trashed vascular system?”

This story is part of a partnership that includes NPR and Kaiser Health News.

Kaiser Health News (KHN) is a national health policy news service. It is an editorially independent program of the Henry J. Kaiser Family Foundation which is not affiliated with Kaiser Permanente.

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KHN’s ‘What the Health?’: Transition Interrupted

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Five days after the election was called for President-elect Joe Biden, President Donald Trump has not conceded — and instead ordered his administration not to begin the transition of power. That could have serious ramifications for health care, particularly as nearly every state is experiencing a spike in COVID-19 cases.

One piece of good news is that early results for a coronavirus vaccine made by Pfizer look promising. But that vaccine, even if it is approved soon, won’t likely be ready for wide distribution for several months.

And for the third time in eight years, the Supreme Court heard a case that could invalidate the Affordable Care Act. Judging from the oral arguments, though, it appears the justices are likely to leave most or even all of the law intact.

This week’s panelists are Julie Rovner of Kaiser Health News, Joanne Kenen of Politico, Stephanie Armour of The Wall Street Journal and Shefali Luthra of the 19th News.

Among the takeaways from this week’s podcast:

• The transition teams advising Biden cannot officially contact current government officials. But many team members have long-standing relationships with people in the government and were talking to those officials before the election, so they have a good sense of what is happening in the administration.
• The pandemic further complicates the handoff. The new administration will need to hit the ground running to distribute any coronavirus vaccine, so communication with Trump administration officials would be beneficial for the Biden team.
• Two members of Biden’s COVID task force, Drs. Vivek Murthy, former surgeon general, and David Kessler, former commissioner of the Food and Drug Administration, have been briefing the former vice president since March on the threats of the coronavirus.
• Since Democrats may not control the Senate — and if they do have control, it will be by the slimmest majority — Biden may be forced to make changes to health policy through executive actions and regulations. That will limit his ambitions.
• Still, even these smaller moves can have major results, such as allowing Planned Parenthood to again participate in federal health programs to expand the number of providers from which low-income women can seek care.
• The Pfizer vaccine requires extremely cold temperatures for storage, complicating the logistics for distribution. It is an obstacle but not an insurmountable one for most areas in this country.
• Supreme Court justices signaled this week they might not strike the Affordable Care Act in its entirety. Several of the conservatives, including Justice Brett Kavanaugh, who was appointed by President Donald Trump, suggested that any ruling that the mandate to have insurance is unconstitutional does not have to doom the rest of the law.

Plus, for extra credit, the panelists recommend their favorite health policy stories of the week they think you should read too:

Julie Rovner: KHN and The Washington Post’s “In Medical Schools, Students Seek Robust and Mandatory Anti-Racist Training,” by Elizabeth Lawrence

Joanne Kenen: KHN’s “Trump’s Anti-Abortion Zeal Shook Fragile Health Systems Around the World,” by Sarah Varney

Stephanie Armour: KHN’s “Biden Plan to Lower Medicare Eligibility Age to 60 Faces Hostility From Hospitals,” by Phil Galewitz

Shefali Luthra: Stat News’ “With a Meteoric Rise in Deaths, Talk of Waves Is Misguided, Say Covid-19 Modelers,” by Elizabeth Cooney

To hear all our podcasts, click here.

And subscribe to What the Health? on iTunes, Stitcher, Google Play, Spotify, or Pocket Casts.

Kaiser Health News (KHN) is a national health policy news service. It is an editorially independent program of the Henry J. Kaiser Family Foundation which is not affiliated with Kaiser Permanente.

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