‘Munchausen by Internet’ crises a warning for all HCPs

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Mon, 08/09/2021 - 08:02

A new study documents a handful of cases of women with Munchausen syndrome by Internet who targeted doulas in the United Kingdom during the COVID-19 lockdown. The women pretended to have a variety of dramatic perinatal crises that garnered them significant attention from birth support professionals.

Dr. Kathryn Newns

The five cases were investigated by Kathryn Newns, MSc, DClinPsy, a clinical psychologist in Cambridge, England, who said the cases were brought to her attention by a doula she herself had used for the birth of her own child a decade earlier.

Dr. Newns said she believes these are not isolated cases – either geographically or in terms of the specialty involved.

“I don’t think it is likely that this is only happening in the United Kingdom. And I’m sure it’s not just happening in the doula world,” Dr. Newns told this news organization.

Coinvestigator Marc Feldman, MD, a clinical professor of psychiatry at the University of Alabama, Tuscaloosa, coined the term “Munchausen by Internet” in a 2000 article. The expression refers to use of electronic media to perpetrate hoaxes that reward posers with sympathy, control, or emotional gratification. The hoaxers do not seek financial gain.

“The ease of carrying out Munchausen behaviors makes me think that it must be much more common than it ever was,” Dr. Feldman said in an interview.

He noted that the new DSM-5 will eliminate the terms “Munchausen” and “Munchausen by Internet” and will clarify that “factitious disorder” can be partly or wholly carried out online.

The study was published in the May issue of the Annals of Clinical Psychiatry.
 

A warning for others

In the past, those with factitious disorder had to go to medical libraries to study up on the ailment they wanted to feign. They would then present to an emergency department or a doctor’s office and act convincingly, Dr. Feldman said.

“Now all you have to do is go to Wikipedia and you can become an expert on a medical ailment within a few minutes,” he added.

In the five cases described in the study, the hoaxers created rich stories, especially in cases 1 and 2. In those cases, the perpetrator turned out to be the same person. Subterfuge “obviously made it much harder to know she wasn’t who she purported to be,” said Dr. Newns.

Dr. Feldman noted that in Munchausen by Internet, there may be some element of truth within the stories.

For health care professionals, “it takes a considerable leap to assume that somebody who’s talking about some dreaded ailment is in fact exaggerating or outright lying,” he said.

In the five cases described in the study, persons contacted doulas, then related traumatic stories and described dramatic, immediate needs. All of the doulas were working remotely because of the COVID-19 pandemic. This likely made it easier for the perpetrators to pull off the hoaxes. The health care professionals agreed to share their experiences in the hopes of warning others.
 

Elaborate scenarios

The first two cases were ultimately determined to involve one person who had created elaborate scenarios.

In case 1, the hoaxer, who called herself “Jessica,” texted the doula “Charlotte” when she was allegedly 39 weeks’ pregnant. She said she was unable to go to the hospital because of the COVID-19 risks to her husband, who had cystic fibrosis and had recently undergone a heart and lung transplant.

The husband “Jordan” took over communications, using the same WhatsApp number as Jessica, as Jessica went into labor.

Ostensibly, a midwife team had come to Jessica’s and Jordan’s house. When the doula was on the phone with Jordan, she heard Jessica crying, grunting, and screaming, and then, at 2:00 a.m., she heard the sound of a baby crying. A photo of the baby was texted to Charlotte.

Soon, there were many problems. Jessica allegedly had a postpartum hemorrhage, and mother and baby were taken to separate hospitals. The baby was then diagnosed with congenital heart disease.

Over the next week, “midwives” started texting back and forth with Charlotte. The doula began to have doubts and asked a midwife to share a visual communication.

After receiving no response, Charlotte used a video call, got Jessica on screen, and told her she thought there was no baby. Jessica said the baby was real and showed a “growth chart” as proof of the 5-day-old baby’s existence. The birth and baby noises were later determined to be recordings.
 

Child deaths

After sharing information among themselves on a private Facebook group, the doulas determined that the person in case 2, “Dakota,” was the same woman who was involved in case 1.

In case 2, a doula had spent 2 years supporting Dakota through the deaths of a parent and her baby, who had a congenital defect. A baby-loss charity had also worked with Dakota but could not confirm the baby’s existence.

Dakota had gone so far as to make a video for the doula that showed a hospital room. In a voice-over, Dakota thanks everyone for the support she received as the baby died.

In case 3, “Hannah” texted a doula seeking emotional but not birth support. The doula, Nikki Barrow, has recounted the case on her own blog.

Hannah became desperate when she went into labor. Ms. Barrow remained close via texts, phone, and video calls, even as the baby supposedly died after 3 days. The doula lit a candle for the baby and cried with Hannah.

Ms. Barrow was eventually able to break away from Hannah, saying she was not a bereavement specialist. However, days later, Hannah tracked her down and claimed she had an infection in her heart and did not have much time to live. At that point, Ms. Barrow stopped all contact.

She determined from other doulas that Hannah had been hoaxing doulas for 4 or 5 years. Some had offered to get her help, but she refused and ended all contact.
 

Multiple COVID crises?

In case 4, a woman sought support on a doula-centered Facebook page and said her partner “Jack” would be in touch. Jack sent the doula hundreds of emails, texts, and WhatsApp messages and then said he was hospitalized with COVID. The woman, “Hayley,” was also soon diagnosed with COVID.

Hayley refused video contact and did not share photos. Drama continued to unfold. She reported that her baby was breach, that she had a second uterus with a second pregnancy simultaneously, and that the baby had COVID.

Hayley also claimed that her partner had come to the hospital, had raped her, and had brandished a gun. When the doula called the police, they did not find Hayley at the hospital or elsewhere.

In case 5, a “grandmother” contacted “Lisa” to find a doula for her daughter-in-law, “Anna.” Hours later, Anna was giving birth, and the baby had to be taken to the hospital because of cardiac and breathing problems. The doula heard nothing more after a few weeks.

However, at least three other doulas said they had supported the same “family.”
 

Online training program

In all cases, the doulas were not paid for their time. Reports to the police prompted no action because no money had changed hands. Some doulas said they felt bereaved, angry, or “silly” that they had been hoodwinked. All noted how difficult it was to disengage from clients who seemed to be in peril.

Ms. Barrow decided to create an online training program in which doulas are advised on how to stay safe while working online.

DoulaMatch, which matches birth support specialists with women in the United States and Canada, offers tips to help protect doulas from hoaxes.

Kim James, BDT(DONA), ICCE, LCCE, CLE, the owner and operator of DoulaMatch, said the organization is aware of “scammers who waste everyone’s time and have found doulas to be the latest easy targets.”

However, she noted, “I’ve only very occasionally and anecdotally heard about people fabricating a pregnancy for emotional gratification.”

In his 2000 article, Dr. Feldman offers clues to help detect hoaxers. He advises clinicians to be wary of the following:

  • Cases in which the length, frequency, and duration of posts are incongruous with the severity of the illness the person is claiming to have; for example, someone who claims to be in  submitting detailed posts.
  • Near-fatal exacerbations of illness alternating with miraculous recoveries.
  • Personal claims that are fantastic, are contradicted by later posts, or are disproved.
  • Continual dramatic events occurring in the person’s life, especially when others in a group become the focus of attention.
  • Others ostensibly posting on behalf of the individual who have identical patterns of writing, such as making grammatical errors, misspellings, and using stylistic idiosyncrasies.

A version of this article first appeared on Medscape.com.

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A new study documents a handful of cases of women with Munchausen syndrome by Internet who targeted doulas in the United Kingdom during the COVID-19 lockdown. The women pretended to have a variety of dramatic perinatal crises that garnered them significant attention from birth support professionals.

Dr. Kathryn Newns

The five cases were investigated by Kathryn Newns, MSc, DClinPsy, a clinical psychologist in Cambridge, England, who said the cases were brought to her attention by a doula she herself had used for the birth of her own child a decade earlier.

Dr. Newns said she believes these are not isolated cases – either geographically or in terms of the specialty involved.

“I don’t think it is likely that this is only happening in the United Kingdom. And I’m sure it’s not just happening in the doula world,” Dr. Newns told this news organization.

Coinvestigator Marc Feldman, MD, a clinical professor of psychiatry at the University of Alabama, Tuscaloosa, coined the term “Munchausen by Internet” in a 2000 article. The expression refers to use of electronic media to perpetrate hoaxes that reward posers with sympathy, control, or emotional gratification. The hoaxers do not seek financial gain.

“The ease of carrying out Munchausen behaviors makes me think that it must be much more common than it ever was,” Dr. Feldman said in an interview.

He noted that the new DSM-5 will eliminate the terms “Munchausen” and “Munchausen by Internet” and will clarify that “factitious disorder” can be partly or wholly carried out online.

The study was published in the May issue of the Annals of Clinical Psychiatry.
 

A warning for others

In the past, those with factitious disorder had to go to medical libraries to study up on the ailment they wanted to feign. They would then present to an emergency department or a doctor’s office and act convincingly, Dr. Feldman said.

“Now all you have to do is go to Wikipedia and you can become an expert on a medical ailment within a few minutes,” he added.

In the five cases described in the study, the hoaxers created rich stories, especially in cases 1 and 2. In those cases, the perpetrator turned out to be the same person. Subterfuge “obviously made it much harder to know she wasn’t who she purported to be,” said Dr. Newns.

Dr. Feldman noted that in Munchausen by Internet, there may be some element of truth within the stories.

For health care professionals, “it takes a considerable leap to assume that somebody who’s talking about some dreaded ailment is in fact exaggerating or outright lying,” he said.

In the five cases described in the study, persons contacted doulas, then related traumatic stories and described dramatic, immediate needs. All of the doulas were working remotely because of the COVID-19 pandemic. This likely made it easier for the perpetrators to pull off the hoaxes. The health care professionals agreed to share their experiences in the hopes of warning others.
 

Elaborate scenarios

The first two cases were ultimately determined to involve one person who had created elaborate scenarios.

In case 1, the hoaxer, who called herself “Jessica,” texted the doula “Charlotte” when she was allegedly 39 weeks’ pregnant. She said she was unable to go to the hospital because of the COVID-19 risks to her husband, who had cystic fibrosis and had recently undergone a heart and lung transplant.

The husband “Jordan” took over communications, using the same WhatsApp number as Jessica, as Jessica went into labor.

Ostensibly, a midwife team had come to Jessica’s and Jordan’s house. When the doula was on the phone with Jordan, she heard Jessica crying, grunting, and screaming, and then, at 2:00 a.m., she heard the sound of a baby crying. A photo of the baby was texted to Charlotte.

Soon, there were many problems. Jessica allegedly had a postpartum hemorrhage, and mother and baby were taken to separate hospitals. The baby was then diagnosed with congenital heart disease.

Over the next week, “midwives” started texting back and forth with Charlotte. The doula began to have doubts and asked a midwife to share a visual communication.

After receiving no response, Charlotte used a video call, got Jessica on screen, and told her she thought there was no baby. Jessica said the baby was real and showed a “growth chart” as proof of the 5-day-old baby’s existence. The birth and baby noises were later determined to be recordings.
 

Child deaths

After sharing information among themselves on a private Facebook group, the doulas determined that the person in case 2, “Dakota,” was the same woman who was involved in case 1.

In case 2, a doula had spent 2 years supporting Dakota through the deaths of a parent and her baby, who had a congenital defect. A baby-loss charity had also worked with Dakota but could not confirm the baby’s existence.

Dakota had gone so far as to make a video for the doula that showed a hospital room. In a voice-over, Dakota thanks everyone for the support she received as the baby died.

In case 3, “Hannah” texted a doula seeking emotional but not birth support. The doula, Nikki Barrow, has recounted the case on her own blog.

Hannah became desperate when she went into labor. Ms. Barrow remained close via texts, phone, and video calls, even as the baby supposedly died after 3 days. The doula lit a candle for the baby and cried with Hannah.

Ms. Barrow was eventually able to break away from Hannah, saying she was not a bereavement specialist. However, days later, Hannah tracked her down and claimed she had an infection in her heart and did not have much time to live. At that point, Ms. Barrow stopped all contact.

She determined from other doulas that Hannah had been hoaxing doulas for 4 or 5 years. Some had offered to get her help, but she refused and ended all contact.
 

Multiple COVID crises?

In case 4, a woman sought support on a doula-centered Facebook page and said her partner “Jack” would be in touch. Jack sent the doula hundreds of emails, texts, and WhatsApp messages and then said he was hospitalized with COVID. The woman, “Hayley,” was also soon diagnosed with COVID.

Hayley refused video contact and did not share photos. Drama continued to unfold. She reported that her baby was breach, that she had a second uterus with a second pregnancy simultaneously, and that the baby had COVID.

Hayley also claimed that her partner had come to the hospital, had raped her, and had brandished a gun. When the doula called the police, they did not find Hayley at the hospital or elsewhere.

In case 5, a “grandmother” contacted “Lisa” to find a doula for her daughter-in-law, “Anna.” Hours later, Anna was giving birth, and the baby had to be taken to the hospital because of cardiac and breathing problems. The doula heard nothing more after a few weeks.

However, at least three other doulas said they had supported the same “family.”
 

Online training program

In all cases, the doulas were not paid for their time. Reports to the police prompted no action because no money had changed hands. Some doulas said they felt bereaved, angry, or “silly” that they had been hoodwinked. All noted how difficult it was to disengage from clients who seemed to be in peril.

Ms. Barrow decided to create an online training program in which doulas are advised on how to stay safe while working online.

DoulaMatch, which matches birth support specialists with women in the United States and Canada, offers tips to help protect doulas from hoaxes.

Kim James, BDT(DONA), ICCE, LCCE, CLE, the owner and operator of DoulaMatch, said the organization is aware of “scammers who waste everyone’s time and have found doulas to be the latest easy targets.”

However, she noted, “I’ve only very occasionally and anecdotally heard about people fabricating a pregnancy for emotional gratification.”

In his 2000 article, Dr. Feldman offers clues to help detect hoaxers. He advises clinicians to be wary of the following:

  • Cases in which the length, frequency, and duration of posts are incongruous with the severity of the illness the person is claiming to have; for example, someone who claims to be in  submitting detailed posts.
  • Near-fatal exacerbations of illness alternating with miraculous recoveries.
  • Personal claims that are fantastic, are contradicted by later posts, or are disproved.
  • Continual dramatic events occurring in the person’s life, especially when others in a group become the focus of attention.
  • Others ostensibly posting on behalf of the individual who have identical patterns of writing, such as making grammatical errors, misspellings, and using stylistic idiosyncrasies.

A version of this article first appeared on Medscape.com.

A new study documents a handful of cases of women with Munchausen syndrome by Internet who targeted doulas in the United Kingdom during the COVID-19 lockdown. The women pretended to have a variety of dramatic perinatal crises that garnered them significant attention from birth support professionals.

Dr. Kathryn Newns

The five cases were investigated by Kathryn Newns, MSc, DClinPsy, a clinical psychologist in Cambridge, England, who said the cases were brought to her attention by a doula she herself had used for the birth of her own child a decade earlier.

Dr. Newns said she believes these are not isolated cases – either geographically or in terms of the specialty involved.

“I don’t think it is likely that this is only happening in the United Kingdom. And I’m sure it’s not just happening in the doula world,” Dr. Newns told this news organization.

Coinvestigator Marc Feldman, MD, a clinical professor of psychiatry at the University of Alabama, Tuscaloosa, coined the term “Munchausen by Internet” in a 2000 article. The expression refers to use of electronic media to perpetrate hoaxes that reward posers with sympathy, control, or emotional gratification. The hoaxers do not seek financial gain.

“The ease of carrying out Munchausen behaviors makes me think that it must be much more common than it ever was,” Dr. Feldman said in an interview.

He noted that the new DSM-5 will eliminate the terms “Munchausen” and “Munchausen by Internet” and will clarify that “factitious disorder” can be partly or wholly carried out online.

The study was published in the May issue of the Annals of Clinical Psychiatry.
 

A warning for others

In the past, those with factitious disorder had to go to medical libraries to study up on the ailment they wanted to feign. They would then present to an emergency department or a doctor’s office and act convincingly, Dr. Feldman said.

“Now all you have to do is go to Wikipedia and you can become an expert on a medical ailment within a few minutes,” he added.

In the five cases described in the study, the hoaxers created rich stories, especially in cases 1 and 2. In those cases, the perpetrator turned out to be the same person. Subterfuge “obviously made it much harder to know she wasn’t who she purported to be,” said Dr. Newns.

Dr. Feldman noted that in Munchausen by Internet, there may be some element of truth within the stories.

For health care professionals, “it takes a considerable leap to assume that somebody who’s talking about some dreaded ailment is in fact exaggerating or outright lying,” he said.

In the five cases described in the study, persons contacted doulas, then related traumatic stories and described dramatic, immediate needs. All of the doulas were working remotely because of the COVID-19 pandemic. This likely made it easier for the perpetrators to pull off the hoaxes. The health care professionals agreed to share their experiences in the hopes of warning others.
 

Elaborate scenarios

The first two cases were ultimately determined to involve one person who had created elaborate scenarios.

In case 1, the hoaxer, who called herself “Jessica,” texted the doula “Charlotte” when she was allegedly 39 weeks’ pregnant. She said she was unable to go to the hospital because of the COVID-19 risks to her husband, who had cystic fibrosis and had recently undergone a heart and lung transplant.

The husband “Jordan” took over communications, using the same WhatsApp number as Jessica, as Jessica went into labor.

Ostensibly, a midwife team had come to Jessica’s and Jordan’s house. When the doula was on the phone with Jordan, she heard Jessica crying, grunting, and screaming, and then, at 2:00 a.m., she heard the sound of a baby crying. A photo of the baby was texted to Charlotte.

Soon, there were many problems. Jessica allegedly had a postpartum hemorrhage, and mother and baby were taken to separate hospitals. The baby was then diagnosed with congenital heart disease.

Over the next week, “midwives” started texting back and forth with Charlotte. The doula began to have doubts and asked a midwife to share a visual communication.

After receiving no response, Charlotte used a video call, got Jessica on screen, and told her she thought there was no baby. Jessica said the baby was real and showed a “growth chart” as proof of the 5-day-old baby’s existence. The birth and baby noises were later determined to be recordings.
 

Child deaths

After sharing information among themselves on a private Facebook group, the doulas determined that the person in case 2, “Dakota,” was the same woman who was involved in case 1.

In case 2, a doula had spent 2 years supporting Dakota through the deaths of a parent and her baby, who had a congenital defect. A baby-loss charity had also worked with Dakota but could not confirm the baby’s existence.

Dakota had gone so far as to make a video for the doula that showed a hospital room. In a voice-over, Dakota thanks everyone for the support she received as the baby died.

In case 3, “Hannah” texted a doula seeking emotional but not birth support. The doula, Nikki Barrow, has recounted the case on her own blog.

Hannah became desperate when she went into labor. Ms. Barrow remained close via texts, phone, and video calls, even as the baby supposedly died after 3 days. The doula lit a candle for the baby and cried with Hannah.

Ms. Barrow was eventually able to break away from Hannah, saying she was not a bereavement specialist. However, days later, Hannah tracked her down and claimed she had an infection in her heart and did not have much time to live. At that point, Ms. Barrow stopped all contact.

She determined from other doulas that Hannah had been hoaxing doulas for 4 or 5 years. Some had offered to get her help, but she refused and ended all contact.
 

Multiple COVID crises?

In case 4, a woman sought support on a doula-centered Facebook page and said her partner “Jack” would be in touch. Jack sent the doula hundreds of emails, texts, and WhatsApp messages and then said he was hospitalized with COVID. The woman, “Hayley,” was also soon diagnosed with COVID.

Hayley refused video contact and did not share photos. Drama continued to unfold. She reported that her baby was breach, that she had a second uterus with a second pregnancy simultaneously, and that the baby had COVID.

Hayley also claimed that her partner had come to the hospital, had raped her, and had brandished a gun. When the doula called the police, they did not find Hayley at the hospital or elsewhere.

In case 5, a “grandmother” contacted “Lisa” to find a doula for her daughter-in-law, “Anna.” Hours later, Anna was giving birth, and the baby had to be taken to the hospital because of cardiac and breathing problems. The doula heard nothing more after a few weeks.

However, at least three other doulas said they had supported the same “family.”
 

Online training program

In all cases, the doulas were not paid for their time. Reports to the police prompted no action because no money had changed hands. Some doulas said they felt bereaved, angry, or “silly” that they had been hoodwinked. All noted how difficult it was to disengage from clients who seemed to be in peril.

Ms. Barrow decided to create an online training program in which doulas are advised on how to stay safe while working online.

DoulaMatch, which matches birth support specialists with women in the United States and Canada, offers tips to help protect doulas from hoaxes.

Kim James, BDT(DONA), ICCE, LCCE, CLE, the owner and operator of DoulaMatch, said the organization is aware of “scammers who waste everyone’s time and have found doulas to be the latest easy targets.”

However, she noted, “I’ve only very occasionally and anecdotally heard about people fabricating a pregnancy for emotional gratification.”

In his 2000 article, Dr. Feldman offers clues to help detect hoaxers. He advises clinicians to be wary of the following:

  • Cases in which the length, frequency, and duration of posts are incongruous with the severity of the illness the person is claiming to have; for example, someone who claims to be in  submitting detailed posts.
  • Near-fatal exacerbations of illness alternating with miraculous recoveries.
  • Personal claims that are fantastic, are contradicted by later posts, or are disproved.
  • Continual dramatic events occurring in the person’s life, especially when others in a group become the focus of attention.
  • Others ostensibly posting on behalf of the individual who have identical patterns of writing, such as making grammatical errors, misspellings, and using stylistic idiosyncrasies.

A version of this article first appeared on Medscape.com.

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Oncologists face nightmares every day with prior authorization

Article Type
Changed
Thu, 08/05/2021 - 14:34

 

Editor’s note: Prior authorization has been flagged as the biggest payer-related cause of stress for U.S. oncologists. In one survey, 75% said prior authorization was their biggest burden, followed by coverage denials and appeals (62%). Another survey found that practices spent on average 16.4 hours a week dealing with prior authorizations.

In the 16 years since I went into practice as a medical oncologist, the issue of prior authorization has become a nightmare.

Around 5% of my emails every day are from insurance companies denying my patients the treatments I have recommended. A part of every day is spent worrying about how I’m going to cover my patients’ therapy and what I need to order to make sure it doesn’t get delayed.

Many doctors are retiring because they don’t want to deal with this anymore. There are many times that I have thought about quitting for this reason. A partner of mine had a heart attack last year. He’s a few years older than I am – in his mid-50s – and that scared me. I actually had a CT angiogram just to make sure. They told me my heart is fine, but I worry because of all these frustrations every day. And I’m not alone. For every doctor I work with, it’s the same story, and it’s just ridiculous.

For example, I had a patient with a huge breast mass. My nurse got me the prior authorization for an emergency biopsy. I got back the results for estrogen and progesterone receptor status, but not the HER2-neu results because that test required another authorization.

Authorization shouldn’t be required for every single step. I understand if maybe you need to get an authorization to do something outside the standard of care or something that is unique or unheard of, but HER2-neu biopsy is standard of care and should not require additional authorization.

And the sad part is, that patient turned out to be HER2-neu positive. She lost 4 weeks just waiting for an authorization of a test that should be a no-brainer.

We cannot even do a blood count in our office before getting authorization from some insurances. This is a very important test when we give chemotherapy, and it’s very cheap.

And then another nightmare is if you want to give a patient growth factors when you see their blood count is going down. Sometimes the insurance company will say, “When they get neutropenic fever, we’ll allow it with the next cycle.” Why do I have to wait until the patient develops such a problem to start with a treatment that could avoid it? They may end up in the hospital.

I think I’m one of the more conservative doctors; I try to do everything scientifically and only order a test or a treatment if it’s indicated. But sometimes this guidance costs more money. For example, an insurance company may say to order a CT scan first and if you don’t find your answer, then get a PET scan.

So I order a CT scan, knowing it’s not going to help, and then I tell them, “Now I need a PET scan.” That’s another week delay and an extra cost that I don’t want the system to incur.

I’ve even had some issues with lung screening scans for smokers. This screening has reduced mortality by 20%; it should be a no-brainer to encourage smokers to do it because many of them may not even need chemotherapy if you find early-stage lung cancer. And the screening is not expensive, you can do it for $90 to $100. So why do we have to get authorization for that?

Sometimes I push back and request a “peer-to-peer,” where you challenge the decision of the insurance company and speak to one of their doctors. Out of 10 doctors, maybe three or four will do the peer-to-peer. The rest will give up because it’s so frustrating.

In one case, I wanted to modify a standard regimen and give only two out of three drugs because I thought the third would be too toxic. But the insurance company wouldn’t approve the regimen because the guidelines say you have to give three drugs.

Guidelines are guidance, they should not dictate how you treat an individual patient – there should be some allowance in there for a doctor’s discretion. If not, why do we even need doctors? We could just follow treatment regimens dictated by computers. They have to allow me to personalize the care that my patient deserves and make changes so that the treatment can be tolerated.

But then, I get that one patient whom I feel I really helped and I realize, “Okay, I can help more people.”

I had this one patient, a young, 40-year-old nurse with breast cancer – also HER2-neu positive. She’d had her surgery and finished her adjuvant chemotherapy. One of the things that you do as standard of care, after a year of trastuzumab, is you start them on neratinib. There are studies that show it improves progression-free survival if you give them an extra year of this drug as an adjuvant.

I prescribed the neratinib, but the insurance company denied it because the patient “did not have positive lymph nodes and was not considered high risk.” I told them, “That’s BS, that’s not what the indication is for.” I asked for a peer-to-peer and they said the policy did not allow for peer-to-peer. So, I made a big fuss about it. We appealed, and I finally spoke to a pharmacist who worked for the insurance company. I told him, “Why did you guys deny this? It’s standard of care.” He said, “Oh, I agree with you, this will be approved. And actually, we’re going to change the policy now.”

When that pharmacist told me they were going to change the policy, it was like someone gave me 1 million dollars. Because, you know what? I didn’t just help my patient; now other patients will also get it. The hope is that if you keep fighting for something, they will change it.

I think every doctor wants to do the best for their patients. It’s not like they don’t want to, but really, I am fortunate that I have the means to do it. We’re a big practice and we have dedicated staff who can help.

If you’re a small practice, it’s almost impossible to deal with this. I have two nurse practitioners, and a lot of their work is filling out paperwork for insurance companies.

We had a colleague, a solo practitioner, who would send us his patients with complicated therapies, because he couldn’t afford the time or the effort or the risk of not getting reimbursed. His practice could have paid out $100,000 for drugs and not get a reimbursement for a few months.

Even when an insurance company does give the preauthorization, there’s always this disclaimer that it doesn’t guarantee payment. If they find in the future that your patient didn’t meet the criteria, they can still deny payment.

If the insurers refuse coverage, we really work hard at getting patients free drugs, and most of the time, we manage to do that. We either look to charitable organizations, like the Leukemia and Lymphoma Society, or we look for rare disease societies or we go to the pharmaceutical company.

For really expensive drugs, pharmaceutical companies have a program where you can enroll the patient and they can help copay or even cover the drug. For less expensive drugs, it might not be a big problem, but for a drug that can cost $18,000 to $20,000 a month, that’s a big risk to take.

It’s confusing for patients, too. They get angry and frustrated, and that’s not good for their treatment, because attitude and psychology are very important. Sometimes they yell at us because they think it’s our fault. I encourage them to call their insurance companies themselves, and some of them do.

I don’t do it with every patient, but there are some more educated patients who are advocates, and if their condition is stable, I do encourage them to call their senators or congressmen or congresswomen to complain.

I don’t mind treating complicated patients. I don’t want to say I enjoy it, but I like challenges. That’s my field, that’s medicine, that’s what I’m supposed to do. But it’s really sad and frustrating that, when you want to treat a patient, you first have to look at their insurance to see how much care you can actually give them.

Maen Hussein, MD, is physician director of finance at Florida Cancer Specialists and Research Institute, Fort Myers. He is a board member of the Florida Cancer Specialists Foundation and sits on the board of directors for the Florida Society of Clinical Oncology.

A version of this article first appeared on Medscape.com.

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Editor’s note: Prior authorization has been flagged as the biggest payer-related cause of stress for U.S. oncologists. In one survey, 75% said prior authorization was their biggest burden, followed by coverage denials and appeals (62%). Another survey found that practices spent on average 16.4 hours a week dealing with prior authorizations.

In the 16 years since I went into practice as a medical oncologist, the issue of prior authorization has become a nightmare.

Around 5% of my emails every day are from insurance companies denying my patients the treatments I have recommended. A part of every day is spent worrying about how I’m going to cover my patients’ therapy and what I need to order to make sure it doesn’t get delayed.

Many doctors are retiring because they don’t want to deal with this anymore. There are many times that I have thought about quitting for this reason. A partner of mine had a heart attack last year. He’s a few years older than I am – in his mid-50s – and that scared me. I actually had a CT angiogram just to make sure. They told me my heart is fine, but I worry because of all these frustrations every day. And I’m not alone. For every doctor I work with, it’s the same story, and it’s just ridiculous.

For example, I had a patient with a huge breast mass. My nurse got me the prior authorization for an emergency biopsy. I got back the results for estrogen and progesterone receptor status, but not the HER2-neu results because that test required another authorization.

Authorization shouldn’t be required for every single step. I understand if maybe you need to get an authorization to do something outside the standard of care or something that is unique or unheard of, but HER2-neu biopsy is standard of care and should not require additional authorization.

And the sad part is, that patient turned out to be HER2-neu positive. She lost 4 weeks just waiting for an authorization of a test that should be a no-brainer.

We cannot even do a blood count in our office before getting authorization from some insurances. This is a very important test when we give chemotherapy, and it’s very cheap.

And then another nightmare is if you want to give a patient growth factors when you see their blood count is going down. Sometimes the insurance company will say, “When they get neutropenic fever, we’ll allow it with the next cycle.” Why do I have to wait until the patient develops such a problem to start with a treatment that could avoid it? They may end up in the hospital.

I think I’m one of the more conservative doctors; I try to do everything scientifically and only order a test or a treatment if it’s indicated. But sometimes this guidance costs more money. For example, an insurance company may say to order a CT scan first and if you don’t find your answer, then get a PET scan.

So I order a CT scan, knowing it’s not going to help, and then I tell them, “Now I need a PET scan.” That’s another week delay and an extra cost that I don’t want the system to incur.

I’ve even had some issues with lung screening scans for smokers. This screening has reduced mortality by 20%; it should be a no-brainer to encourage smokers to do it because many of them may not even need chemotherapy if you find early-stage lung cancer. And the screening is not expensive, you can do it for $90 to $100. So why do we have to get authorization for that?

Sometimes I push back and request a “peer-to-peer,” where you challenge the decision of the insurance company and speak to one of their doctors. Out of 10 doctors, maybe three or four will do the peer-to-peer. The rest will give up because it’s so frustrating.

In one case, I wanted to modify a standard regimen and give only two out of three drugs because I thought the third would be too toxic. But the insurance company wouldn’t approve the regimen because the guidelines say you have to give three drugs.

Guidelines are guidance, they should not dictate how you treat an individual patient – there should be some allowance in there for a doctor’s discretion. If not, why do we even need doctors? We could just follow treatment regimens dictated by computers. They have to allow me to personalize the care that my patient deserves and make changes so that the treatment can be tolerated.

But then, I get that one patient whom I feel I really helped and I realize, “Okay, I can help more people.”

I had this one patient, a young, 40-year-old nurse with breast cancer – also HER2-neu positive. She’d had her surgery and finished her adjuvant chemotherapy. One of the things that you do as standard of care, after a year of trastuzumab, is you start them on neratinib. There are studies that show it improves progression-free survival if you give them an extra year of this drug as an adjuvant.

I prescribed the neratinib, but the insurance company denied it because the patient “did not have positive lymph nodes and was not considered high risk.” I told them, “That’s BS, that’s not what the indication is for.” I asked for a peer-to-peer and they said the policy did not allow for peer-to-peer. So, I made a big fuss about it. We appealed, and I finally spoke to a pharmacist who worked for the insurance company. I told him, “Why did you guys deny this? It’s standard of care.” He said, “Oh, I agree with you, this will be approved. And actually, we’re going to change the policy now.”

When that pharmacist told me they were going to change the policy, it was like someone gave me 1 million dollars. Because, you know what? I didn’t just help my patient; now other patients will also get it. The hope is that if you keep fighting for something, they will change it.

I think every doctor wants to do the best for their patients. It’s not like they don’t want to, but really, I am fortunate that I have the means to do it. We’re a big practice and we have dedicated staff who can help.

If you’re a small practice, it’s almost impossible to deal with this. I have two nurse practitioners, and a lot of their work is filling out paperwork for insurance companies.

We had a colleague, a solo practitioner, who would send us his patients with complicated therapies, because he couldn’t afford the time or the effort or the risk of not getting reimbursed. His practice could have paid out $100,000 for drugs and not get a reimbursement for a few months.

Even when an insurance company does give the preauthorization, there’s always this disclaimer that it doesn’t guarantee payment. If they find in the future that your patient didn’t meet the criteria, they can still deny payment.

If the insurers refuse coverage, we really work hard at getting patients free drugs, and most of the time, we manage to do that. We either look to charitable organizations, like the Leukemia and Lymphoma Society, or we look for rare disease societies or we go to the pharmaceutical company.

For really expensive drugs, pharmaceutical companies have a program where you can enroll the patient and they can help copay or even cover the drug. For less expensive drugs, it might not be a big problem, but for a drug that can cost $18,000 to $20,000 a month, that’s a big risk to take.

It’s confusing for patients, too. They get angry and frustrated, and that’s not good for their treatment, because attitude and psychology are very important. Sometimes they yell at us because they think it’s our fault. I encourage them to call their insurance companies themselves, and some of them do.

I don’t do it with every patient, but there are some more educated patients who are advocates, and if their condition is stable, I do encourage them to call their senators or congressmen or congresswomen to complain.

I don’t mind treating complicated patients. I don’t want to say I enjoy it, but I like challenges. That’s my field, that’s medicine, that’s what I’m supposed to do. But it’s really sad and frustrating that, when you want to treat a patient, you first have to look at their insurance to see how much care you can actually give them.

Maen Hussein, MD, is physician director of finance at Florida Cancer Specialists and Research Institute, Fort Myers. He is a board member of the Florida Cancer Specialists Foundation and sits on the board of directors for the Florida Society of Clinical Oncology.

A version of this article first appeared on Medscape.com.

 

Editor’s note: Prior authorization has been flagged as the biggest payer-related cause of stress for U.S. oncologists. In one survey, 75% said prior authorization was their biggest burden, followed by coverage denials and appeals (62%). Another survey found that practices spent on average 16.4 hours a week dealing with prior authorizations.

In the 16 years since I went into practice as a medical oncologist, the issue of prior authorization has become a nightmare.

Around 5% of my emails every day are from insurance companies denying my patients the treatments I have recommended. A part of every day is spent worrying about how I’m going to cover my patients’ therapy and what I need to order to make sure it doesn’t get delayed.

Many doctors are retiring because they don’t want to deal with this anymore. There are many times that I have thought about quitting for this reason. A partner of mine had a heart attack last year. He’s a few years older than I am – in his mid-50s – and that scared me. I actually had a CT angiogram just to make sure. They told me my heart is fine, but I worry because of all these frustrations every day. And I’m not alone. For every doctor I work with, it’s the same story, and it’s just ridiculous.

For example, I had a patient with a huge breast mass. My nurse got me the prior authorization for an emergency biopsy. I got back the results for estrogen and progesterone receptor status, but not the HER2-neu results because that test required another authorization.

Authorization shouldn’t be required for every single step. I understand if maybe you need to get an authorization to do something outside the standard of care or something that is unique or unheard of, but HER2-neu biopsy is standard of care and should not require additional authorization.

And the sad part is, that patient turned out to be HER2-neu positive. She lost 4 weeks just waiting for an authorization of a test that should be a no-brainer.

We cannot even do a blood count in our office before getting authorization from some insurances. This is a very important test when we give chemotherapy, and it’s very cheap.

And then another nightmare is if you want to give a patient growth factors when you see their blood count is going down. Sometimes the insurance company will say, “When they get neutropenic fever, we’ll allow it with the next cycle.” Why do I have to wait until the patient develops such a problem to start with a treatment that could avoid it? They may end up in the hospital.

I think I’m one of the more conservative doctors; I try to do everything scientifically and only order a test or a treatment if it’s indicated. But sometimes this guidance costs more money. For example, an insurance company may say to order a CT scan first and if you don’t find your answer, then get a PET scan.

So I order a CT scan, knowing it’s not going to help, and then I tell them, “Now I need a PET scan.” That’s another week delay and an extra cost that I don’t want the system to incur.

I’ve even had some issues with lung screening scans for smokers. This screening has reduced mortality by 20%; it should be a no-brainer to encourage smokers to do it because many of them may not even need chemotherapy if you find early-stage lung cancer. And the screening is not expensive, you can do it for $90 to $100. So why do we have to get authorization for that?

Sometimes I push back and request a “peer-to-peer,” where you challenge the decision of the insurance company and speak to one of their doctors. Out of 10 doctors, maybe three or four will do the peer-to-peer. The rest will give up because it’s so frustrating.

In one case, I wanted to modify a standard regimen and give only two out of three drugs because I thought the third would be too toxic. But the insurance company wouldn’t approve the regimen because the guidelines say you have to give three drugs.

Guidelines are guidance, they should not dictate how you treat an individual patient – there should be some allowance in there for a doctor’s discretion. If not, why do we even need doctors? We could just follow treatment regimens dictated by computers. They have to allow me to personalize the care that my patient deserves and make changes so that the treatment can be tolerated.

But then, I get that one patient whom I feel I really helped and I realize, “Okay, I can help more people.”

I had this one patient, a young, 40-year-old nurse with breast cancer – also HER2-neu positive. She’d had her surgery and finished her adjuvant chemotherapy. One of the things that you do as standard of care, after a year of trastuzumab, is you start them on neratinib. There are studies that show it improves progression-free survival if you give them an extra year of this drug as an adjuvant.

I prescribed the neratinib, but the insurance company denied it because the patient “did not have positive lymph nodes and was not considered high risk.” I told them, “That’s BS, that’s not what the indication is for.” I asked for a peer-to-peer and they said the policy did not allow for peer-to-peer. So, I made a big fuss about it. We appealed, and I finally spoke to a pharmacist who worked for the insurance company. I told him, “Why did you guys deny this? It’s standard of care.” He said, “Oh, I agree with you, this will be approved. And actually, we’re going to change the policy now.”

When that pharmacist told me they were going to change the policy, it was like someone gave me 1 million dollars. Because, you know what? I didn’t just help my patient; now other patients will also get it. The hope is that if you keep fighting for something, they will change it.

I think every doctor wants to do the best for their patients. It’s not like they don’t want to, but really, I am fortunate that I have the means to do it. We’re a big practice and we have dedicated staff who can help.

If you’re a small practice, it’s almost impossible to deal with this. I have two nurse practitioners, and a lot of their work is filling out paperwork for insurance companies.

We had a colleague, a solo practitioner, who would send us his patients with complicated therapies, because he couldn’t afford the time or the effort or the risk of not getting reimbursed. His practice could have paid out $100,000 for drugs and not get a reimbursement for a few months.

Even when an insurance company does give the preauthorization, there’s always this disclaimer that it doesn’t guarantee payment. If they find in the future that your patient didn’t meet the criteria, they can still deny payment.

If the insurers refuse coverage, we really work hard at getting patients free drugs, and most of the time, we manage to do that. We either look to charitable organizations, like the Leukemia and Lymphoma Society, or we look for rare disease societies or we go to the pharmaceutical company.

For really expensive drugs, pharmaceutical companies have a program where you can enroll the patient and they can help copay or even cover the drug. For less expensive drugs, it might not be a big problem, but for a drug that can cost $18,000 to $20,000 a month, that’s a big risk to take.

It’s confusing for patients, too. They get angry and frustrated, and that’s not good for their treatment, because attitude and psychology are very important. Sometimes they yell at us because they think it’s our fault. I encourage them to call their insurance companies themselves, and some of them do.

I don’t do it with every patient, but there are some more educated patients who are advocates, and if their condition is stable, I do encourage them to call their senators or congressmen or congresswomen to complain.

I don’t mind treating complicated patients. I don’t want to say I enjoy it, but I like challenges. That’s my field, that’s medicine, that’s what I’m supposed to do. But it’s really sad and frustrating that, when you want to treat a patient, you first have to look at their insurance to see how much care you can actually give them.

Maen Hussein, MD, is physician director of finance at Florida Cancer Specialists and Research Institute, Fort Myers. He is a board member of the Florida Cancer Specialists Foundation and sits on the board of directors for the Florida Society of Clinical Oncology.

A version of this article first appeared on Medscape.com.

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Androgenetic alopecia fuels negative emotions and poor quality of life

Article Type
Changed
Thu, 08/05/2021 - 11:43

Androgenetic alopecia significantly impairs patients’ overall quality of life and emotional health, but does not have a notable impact on the incidence of depression, according a systematic review and meta-analysis of 41 studies.

“Hair loss affects self-image, causes trichodynia, and plays a role in emotions and social activity, which may be associated with psychiatric problems and impaired health-related quality of life,” wrote Chun-Hsien Huang, MD, of Chang Gung Memorial Hospital, Linkou, Taiwan, and colleagues. However, systematic reviews of the associations between androgenetic alopecia (AGA) and health-related quality of life (HRQOL) are lacking, they said.

In a study published in JAMA Dermatology, the researchers reviewed data from a total of 7,995 AGA patients in 41 studies. The studies included 11 tools for HRQOL assessment and 29 tools for psychological assessment. Of these, the Dermatology Life Quality Index (DLQI) and the Hair-Specific Skindex-29 were used to assess quality of life, and the Center for Epidemiologic Studies Depression Scale (CES-D) was used for psychological assessment in the meta-analysis.

Overall, 27 studies identified 18 factors associated with HRQOL; those with an inverse effect were higher self-rated hair loss severity, lower VAS score, and higher educational level. Of note, neither physician-rated hair loss severity nor treatment response were factors in HRQOL, the researchers said.

The pooled DLQI score across studies was 8.16, and subgroup analysis showed no differences in HRQOL between men and women or between patients from European vs. Asian countries. However, five studies showed significant differences in HRQOL between men and women when different assessment tools were used, which emphasized the need for more studies to examine the association of AGA with HRQOL by sex, the researchers said.



The meta-analysis of the Hair-Specific Skindex-29 scores showed pooled averages of 21.95 for symptom dimension, 18.52 in function dimension, and 29.22 in emotion dimension. Of these, the emotion dimension scores indicated moderate emotional impairment.

The average pooled score on the CES-D in the meta-analysis was 14.98, indicating no association between AGA and depression, the researchers said. However, “depression accounts for only a part of the emotion dimension,” they said. “Therefore, emotion dimension could be impaired even if no depressive symptoms were noted.”

The pooled DLQI scores for AGA (8.16) were higher than scores for other skin conditions including alopecia areata (6.3), contact dermatitis (7.35), and acne vulgaris (7.45), but lower than the pooled scores for vitiligo (9.11), urticaria (9.8), psoriasis (10.53), and atopic dermatitis (11.2), the researchers noted. “However, additional head-to-head studies are needed for direct comparisons of HRQOL in patients with various dermatoses,” they said.

The study findings were limited by the cross-sectional design of many of the included studies, and the limited number of assessment tools included in the analysis, the researchers noted. Other limitations were the lack of specific domain scores and the inclusion of only three studies from China, they said.

However, the results are consistent with findings from previous studies, and suggest that patients with AGA may benefit from psychological and psychosocial support, the researchers said.

Quality of life issues deserve attention

“Studies of the quality-of-life impact of various conditions are becoming more common in the medical literature,” Jamie B. MacKelfresh, MD, associate professor of dermatology, Emory University, Atlanta, said in an interview.

Dr. Jamie B. MacKelfresh

“Androgenetic alopecia is the most common type of hair loss in men and women,” she noted. “Hair loss can be labeled as a cosmetic concern, so it is important that providers understand the significant quality-of-life impact androgenetic alopecia has on the many people with this diagnosis,” she emphasized.

Dr. MacKelfresh, who was asked to comment on the study, said she was surprised that the subgroup analysis of the DLQI showed no significant difference between men and women. “This surprised me because a number of past studies have highlighted the relatively greater quality-of-life impact of hair loss on women compared to men,” she noted.

However, she added, “I was not surprised to see that androgenetic alopecia has a significant quality-of-life impact on many patients, and that physician objective assessments of the hair loss do not always correlate with the amount of quality-of-life impact,” said Dr. MacKelfresh. “In the patients I see, I find hair loss very often has a significant quality-of-life impact on patients, regardless of gender, and the amount of quality-of-life impact definitely does not always correlate with the objective amount of hair loss,” she noted.

A takeaway message for clinicians is to be aware that androgenetic alopecia frequently has a significant impact on patients, “particularly in the emotional dimension,” and can affect both men and women, Dr. MacKelfresh said. “Objective assessments of hair loss severity by providers may not accurately predict the degree of quality-of-life impact a patient may experience; therefore providers should include quality-of-life questions as part of their standard evaluation of patients with androgenetic alopecia,” she said. In addition to treating the hair loss, providers can help these patients by guiding them to psychological support resources, she emphasized.

More research is needed to assess the impact of androgenetic alopecia on “men, women, and the non-binary gender population,” as well as the relationship between self-esteem and hair loss, she said. “Finally, it would be helpful to understand what interventions can best help improve androgenetic alopecia patients’ quality of life,” she noted.

The study received no outside funding. The researchers had no financial conflicts to disclose. Dr. MacKelfresh had no financial conflicts to disclose.

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Androgenetic alopecia significantly impairs patients’ overall quality of life and emotional health, but does not have a notable impact on the incidence of depression, according a systematic review and meta-analysis of 41 studies.

“Hair loss affects self-image, causes trichodynia, and plays a role in emotions and social activity, which may be associated with psychiatric problems and impaired health-related quality of life,” wrote Chun-Hsien Huang, MD, of Chang Gung Memorial Hospital, Linkou, Taiwan, and colleagues. However, systematic reviews of the associations between androgenetic alopecia (AGA) and health-related quality of life (HRQOL) are lacking, they said.

In a study published in JAMA Dermatology, the researchers reviewed data from a total of 7,995 AGA patients in 41 studies. The studies included 11 tools for HRQOL assessment and 29 tools for psychological assessment. Of these, the Dermatology Life Quality Index (DLQI) and the Hair-Specific Skindex-29 were used to assess quality of life, and the Center for Epidemiologic Studies Depression Scale (CES-D) was used for psychological assessment in the meta-analysis.

Overall, 27 studies identified 18 factors associated with HRQOL; those with an inverse effect were higher self-rated hair loss severity, lower VAS score, and higher educational level. Of note, neither physician-rated hair loss severity nor treatment response were factors in HRQOL, the researchers said.

The pooled DLQI score across studies was 8.16, and subgroup analysis showed no differences in HRQOL between men and women or between patients from European vs. Asian countries. However, five studies showed significant differences in HRQOL between men and women when different assessment tools were used, which emphasized the need for more studies to examine the association of AGA with HRQOL by sex, the researchers said.



The meta-analysis of the Hair-Specific Skindex-29 scores showed pooled averages of 21.95 for symptom dimension, 18.52 in function dimension, and 29.22 in emotion dimension. Of these, the emotion dimension scores indicated moderate emotional impairment.

The average pooled score on the CES-D in the meta-analysis was 14.98, indicating no association between AGA and depression, the researchers said. However, “depression accounts for only a part of the emotion dimension,” they said. “Therefore, emotion dimension could be impaired even if no depressive symptoms were noted.”

The pooled DLQI scores for AGA (8.16) were higher than scores for other skin conditions including alopecia areata (6.3), contact dermatitis (7.35), and acne vulgaris (7.45), but lower than the pooled scores for vitiligo (9.11), urticaria (9.8), psoriasis (10.53), and atopic dermatitis (11.2), the researchers noted. “However, additional head-to-head studies are needed for direct comparisons of HRQOL in patients with various dermatoses,” they said.

The study findings were limited by the cross-sectional design of many of the included studies, and the limited number of assessment tools included in the analysis, the researchers noted. Other limitations were the lack of specific domain scores and the inclusion of only three studies from China, they said.

However, the results are consistent with findings from previous studies, and suggest that patients with AGA may benefit from psychological and psychosocial support, the researchers said.

Quality of life issues deserve attention

“Studies of the quality-of-life impact of various conditions are becoming more common in the medical literature,” Jamie B. MacKelfresh, MD, associate professor of dermatology, Emory University, Atlanta, said in an interview.

Dr. Jamie B. MacKelfresh

“Androgenetic alopecia is the most common type of hair loss in men and women,” she noted. “Hair loss can be labeled as a cosmetic concern, so it is important that providers understand the significant quality-of-life impact androgenetic alopecia has on the many people with this diagnosis,” she emphasized.

Dr. MacKelfresh, who was asked to comment on the study, said she was surprised that the subgroup analysis of the DLQI showed no significant difference between men and women. “This surprised me because a number of past studies have highlighted the relatively greater quality-of-life impact of hair loss on women compared to men,” she noted.

However, she added, “I was not surprised to see that androgenetic alopecia has a significant quality-of-life impact on many patients, and that physician objective assessments of the hair loss do not always correlate with the amount of quality-of-life impact,” said Dr. MacKelfresh. “In the patients I see, I find hair loss very often has a significant quality-of-life impact on patients, regardless of gender, and the amount of quality-of-life impact definitely does not always correlate with the objective amount of hair loss,” she noted.

A takeaway message for clinicians is to be aware that androgenetic alopecia frequently has a significant impact on patients, “particularly in the emotional dimension,” and can affect both men and women, Dr. MacKelfresh said. “Objective assessments of hair loss severity by providers may not accurately predict the degree of quality-of-life impact a patient may experience; therefore providers should include quality-of-life questions as part of their standard evaluation of patients with androgenetic alopecia,” she said. In addition to treating the hair loss, providers can help these patients by guiding them to psychological support resources, she emphasized.

More research is needed to assess the impact of androgenetic alopecia on “men, women, and the non-binary gender population,” as well as the relationship between self-esteem and hair loss, she said. “Finally, it would be helpful to understand what interventions can best help improve androgenetic alopecia patients’ quality of life,” she noted.

The study received no outside funding. The researchers had no financial conflicts to disclose. Dr. MacKelfresh had no financial conflicts to disclose.

Androgenetic alopecia significantly impairs patients’ overall quality of life and emotional health, but does not have a notable impact on the incidence of depression, according a systematic review and meta-analysis of 41 studies.

“Hair loss affects self-image, causes trichodynia, and plays a role in emotions and social activity, which may be associated with psychiatric problems and impaired health-related quality of life,” wrote Chun-Hsien Huang, MD, of Chang Gung Memorial Hospital, Linkou, Taiwan, and colleagues. However, systematic reviews of the associations between androgenetic alopecia (AGA) and health-related quality of life (HRQOL) are lacking, they said.

In a study published in JAMA Dermatology, the researchers reviewed data from a total of 7,995 AGA patients in 41 studies. The studies included 11 tools for HRQOL assessment and 29 tools for psychological assessment. Of these, the Dermatology Life Quality Index (DLQI) and the Hair-Specific Skindex-29 were used to assess quality of life, and the Center for Epidemiologic Studies Depression Scale (CES-D) was used for psychological assessment in the meta-analysis.

Overall, 27 studies identified 18 factors associated with HRQOL; those with an inverse effect were higher self-rated hair loss severity, lower VAS score, and higher educational level. Of note, neither physician-rated hair loss severity nor treatment response were factors in HRQOL, the researchers said.

The pooled DLQI score across studies was 8.16, and subgroup analysis showed no differences in HRQOL between men and women or between patients from European vs. Asian countries. However, five studies showed significant differences in HRQOL between men and women when different assessment tools were used, which emphasized the need for more studies to examine the association of AGA with HRQOL by sex, the researchers said.



The meta-analysis of the Hair-Specific Skindex-29 scores showed pooled averages of 21.95 for symptom dimension, 18.52 in function dimension, and 29.22 in emotion dimension. Of these, the emotion dimension scores indicated moderate emotional impairment.

The average pooled score on the CES-D in the meta-analysis was 14.98, indicating no association between AGA and depression, the researchers said. However, “depression accounts for only a part of the emotion dimension,” they said. “Therefore, emotion dimension could be impaired even if no depressive symptoms were noted.”

The pooled DLQI scores for AGA (8.16) were higher than scores for other skin conditions including alopecia areata (6.3), contact dermatitis (7.35), and acne vulgaris (7.45), but lower than the pooled scores for vitiligo (9.11), urticaria (9.8), psoriasis (10.53), and atopic dermatitis (11.2), the researchers noted. “However, additional head-to-head studies are needed for direct comparisons of HRQOL in patients with various dermatoses,” they said.

The study findings were limited by the cross-sectional design of many of the included studies, and the limited number of assessment tools included in the analysis, the researchers noted. Other limitations were the lack of specific domain scores and the inclusion of only three studies from China, they said.

However, the results are consistent with findings from previous studies, and suggest that patients with AGA may benefit from psychological and psychosocial support, the researchers said.

Quality of life issues deserve attention

“Studies of the quality-of-life impact of various conditions are becoming more common in the medical literature,” Jamie B. MacKelfresh, MD, associate professor of dermatology, Emory University, Atlanta, said in an interview.

Dr. Jamie B. MacKelfresh

“Androgenetic alopecia is the most common type of hair loss in men and women,” she noted. “Hair loss can be labeled as a cosmetic concern, so it is important that providers understand the significant quality-of-life impact androgenetic alopecia has on the many people with this diagnosis,” she emphasized.

Dr. MacKelfresh, who was asked to comment on the study, said she was surprised that the subgroup analysis of the DLQI showed no significant difference between men and women. “This surprised me because a number of past studies have highlighted the relatively greater quality-of-life impact of hair loss on women compared to men,” she noted.

However, she added, “I was not surprised to see that androgenetic alopecia has a significant quality-of-life impact on many patients, and that physician objective assessments of the hair loss do not always correlate with the amount of quality-of-life impact,” said Dr. MacKelfresh. “In the patients I see, I find hair loss very often has a significant quality-of-life impact on patients, regardless of gender, and the amount of quality-of-life impact definitely does not always correlate with the objective amount of hair loss,” she noted.

A takeaway message for clinicians is to be aware that androgenetic alopecia frequently has a significant impact on patients, “particularly in the emotional dimension,” and can affect both men and women, Dr. MacKelfresh said. “Objective assessments of hair loss severity by providers may not accurately predict the degree of quality-of-life impact a patient may experience; therefore providers should include quality-of-life questions as part of their standard evaluation of patients with androgenetic alopecia,” she said. In addition to treating the hair loss, providers can help these patients by guiding them to psychological support resources, she emphasized.

More research is needed to assess the impact of androgenetic alopecia on “men, women, and the non-binary gender population,” as well as the relationship between self-esteem and hair loss, she said. “Finally, it would be helpful to understand what interventions can best help improve androgenetic alopecia patients’ quality of life,” she noted.

The study received no outside funding. The researchers had no financial conflicts to disclose. Dr. MacKelfresh had no financial conflicts to disclose.

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Isolated Scrotal Granular Parakeratosis: An Atypical Clinical Presentation

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To the Editor:

Granular parakeratosis is a rare condition with an unclear etiology that results from a myriad of factors, including exposure to irritants, friction, moisture, and heat. The diagnosis is made based on a distinct histologic reaction pattern that may be protective against the triggers. We present a case of isolated scrotal granular parakeratosis in a patient with compensatory hyperhidrosis after endoscopic thoracic sympathectomy.

A 52-year-old man presented with a 5-year history of a recurrent rash affecting the scrotum. He experienced monthly flares that were exacerbated by inguinal hyperhidrosis. His symptoms included a burning sensation and pruritus followed by superficial desquamation, with gradual yet temporary improvement. His medical history was remarkable for primary axillary and palmoplantar hyperhidrosis, with compensatory inguinal hyperhidrosis after endoscopic thoracic sympathectomy 8 years prior to presentation.

Physical examination revealed a well-demarcated, scaly, erythematous plaque affecting the scrotal skin with sparing of the median raphe, penis, and inguinal folds (Figure 1). There were no other lesions noted in the axillary region or other skin folds.

Figure 1. Well-demarcated, scaly, erythematous plaque affecting the scrotal skin and sparing the median raphe, penis, and inguinal folds in a 52-year-old man.


Prior treatments prescribed by other providers included topical pimecrolimus, antifungal creams, topical corticosteroids, zinc oxide ointment, and daily application of an over-the-counter medicated powder with no resolution.

A punch biopsy performed at the current presentation showed psoriasiform hyperplasia of the epidermis with only a focally diminished granular layer. There was overlying thick parakeratosis and retention of keratohyalin granules (Figure 2). Grocott-Gomori methenamine- silver staining was negative for fungal elements in the sections examined. Clinical history, morphology of the eruption, and histologic features were consistent with granular parakeratosis.

Figure 2. A punch biopsy showed psoriasiform hyperplasia of the epidermis with a thick parakeratotic layer and retention of keratohyalin granules (H&E, original magnification ×400).


Since the first reported incident of granular parakeratosis of the axilla in 1991,1 granular parakeratosis has been reported in other intertriginous areas, including the inframammary folds, inguinal folds, genitalia, perianal skin, and beneath the abdominal pannus.2 One case study in 1998 reported a patient with isolated involvement of the inguinal region3; however, this presentation is rare.4 This condition has been reported in both sexes and all age groups, including children.5

Granular parakeratosis classically presents as erythematous to brown hyperkeratotic papules that coalesce into plaques.6 It is thought to be a reactive inflammatory condition secondary to aggravating factors such as exposure to heat,7 moisture, and friction; skin occlusion; repeated washing; irritation from external agents; antiperspirants; and use of depilatory creams.8 Histopathology is characteristic and consists of retained nuclei and keratohyalin granules within the stratum corneum, beneath which there is a retained stratum granulosum. Epidermal changes may be varied and include atrophy or hyperplasia.



Murine models have postulated that granular parakeratosis may result from a deficiency in caspase 14, a protease vital to the formation of a well-functioning skin barrier.9 A cornified envelope often is noted in granular parakeratotic cells with no defects in desmosomes and cell membranes, suggesting that the pathogenesis lies within processing of profilaggrin to filaggrin, resulting in a failure to degrade keratohyalin granules and aggregation of keratin filaments.10 Granular parakeratosis is not known to be associated with other medical conditions, but it has been observed in patients receiving chemotherapy for breast11 and ovarian12 carcinomas. In infants with atopic dermatitis, granular parakeratosis was reported in 5 out of 7 cases.6 In our patient with secondary inguinal hyperhidrosis after thoracic sympathectomy, granular parakeratosis may be reactive to excess sweating and friction in the scrotal area.

Granular parakeratosis follows a waxing and waning pattern that may spontaneously resolve without any treatment; it also can follow a protracted course, as in a case with associated facial papules that persisted for 20 years.13 Topical corticosteroids alone or in combination with topical antifungal agents have been used for the treatment of granular parakeratosis with the goal of accelerating resolution.2,14 However, the efficacy of these therapeutic interventions is limited, and no controlled trials are underway. Topical vitamin D analogues15,16 and topical retinoids17 also have been reported with successful outcomes. Spontaneous resolution also has been observed in 2 different cases after previously being unresponsive to topical treatment.18,19 Treatment with Clostridium botulinum toxin A resulted in complete remission of the disease observed at 6-month follow-up. The pharmacologic action of the neurotoxin disrupts the stimulation of eccrine sweat glands, resulting in decreased sweating, a known exacerbating factor of granular parakeratosis.20

In summary, our case represents a unique clinical presentation of granular parakeratosis with classic histopathologic features. A high index of suspicion and a biopsy are vital to arriving at the correct diagnosis.

References
  1. Northcutt AD, Nelson DM, Tschen JA. Axillary granular parakeratosis. J Am Acad Dermatol. 1991;24:541-544.
  2. Burford C. Granular parakeratosis of multiple intertriginous areas. Australas J Dermatol. 2008;49:35-38.
  3. Mehregan DA, Thomas JE, Mehregan DR. Intertriginous granular parakeratosis. J Am Acad Dermatol. 1998;39:495-496.
  4. Leclerc-Mercier S, Prost-Squarcioni C, Hamel-Teillac D, et al. A case of congenital granular parakeratosis. Am J Dermatopathol. 2011;33:531-533.
  5. Scheinfeld NS, Mones J. Granular parakeratosis: pathologic and clinical correlation of 18 cases of granular parakeratosis. J Am Acad Dermatol. 2005;52:863-867.
  6. Akkaya AD, Oram Y, Aydin O. Infantile granular parakeratosis: cytologic examination of superficial scrapings as an aid to diagnosis. Pediatr Dermatol. 2015;32:392-396.
  7. Rodríguez G. Axillary granular parakeratosis [in Spanish]. Biomedica. 2002;22:519-523.
  8. Samrao A, Reis M, Niedt G, et al. Granular parakeratosis: response to calcipotriene and brief review of current therapeutic options. Skinmed. 2010;8:357-359.
  9. Hoste E, Denecker G, Gilbert B, et al. Caspase-14-deficient mice are more prone to the development of parakeratosis. J Invest Dermatol. 2013;133:742-750.
  10. Metze D, Rutten A. Granular parakeratosis—a unique acquired disorder of keratinization. J Cutan Pathol. 1999;26:339-352.
  11. Wallace CA, Pichardo RO, Yosipovitch G, et al. Granular parakeratosis: a case report and literature review. J Cutan Pathol. 2003;30:332-335.
  12. Jaconelli L, Doebelin B, Kanitakis J, et al. Granular parakeratosis in a patient treated with liposomal doxorubicin for ovarian carcinoma. J Am Acad Dermatol. 2008;58(5 suppl 1):S84-S87.
  13. Reddy IS, Swarnalata G, Mody T. Intertriginous granular parakeratosis persisting for 20 years. Indian J Dermatol Venereol Leprol. 2008;74:405-407.
  14. Dearden C, al-Nakib W, Andries K, et al. Drug resistant rhinoviruses from the nose of experimentally treated volunteers. Arch Virol. 1989;109:71-81.
  15. Patel U, Patel T, Skinner RB Jr. Resolution of granular parakeratosis with topical calcitriol. Arch Dermatol. 2011;147:997-998.
  16. Contreras ME, Gottfried LC, Bang RH, et al. Axillary intertriginous granular parakeratosis responsive to topical calcipotriene and ammonium lactate. Int J Dermatol. 2003;42:382-383.
  17. Brown SK, Heilman ER. Granular parakeratosis: resolution with topical tretinoin. J Am Acad Dermatol. 2002;47(5 suppl):S279-S280.
  18. Compton AK, Jackson JM. Isotretinoin as a treatment for axillary granular parakeratosis. Cutis. 2007;80:55-56.
  19. Webster CG, Resnik KS, Webster GF. Axillary granular parakeratosis: response to isotretinoin. J Am Acad Dermatol. 1997; 37:789-790.
  20. Ravitskiy L, Heymann WR. Botulinum toxin-induced resolution of axillary granular parakeratosis. Skinmed. 2005;4:118-120.
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From the Department of Dermatology, Saint Louis University School of Medicine, Missouri.

The authors report no conflict of interest.

Correspondence: A. Mary Guo, MD, SLUCare Academic Pavilion, 3rd Floor, Dermatology, 1008 Spring Ave, St. Louis, MO 63110([email protected]).

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Correspondence: A. Mary Guo, MD, SLUCare Academic Pavilion, 3rd Floor, Dermatology, 1008 Spring Ave, St. Louis, MO 63110([email protected]).

Author and Disclosure Information

From the Department of Dermatology, Saint Louis University School of Medicine, Missouri.

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Correspondence: A. Mary Guo, MD, SLUCare Academic Pavilion, 3rd Floor, Dermatology, 1008 Spring Ave, St. Louis, MO 63110([email protected]).

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To the Editor:

Granular parakeratosis is a rare condition with an unclear etiology that results from a myriad of factors, including exposure to irritants, friction, moisture, and heat. The diagnosis is made based on a distinct histologic reaction pattern that may be protective against the triggers. We present a case of isolated scrotal granular parakeratosis in a patient with compensatory hyperhidrosis after endoscopic thoracic sympathectomy.

A 52-year-old man presented with a 5-year history of a recurrent rash affecting the scrotum. He experienced monthly flares that were exacerbated by inguinal hyperhidrosis. His symptoms included a burning sensation and pruritus followed by superficial desquamation, with gradual yet temporary improvement. His medical history was remarkable for primary axillary and palmoplantar hyperhidrosis, with compensatory inguinal hyperhidrosis after endoscopic thoracic sympathectomy 8 years prior to presentation.

Physical examination revealed a well-demarcated, scaly, erythematous plaque affecting the scrotal skin with sparing of the median raphe, penis, and inguinal folds (Figure 1). There were no other lesions noted in the axillary region or other skin folds.

Figure 1. Well-demarcated, scaly, erythematous plaque affecting the scrotal skin and sparing the median raphe, penis, and inguinal folds in a 52-year-old man.


Prior treatments prescribed by other providers included topical pimecrolimus, antifungal creams, topical corticosteroids, zinc oxide ointment, and daily application of an over-the-counter medicated powder with no resolution.

A punch biopsy performed at the current presentation showed psoriasiform hyperplasia of the epidermis with only a focally diminished granular layer. There was overlying thick parakeratosis and retention of keratohyalin granules (Figure 2). Grocott-Gomori methenamine- silver staining was negative for fungal elements in the sections examined. Clinical history, morphology of the eruption, and histologic features were consistent with granular parakeratosis.

Figure 2. A punch biopsy showed psoriasiform hyperplasia of the epidermis with a thick parakeratotic layer and retention of keratohyalin granules (H&E, original magnification ×400).


Since the first reported incident of granular parakeratosis of the axilla in 1991,1 granular parakeratosis has been reported in other intertriginous areas, including the inframammary folds, inguinal folds, genitalia, perianal skin, and beneath the abdominal pannus.2 One case study in 1998 reported a patient with isolated involvement of the inguinal region3; however, this presentation is rare.4 This condition has been reported in both sexes and all age groups, including children.5

Granular parakeratosis classically presents as erythematous to brown hyperkeratotic papules that coalesce into plaques.6 It is thought to be a reactive inflammatory condition secondary to aggravating factors such as exposure to heat,7 moisture, and friction; skin occlusion; repeated washing; irritation from external agents; antiperspirants; and use of depilatory creams.8 Histopathology is characteristic and consists of retained nuclei and keratohyalin granules within the stratum corneum, beneath which there is a retained stratum granulosum. Epidermal changes may be varied and include atrophy or hyperplasia.



Murine models have postulated that granular parakeratosis may result from a deficiency in caspase 14, a protease vital to the formation of a well-functioning skin barrier.9 A cornified envelope often is noted in granular parakeratotic cells with no defects in desmosomes and cell membranes, suggesting that the pathogenesis lies within processing of profilaggrin to filaggrin, resulting in a failure to degrade keratohyalin granules and aggregation of keratin filaments.10 Granular parakeratosis is not known to be associated with other medical conditions, but it has been observed in patients receiving chemotherapy for breast11 and ovarian12 carcinomas. In infants with atopic dermatitis, granular parakeratosis was reported in 5 out of 7 cases.6 In our patient with secondary inguinal hyperhidrosis after thoracic sympathectomy, granular parakeratosis may be reactive to excess sweating and friction in the scrotal area.

Granular parakeratosis follows a waxing and waning pattern that may spontaneously resolve without any treatment; it also can follow a protracted course, as in a case with associated facial papules that persisted for 20 years.13 Topical corticosteroids alone or in combination with topical antifungal agents have been used for the treatment of granular parakeratosis with the goal of accelerating resolution.2,14 However, the efficacy of these therapeutic interventions is limited, and no controlled trials are underway. Topical vitamin D analogues15,16 and topical retinoids17 also have been reported with successful outcomes. Spontaneous resolution also has been observed in 2 different cases after previously being unresponsive to topical treatment.18,19 Treatment with Clostridium botulinum toxin A resulted in complete remission of the disease observed at 6-month follow-up. The pharmacologic action of the neurotoxin disrupts the stimulation of eccrine sweat glands, resulting in decreased sweating, a known exacerbating factor of granular parakeratosis.20

In summary, our case represents a unique clinical presentation of granular parakeratosis with classic histopathologic features. A high index of suspicion and a biopsy are vital to arriving at the correct diagnosis.

To the Editor:

Granular parakeratosis is a rare condition with an unclear etiology that results from a myriad of factors, including exposure to irritants, friction, moisture, and heat. The diagnosis is made based on a distinct histologic reaction pattern that may be protective against the triggers. We present a case of isolated scrotal granular parakeratosis in a patient with compensatory hyperhidrosis after endoscopic thoracic sympathectomy.

A 52-year-old man presented with a 5-year history of a recurrent rash affecting the scrotum. He experienced monthly flares that were exacerbated by inguinal hyperhidrosis. His symptoms included a burning sensation and pruritus followed by superficial desquamation, with gradual yet temporary improvement. His medical history was remarkable for primary axillary and palmoplantar hyperhidrosis, with compensatory inguinal hyperhidrosis after endoscopic thoracic sympathectomy 8 years prior to presentation.

Physical examination revealed a well-demarcated, scaly, erythematous plaque affecting the scrotal skin with sparing of the median raphe, penis, and inguinal folds (Figure 1). There were no other lesions noted in the axillary region or other skin folds.

Figure 1. Well-demarcated, scaly, erythematous plaque affecting the scrotal skin and sparing the median raphe, penis, and inguinal folds in a 52-year-old man.


Prior treatments prescribed by other providers included topical pimecrolimus, antifungal creams, topical corticosteroids, zinc oxide ointment, and daily application of an over-the-counter medicated powder with no resolution.

A punch biopsy performed at the current presentation showed psoriasiform hyperplasia of the epidermis with only a focally diminished granular layer. There was overlying thick parakeratosis and retention of keratohyalin granules (Figure 2). Grocott-Gomori methenamine- silver staining was negative for fungal elements in the sections examined. Clinical history, morphology of the eruption, and histologic features were consistent with granular parakeratosis.

Figure 2. A punch biopsy showed psoriasiform hyperplasia of the epidermis with a thick parakeratotic layer and retention of keratohyalin granules (H&E, original magnification ×400).


Since the first reported incident of granular parakeratosis of the axilla in 1991,1 granular parakeratosis has been reported in other intertriginous areas, including the inframammary folds, inguinal folds, genitalia, perianal skin, and beneath the abdominal pannus.2 One case study in 1998 reported a patient with isolated involvement of the inguinal region3; however, this presentation is rare.4 This condition has been reported in both sexes and all age groups, including children.5

Granular parakeratosis classically presents as erythematous to brown hyperkeratotic papules that coalesce into plaques.6 It is thought to be a reactive inflammatory condition secondary to aggravating factors such as exposure to heat,7 moisture, and friction; skin occlusion; repeated washing; irritation from external agents; antiperspirants; and use of depilatory creams.8 Histopathology is characteristic and consists of retained nuclei and keratohyalin granules within the stratum corneum, beneath which there is a retained stratum granulosum. Epidermal changes may be varied and include atrophy or hyperplasia.



Murine models have postulated that granular parakeratosis may result from a deficiency in caspase 14, a protease vital to the formation of a well-functioning skin barrier.9 A cornified envelope often is noted in granular parakeratotic cells with no defects in desmosomes and cell membranes, suggesting that the pathogenesis lies within processing of profilaggrin to filaggrin, resulting in a failure to degrade keratohyalin granules and aggregation of keratin filaments.10 Granular parakeratosis is not known to be associated with other medical conditions, but it has been observed in patients receiving chemotherapy for breast11 and ovarian12 carcinomas. In infants with atopic dermatitis, granular parakeratosis was reported in 5 out of 7 cases.6 In our patient with secondary inguinal hyperhidrosis after thoracic sympathectomy, granular parakeratosis may be reactive to excess sweating and friction in the scrotal area.

Granular parakeratosis follows a waxing and waning pattern that may spontaneously resolve without any treatment; it also can follow a protracted course, as in a case with associated facial papules that persisted for 20 years.13 Topical corticosteroids alone or in combination with topical antifungal agents have been used for the treatment of granular parakeratosis with the goal of accelerating resolution.2,14 However, the efficacy of these therapeutic interventions is limited, and no controlled trials are underway. Topical vitamin D analogues15,16 and topical retinoids17 also have been reported with successful outcomes. Spontaneous resolution also has been observed in 2 different cases after previously being unresponsive to topical treatment.18,19 Treatment with Clostridium botulinum toxin A resulted in complete remission of the disease observed at 6-month follow-up. The pharmacologic action of the neurotoxin disrupts the stimulation of eccrine sweat glands, resulting in decreased sweating, a known exacerbating factor of granular parakeratosis.20

In summary, our case represents a unique clinical presentation of granular parakeratosis with classic histopathologic features. A high index of suspicion and a biopsy are vital to arriving at the correct diagnosis.

References
  1. Northcutt AD, Nelson DM, Tschen JA. Axillary granular parakeratosis. J Am Acad Dermatol. 1991;24:541-544.
  2. Burford C. Granular parakeratosis of multiple intertriginous areas. Australas J Dermatol. 2008;49:35-38.
  3. Mehregan DA, Thomas JE, Mehregan DR. Intertriginous granular parakeratosis. J Am Acad Dermatol. 1998;39:495-496.
  4. Leclerc-Mercier S, Prost-Squarcioni C, Hamel-Teillac D, et al. A case of congenital granular parakeratosis. Am J Dermatopathol. 2011;33:531-533.
  5. Scheinfeld NS, Mones J. Granular parakeratosis: pathologic and clinical correlation of 18 cases of granular parakeratosis. J Am Acad Dermatol. 2005;52:863-867.
  6. Akkaya AD, Oram Y, Aydin O. Infantile granular parakeratosis: cytologic examination of superficial scrapings as an aid to diagnosis. Pediatr Dermatol. 2015;32:392-396.
  7. Rodríguez G. Axillary granular parakeratosis [in Spanish]. Biomedica. 2002;22:519-523.
  8. Samrao A, Reis M, Niedt G, et al. Granular parakeratosis: response to calcipotriene and brief review of current therapeutic options. Skinmed. 2010;8:357-359.
  9. Hoste E, Denecker G, Gilbert B, et al. Caspase-14-deficient mice are more prone to the development of parakeratosis. J Invest Dermatol. 2013;133:742-750.
  10. Metze D, Rutten A. Granular parakeratosis—a unique acquired disorder of keratinization. J Cutan Pathol. 1999;26:339-352.
  11. Wallace CA, Pichardo RO, Yosipovitch G, et al. Granular parakeratosis: a case report and literature review. J Cutan Pathol. 2003;30:332-335.
  12. Jaconelli L, Doebelin B, Kanitakis J, et al. Granular parakeratosis in a patient treated with liposomal doxorubicin for ovarian carcinoma. J Am Acad Dermatol. 2008;58(5 suppl 1):S84-S87.
  13. Reddy IS, Swarnalata G, Mody T. Intertriginous granular parakeratosis persisting for 20 years. Indian J Dermatol Venereol Leprol. 2008;74:405-407.
  14. Dearden C, al-Nakib W, Andries K, et al. Drug resistant rhinoviruses from the nose of experimentally treated volunteers. Arch Virol. 1989;109:71-81.
  15. Patel U, Patel T, Skinner RB Jr. Resolution of granular parakeratosis with topical calcitriol. Arch Dermatol. 2011;147:997-998.
  16. Contreras ME, Gottfried LC, Bang RH, et al. Axillary intertriginous granular parakeratosis responsive to topical calcipotriene and ammonium lactate. Int J Dermatol. 2003;42:382-383.
  17. Brown SK, Heilman ER. Granular parakeratosis: resolution with topical tretinoin. J Am Acad Dermatol. 2002;47(5 suppl):S279-S280.
  18. Compton AK, Jackson JM. Isotretinoin as a treatment for axillary granular parakeratosis. Cutis. 2007;80:55-56.
  19. Webster CG, Resnik KS, Webster GF. Axillary granular parakeratosis: response to isotretinoin. J Am Acad Dermatol. 1997; 37:789-790.
  20. Ravitskiy L, Heymann WR. Botulinum toxin-induced resolution of axillary granular parakeratosis. Skinmed. 2005;4:118-120.
References
  1. Northcutt AD, Nelson DM, Tschen JA. Axillary granular parakeratosis. J Am Acad Dermatol. 1991;24:541-544.
  2. Burford C. Granular parakeratosis of multiple intertriginous areas. Australas J Dermatol. 2008;49:35-38.
  3. Mehregan DA, Thomas JE, Mehregan DR. Intertriginous granular parakeratosis. J Am Acad Dermatol. 1998;39:495-496.
  4. Leclerc-Mercier S, Prost-Squarcioni C, Hamel-Teillac D, et al. A case of congenital granular parakeratosis. Am J Dermatopathol. 2011;33:531-533.
  5. Scheinfeld NS, Mones J. Granular parakeratosis: pathologic and clinical correlation of 18 cases of granular parakeratosis. J Am Acad Dermatol. 2005;52:863-867.
  6. Akkaya AD, Oram Y, Aydin O. Infantile granular parakeratosis: cytologic examination of superficial scrapings as an aid to diagnosis. Pediatr Dermatol. 2015;32:392-396.
  7. Rodríguez G. Axillary granular parakeratosis [in Spanish]. Biomedica. 2002;22:519-523.
  8. Samrao A, Reis M, Niedt G, et al. Granular parakeratosis: response to calcipotriene and brief review of current therapeutic options. Skinmed. 2010;8:357-359.
  9. Hoste E, Denecker G, Gilbert B, et al. Caspase-14-deficient mice are more prone to the development of parakeratosis. J Invest Dermatol. 2013;133:742-750.
  10. Metze D, Rutten A. Granular parakeratosis—a unique acquired disorder of keratinization. J Cutan Pathol. 1999;26:339-352.
  11. Wallace CA, Pichardo RO, Yosipovitch G, et al. Granular parakeratosis: a case report and literature review. J Cutan Pathol. 2003;30:332-335.
  12. Jaconelli L, Doebelin B, Kanitakis J, et al. Granular parakeratosis in a patient treated with liposomal doxorubicin for ovarian carcinoma. J Am Acad Dermatol. 2008;58(5 suppl 1):S84-S87.
  13. Reddy IS, Swarnalata G, Mody T. Intertriginous granular parakeratosis persisting for 20 years. Indian J Dermatol Venereol Leprol. 2008;74:405-407.
  14. Dearden C, al-Nakib W, Andries K, et al. Drug resistant rhinoviruses from the nose of experimentally treated volunteers. Arch Virol. 1989;109:71-81.
  15. Patel U, Patel T, Skinner RB Jr. Resolution of granular parakeratosis with topical calcitriol. Arch Dermatol. 2011;147:997-998.
  16. Contreras ME, Gottfried LC, Bang RH, et al. Axillary intertriginous granular parakeratosis responsive to topical calcipotriene and ammonium lactate. Int J Dermatol. 2003;42:382-383.
  17. Brown SK, Heilman ER. Granular parakeratosis: resolution with topical tretinoin. J Am Acad Dermatol. 2002;47(5 suppl):S279-S280.
  18. Compton AK, Jackson JM. Isotretinoin as a treatment for axillary granular parakeratosis. Cutis. 2007;80:55-56.
  19. Webster CG, Resnik KS, Webster GF. Axillary granular parakeratosis: response to isotretinoin. J Am Acad Dermatol. 1997; 37:789-790.
  20. Ravitskiy L, Heymann WR. Botulinum toxin-induced resolution of axillary granular parakeratosis. Skinmed. 2005;4:118-120.
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Practice Points

  • Granular parakeratosis can occur in response to triggers such as irritants, friction, hyperhidrosis, and heat.
  • Granular parakeratosis can have an atypical presentation; therefore, a high index of suspicion and punch biopsy are vital to arrive at the correct diagnosis.
  • Classic histopathology demonstrates retained nuclei and keratohyalin granules within the stratum corneum beneath which there is a retained stratum granulosum.
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How heat kills: Deadly weather ‘cooking’ people from within

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Millions of Americans have been languishing for weeks in the oppressive heat and humidity of a merciless summer. Deadly heat has already taken the lives of hundreds in the Pacific Northwest alone, with numbers likely to grow as the full impact of heat-related deaths eventually comes to light.

In the final week of July, the National Weather Service issued excessive heat warnings for 17 states, stretching from the West Coast, across the Midwest, down south into Louisiana and Georgia. Temperatures 10° to 15° F above average threaten the lives and livelihoods of people all across the country.

After a scorching heat wave in late June, residents of the Pacific Northwest are once again likely to see triple-digit temperatures in the coming days. With the heat, hospitals may face another surge of people with heat-related illnesses.

Erika Moseson, MD, a lung and intensive care specialist, witnessed firsthand the life-threatening impacts of soaring temperatures. She happened to be running her 10-bed intensive care unit in a suburban hospital in Gresham, Ore., about 15 miles east of Portland, the weekend of June 26. Within 12 hours, almost half her ICU beds were filled with people found unconscious on the street, in the bushes, or in their own beds, all because their body’s defenses had become overwhelmed by heat.

“It was unidentified person after unidentified person, coming in, same story, temperatures through the roof, comatose,” Dr. Moseson recalled. Young people in their 20s with muscle breakdown markers through the roof, a sign of rhabdomyolysis; people with no other medical problems that would have put them in a high-risk category.

As a lifelong Oregonian, she’d never seen anything like this before. “We’re all trained for it. I know what happens to you if you have heatstroke, I know how to treat it,” she trailed off, still finding it hard to believe. Still reeling from the number of cases in just a few hours. Still shocked that this happened on what’s supposed to be the cooler, rainforest side of Oregon.

Among those she treated and resuscitated, the memory of a patient that she lost continues to gnaw at her.

“I’ve gone back to it day after day since it happened,” she reflected.

Adults, in their 50s, living at home with their children. Just 1 hour prior, they’d all said goodnight. Then 1 hour later, when a child came to check in, both parents were unconscious.

Dr. Moseson shared how her team tried everything in their power for 18 hours to save the parent that was brought to her ICU. But like hundreds of others who went through the heat wave that weekend, her patient didn’t survive.

It was too late. From Dr. Moseson’s experience, it’s what happens “if you’re cooking a human.”
 

How heat kills

Regardless of where we live on the planet, humans maintain a consistent internal temperature around 98° F for our systems to function properly. 

Our bodies have an entire temperature-regulating system to balance heat gain with heat loss so we don’t stray too far from our ideal range. The hypothalamus functions as the thermostat, communicating with heat sensors in our skin, muscles, and spinal cord. Based on signals about our core body temperature, our nervous system makes many decisions for us – opening up blood vessels in the peripheral parts of our body, pushing more blood toward the skin, and activating sweat glands to produce more sweat.  

Sweat is one of the most powerful tools we have to maintain a safe internal temperature. Of course, there are some things under our control, such as removing clothing, drinking more water, and finding shade (or preferably air conditioning). But beyond that, it’s our ability to sweat that keeps us cool. When sweat evaporates into the air, heat from our skin goes with it, cooling us off.

Over time, our sweat response can work better as we get used to warmer environments, a process that’s known as acclimatization. Over the period of a few days to weeks, the sweat glands of acclimated people can start making sweat at lower temperatures, produce more sweat, and absorb more salt back into our system, all to make us more efficient “sweaters.”

While someone who’s not used to the heat may only produce 1 liter of sweat per hour, people who have become acclimated can produce 2-3 liters every hour, allowing evaporation to eliminate more than two times the amount of heat.   

Because the process of acclimatization can take some time, typically it’s the first throes of summer, or heat waves in places where people don’t typically see high temperatures, that are the most deadly. And of course, the right infrastructure, like access to air conditioning, also plays a large role in limiting heat-related death and hospitalization.

A 2019 study showed that heat-related hospitalizations peak at different temperatures in different places. For example, hospitalizations typically peak in Texas when the temperature hits 105° F. But they might be highest in the Pacific Northwest at just 81° F.

Even with acclimatization, there are limits to how much our bodies can adapt to heat. When the humidity goes up past 75%, there’s already so much moisture in the air that heat loss through evaporation no longer occurs.

It’s this connection between heat and humidity that can be deadly. This is why the heat index (a measure that takes into account temperature and relative humidity) and wet bulb globe temperature (a measure commonly used by the military and competitive athletes that takes into account temperature, humidity, wind speed, sun angle, and cloud cover) are both better at showing how dangerous the heat may be for our health, compared to temperature alone.

Kristie L. Ebi, PhD, a professor in the Center for Health and the Global Environment at the University of Washington, Seattle, has been studying the effects of heat and other climate-sensitive conditions on health for over 20 years. She stresses that it’s not just the recorded temperatures, but the prolonged exposure that kills.

If you never get a chance to bring down that core body temperature, if your internal temperatures stay above the range where your cells and your organs can work well for a long time, that’s when you can have the most dangerous effects of heat.

“It depends then on your age, your fitness, your individual physiology, underlying medical conditions, to how quickly that could affect the functioning of those organs. There’s lots of variability in there,” Dr. Ebi said.

Our hearts take on the brunt of the early response, working harder to pump blood toward the skin. Water and salt loss through our skin can start to cause electrolyte changes that can cause heat cramps and heat exhaustion. We feel tired, nauseated, dizzy. With enough water loss, we may become dehydrated, limiting the blood flow to our brains, causing us to pass out.

These early signs are like a car’s check engine light – systems are already being damaged, but resting, refueling, and, most importantly, turning off the heat are critical steps to prevent fatal injury.

If hazardous heat exposure continues and our internal temperatures continue to rise, nerves stop talking to each other, the proteins in our body unfold and lose their shape, and the cells of our organs disintegrate. This in turn sets off a fire alarm in our blood vessels, where a variety of chemical messengers, including “heat-shock proteins,” are released. The release of these inflammatory proteins, coupled with the loss of blood flow, eventually leads to the death of cells throughout the body, from the brain, to the heart, the muscles, and the kidneys.

This process is referred to as heatstroke. In essence, we melt from the inside.

At a certain point, this cascade can’t be reversed. Just like when you cool a melting block of ice, the parts that have melted will not go back to their original shape. It’s a similar process in our bodies, so delays in cooling and treatment can lead to death rates as high as 80%.

On the outside, we see people who look confused and disoriented, with hot skin and rapid breathing, and they may eventually become unconscious. Core body temperatures over 105° F clinch the diagnosis, but at the first sign of feeling unwell, cooling should be started.

There is no fancier or more effective treatment than that: Cool right away. In emergency rooms in Washington State, doctors used body bags filled with ice and water to cool victims of the heat wave in late June.

“It was all from heat ... that’s the thing, you feel so idiotic ... you’re like, ‘I’ve given you ice’ ... you bring their temperature down. But it’s already set off this cascade that you can’t stop,” Dr. Moseson said.

By the time Dr. Moseson’s patient made it to her, cooling with ice was just the beginning of the attempts to resuscitate and revive. The patient was already showing evidence of a process causing widespread bleeding and clotting, known as disseminated intravascular coagulation, along with damage to the heart and failing kidneys. Over 18 hours, her team cooled the patient, flooded the blood vessels with fluids and blood products, attempted to start dialysis, and inserted a breathing tube – all of the technology that is used to save people from serious cardiovascular collapse from other conditions. But nothing could reverse the melting that had already occurred.

Deaths from heat are 100% preventable. Until they’re not.
 

 

 

No respite

As Dr. Ebi says, the key to preventing heat-related death is to cool down enough to stabilize our internal cells and proteins before the irreversible cascade begins.

But for close to 80% of Americans who live in urban areas, temperatures can be even higher and more intolerable compared to surrounding areas because of the way we’ve designed our cities. In effect, we have unintentionally created hot zones called “urban heat islands.”

Jeremy Hoffman, PhD, chief scientist for the Science Museum of Virginia, explains that things like bricks, asphalt, and parking lots absorb more of the sun’s energy throughout the day and then emit that back into the air as heat throughout the afternoon and into the evening. This raises the air and surface temperatures in cities, relative to rural areas. When temperatures don’t cool enough at night, there’s no way to recover from the day’s heat. You start the next day still depleted, with less reserve to face the heat of a new day.

When you dig even deeper, it turns out that even within the same city, there are huge “thermal inequities,” as Dr. Hoffman calls them. In a 2019 study, he found that wealthier parts of cities had more natural spaces such as parks and tree-lined streets, compared to areas that had been intentionally “redlined,” or systematically deprived of investment. This pattern repeats itself in over 100 urban areas across the country and translates to huge temperature differences on the order of 10-20 degrees Fahrenheit within the same city, at the exact same time during a heat wave.

“In some ways, the way that we’ve decided to plan and build our cities physically turns up the thermostat by several tens of degrees during heat waves in particular neighborhoods,” Dr. Hoffman said.

Dr. Hoffman’s work showed that the city of Portland (where the death toll from the heat wave in late June was the highest) had some of the most intense differences between formerly redlined vs. tree-lined areas out of the more than 100 cities that he studied.  

“Watching it play out, I was really concerned, not only as a climate scientist, but as a human. Understanding the urban heat island effect and the extreme nature of the inequity in our cities, thermally and otherwise, once you start to really recognize it, you can’t forget it.”
 

The most vulnerable

When it comes to identifying and protecting the people most vulnerable to heat stress and heat-related death, there is an ever-growing list of those most at risk. Unfortunately, very few recognize when they themselves are at risk, often until it’s too late.

According to Linda McCauley, PhD, dean of the Emory University School of Nursing in Atlanta, “the scope of who is vulnerable is quickly increasing.”

For example, we’re used to recognizing that pregnant women and young children are at risk. Public health campaigns have long advised us not to leave young children and pets in hot cars. We know that adolescents who play sports during hot summer months are at high risk for heat-related events and even death.

In Georgia, a 15-year-old boy collapsed and died after his first day back at football practice when the heat index was 105° F on July 26, even as it appears that all protocols for heat safety were being followed.

We recognize that outdoor workers face devastating consequences from prolonged exertion in the heat and must have safer working conditions.

The elderly and those with long-term medical and mental health conditions are also more vulnerable to heat. The elderly may not have the same warning signs and may not recognize that they are dehydrated until it is too late. In addition, their sweating mechanism weakens, and they may be taking medicines that interfere with their ability to regulate their temperature.

Poverty and inadequate housing are risk factors, especially for those in urban heat islands. For many people, their housing does not have enough cooling to protect them, and they can’t safely get themselves to cooling shelters.

These patterns for the most vulnerable fit for the majority of deaths in Oregon during the late June heat wave. Most victims were older, lived alone, and didn’t have air conditioning. But with climate change, the predictions are that temperatures will go higher and heat waves will last longer.

“There’s probably very few people today that are ‘immune’ to the effects of heat-related stress with climate change. All of us can be put in situations where we are susceptible,” Dr. McCauley said.

Dr. Moseson agreed. Many of her patients fit none of these risk categories – she treated people with no health problems in their 20s in her ICU, and the patient she lost would not traditionally have been thought of as high risk. That 50-something patient had no long-standing medical problems, and lived with family in a newly renovated suburban home that had air conditioning. The only problem was that the air conditioner had broken and there had been no rush to fix it based on past experience with Oregon summers.
 

 

 

Preventing heat deaths

Protecting ourselves and our families means monitoring the “simple things.” The first three rules are to make sure we’re drinking plenty of water – this means drinking whether we feel thirsty or not. If we’re not in an air-conditioned place, we’ve got to look for shade. And we need to take regular rest breaks.

Inside a home without air conditioning, placing ice in front of a fan to cool the air can work, but realistically, if you are in a place without air conditioning and the temperatures are approaching 90° F, it’s safest to find another place to stay, if possible.

For those playing sports, there are usually 1-week to 2-week protocols that allow for acclimatization when the season begins – this means starting slowly, without gear, and ramping up activity. Still, parents and coaches should watch advanced weather reports to make sure it’s safe to practice outside.

How we dress can also help us, so light clothing is key. And if we’re able to schedule activities for times when it is cooler, that can also protect us from overheating.

If anyone shows early signs of heat stress, removing clothing, cooling their bodies with cold water, and getting them out of the heat is critical. Any evidence of heatstroke is an emergency, and 911 should be called without delay. The faster the core temperature can be dropped, the better the chances for recovery.

On the level of communities, access to natural air conditioning in the form of healthy tree canopies, and trees at bus stops to provide shade can help a lot. According to Dr. Hoffman, these investments help almost right away. Reimagining our cities to remove the “hot zones” that we have created is another key to protecting ourselves as our climate changes.
 

Reaching our limits in a changing climate

Already, we are seeing more intense, more frequent, and longer-lasting heat waves throughout the country and across the globe.

Dr. Ebi, a coauthor of a recently released scientific analysis that found that the late June Pacific Northwest heat wave would have been virtually impossible without climate change, herself lived through the scorching temperatures in Seattle. Her work shows that the changing climate is killing us right now.

We are approaching a time where extreme temperatures and humidity will make it almost impossible for people to be outside in many parts of the world. Researchers have found that periods of extreme humid heat have more than doubled since 1979, and some places have already had wet-bulb temperatures at the limits of what scientists think humans can tolerate under ideal conditions, meaning for people in perfect health, completely unclothed, in gale-force winds, performing no activity. Obviously that’s less than ideal for most of us and helps explain why thousands of people die at temperatures much lower than our upper limit.

Dr. Ebi pointed out that the good news is that many local communities with a long history of managing high temperatures have a lot of knowledge to share with regions that are newly dealing with these conditions. This includes how local areas develop early warning and response systems with specific action plans.

But, she cautions, it’s going to take a lot of coordination and a lot of behavior change to stabilize the earth’s climate, understand our weak points, and protect our health.

For Dr. Moseson, this reality has hit home.

“I already spent the year being terrified that I as an ICU doctor was going to be the one who gave my mom COVID. Finally I’m vaccinated, she’s vaccinated. Now I’ve watched someone die because they don’t have AC. And my parents, they’re old-school Oregonians, they don’t have AC.”

A version of this article originally appeared on WebMD.com.

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Millions of Americans have been languishing for weeks in the oppressive heat and humidity of a merciless summer. Deadly heat has already taken the lives of hundreds in the Pacific Northwest alone, with numbers likely to grow as the full impact of heat-related deaths eventually comes to light.

In the final week of July, the National Weather Service issued excessive heat warnings for 17 states, stretching from the West Coast, across the Midwest, down south into Louisiana and Georgia. Temperatures 10° to 15° F above average threaten the lives and livelihoods of people all across the country.

After a scorching heat wave in late June, residents of the Pacific Northwest are once again likely to see triple-digit temperatures in the coming days. With the heat, hospitals may face another surge of people with heat-related illnesses.

Erika Moseson, MD, a lung and intensive care specialist, witnessed firsthand the life-threatening impacts of soaring temperatures. She happened to be running her 10-bed intensive care unit in a suburban hospital in Gresham, Ore., about 15 miles east of Portland, the weekend of June 26. Within 12 hours, almost half her ICU beds were filled with people found unconscious on the street, in the bushes, or in their own beds, all because their body’s defenses had become overwhelmed by heat.

“It was unidentified person after unidentified person, coming in, same story, temperatures through the roof, comatose,” Dr. Moseson recalled. Young people in their 20s with muscle breakdown markers through the roof, a sign of rhabdomyolysis; people with no other medical problems that would have put them in a high-risk category.

As a lifelong Oregonian, she’d never seen anything like this before. “We’re all trained for it. I know what happens to you if you have heatstroke, I know how to treat it,” she trailed off, still finding it hard to believe. Still reeling from the number of cases in just a few hours. Still shocked that this happened on what’s supposed to be the cooler, rainforest side of Oregon.

Among those she treated and resuscitated, the memory of a patient that she lost continues to gnaw at her.

“I’ve gone back to it day after day since it happened,” she reflected.

Adults, in their 50s, living at home with their children. Just 1 hour prior, they’d all said goodnight. Then 1 hour later, when a child came to check in, both parents were unconscious.

Dr. Moseson shared how her team tried everything in their power for 18 hours to save the parent that was brought to her ICU. But like hundreds of others who went through the heat wave that weekend, her patient didn’t survive.

It was too late. From Dr. Moseson’s experience, it’s what happens “if you’re cooking a human.”
 

How heat kills

Regardless of where we live on the planet, humans maintain a consistent internal temperature around 98° F for our systems to function properly. 

Our bodies have an entire temperature-regulating system to balance heat gain with heat loss so we don’t stray too far from our ideal range. The hypothalamus functions as the thermostat, communicating with heat sensors in our skin, muscles, and spinal cord. Based on signals about our core body temperature, our nervous system makes many decisions for us – opening up blood vessels in the peripheral parts of our body, pushing more blood toward the skin, and activating sweat glands to produce more sweat.  

Sweat is one of the most powerful tools we have to maintain a safe internal temperature. Of course, there are some things under our control, such as removing clothing, drinking more water, and finding shade (or preferably air conditioning). But beyond that, it’s our ability to sweat that keeps us cool. When sweat evaporates into the air, heat from our skin goes with it, cooling us off.

Over time, our sweat response can work better as we get used to warmer environments, a process that’s known as acclimatization. Over the period of a few days to weeks, the sweat glands of acclimated people can start making sweat at lower temperatures, produce more sweat, and absorb more salt back into our system, all to make us more efficient “sweaters.”

While someone who’s not used to the heat may only produce 1 liter of sweat per hour, people who have become acclimated can produce 2-3 liters every hour, allowing evaporation to eliminate more than two times the amount of heat.   

Because the process of acclimatization can take some time, typically it’s the first throes of summer, or heat waves in places where people don’t typically see high temperatures, that are the most deadly. And of course, the right infrastructure, like access to air conditioning, also plays a large role in limiting heat-related death and hospitalization.

A 2019 study showed that heat-related hospitalizations peak at different temperatures in different places. For example, hospitalizations typically peak in Texas when the temperature hits 105° F. But they might be highest in the Pacific Northwest at just 81° F.

Even with acclimatization, there are limits to how much our bodies can adapt to heat. When the humidity goes up past 75%, there’s already so much moisture in the air that heat loss through evaporation no longer occurs.

It’s this connection between heat and humidity that can be deadly. This is why the heat index (a measure that takes into account temperature and relative humidity) and wet bulb globe temperature (a measure commonly used by the military and competitive athletes that takes into account temperature, humidity, wind speed, sun angle, and cloud cover) are both better at showing how dangerous the heat may be for our health, compared to temperature alone.

Kristie L. Ebi, PhD, a professor in the Center for Health and the Global Environment at the University of Washington, Seattle, has been studying the effects of heat and other climate-sensitive conditions on health for over 20 years. She stresses that it’s not just the recorded temperatures, but the prolonged exposure that kills.

If you never get a chance to bring down that core body temperature, if your internal temperatures stay above the range where your cells and your organs can work well for a long time, that’s when you can have the most dangerous effects of heat.

“It depends then on your age, your fitness, your individual physiology, underlying medical conditions, to how quickly that could affect the functioning of those organs. There’s lots of variability in there,” Dr. Ebi said.

Our hearts take on the brunt of the early response, working harder to pump blood toward the skin. Water and salt loss through our skin can start to cause electrolyte changes that can cause heat cramps and heat exhaustion. We feel tired, nauseated, dizzy. With enough water loss, we may become dehydrated, limiting the blood flow to our brains, causing us to pass out.

These early signs are like a car’s check engine light – systems are already being damaged, but resting, refueling, and, most importantly, turning off the heat are critical steps to prevent fatal injury.

If hazardous heat exposure continues and our internal temperatures continue to rise, nerves stop talking to each other, the proteins in our body unfold and lose their shape, and the cells of our organs disintegrate. This in turn sets off a fire alarm in our blood vessels, where a variety of chemical messengers, including “heat-shock proteins,” are released. The release of these inflammatory proteins, coupled with the loss of blood flow, eventually leads to the death of cells throughout the body, from the brain, to the heart, the muscles, and the kidneys.

This process is referred to as heatstroke. In essence, we melt from the inside.

At a certain point, this cascade can’t be reversed. Just like when you cool a melting block of ice, the parts that have melted will not go back to their original shape. It’s a similar process in our bodies, so delays in cooling and treatment can lead to death rates as high as 80%.

On the outside, we see people who look confused and disoriented, with hot skin and rapid breathing, and they may eventually become unconscious. Core body temperatures over 105° F clinch the diagnosis, but at the first sign of feeling unwell, cooling should be started.

There is no fancier or more effective treatment than that: Cool right away. In emergency rooms in Washington State, doctors used body bags filled with ice and water to cool victims of the heat wave in late June.

“It was all from heat ... that’s the thing, you feel so idiotic ... you’re like, ‘I’ve given you ice’ ... you bring their temperature down. But it’s already set off this cascade that you can’t stop,” Dr. Moseson said.

By the time Dr. Moseson’s patient made it to her, cooling with ice was just the beginning of the attempts to resuscitate and revive. The patient was already showing evidence of a process causing widespread bleeding and clotting, known as disseminated intravascular coagulation, along with damage to the heart and failing kidneys. Over 18 hours, her team cooled the patient, flooded the blood vessels with fluids and blood products, attempted to start dialysis, and inserted a breathing tube – all of the technology that is used to save people from serious cardiovascular collapse from other conditions. But nothing could reverse the melting that had already occurred.

Deaths from heat are 100% preventable. Until they’re not.
 

 

 

No respite

As Dr. Ebi says, the key to preventing heat-related death is to cool down enough to stabilize our internal cells and proteins before the irreversible cascade begins.

But for close to 80% of Americans who live in urban areas, temperatures can be even higher and more intolerable compared to surrounding areas because of the way we’ve designed our cities. In effect, we have unintentionally created hot zones called “urban heat islands.”

Jeremy Hoffman, PhD, chief scientist for the Science Museum of Virginia, explains that things like bricks, asphalt, and parking lots absorb more of the sun’s energy throughout the day and then emit that back into the air as heat throughout the afternoon and into the evening. This raises the air and surface temperatures in cities, relative to rural areas. When temperatures don’t cool enough at night, there’s no way to recover from the day’s heat. You start the next day still depleted, with less reserve to face the heat of a new day.

When you dig even deeper, it turns out that even within the same city, there are huge “thermal inequities,” as Dr. Hoffman calls them. In a 2019 study, he found that wealthier parts of cities had more natural spaces such as parks and tree-lined streets, compared to areas that had been intentionally “redlined,” or systematically deprived of investment. This pattern repeats itself in over 100 urban areas across the country and translates to huge temperature differences on the order of 10-20 degrees Fahrenheit within the same city, at the exact same time during a heat wave.

“In some ways, the way that we’ve decided to plan and build our cities physically turns up the thermostat by several tens of degrees during heat waves in particular neighborhoods,” Dr. Hoffman said.

Dr. Hoffman’s work showed that the city of Portland (where the death toll from the heat wave in late June was the highest) had some of the most intense differences between formerly redlined vs. tree-lined areas out of the more than 100 cities that he studied.  

“Watching it play out, I was really concerned, not only as a climate scientist, but as a human. Understanding the urban heat island effect and the extreme nature of the inequity in our cities, thermally and otherwise, once you start to really recognize it, you can’t forget it.”
 

The most vulnerable

When it comes to identifying and protecting the people most vulnerable to heat stress and heat-related death, there is an ever-growing list of those most at risk. Unfortunately, very few recognize when they themselves are at risk, often until it’s too late.

According to Linda McCauley, PhD, dean of the Emory University School of Nursing in Atlanta, “the scope of who is vulnerable is quickly increasing.”

For example, we’re used to recognizing that pregnant women and young children are at risk. Public health campaigns have long advised us not to leave young children and pets in hot cars. We know that adolescents who play sports during hot summer months are at high risk for heat-related events and even death.

In Georgia, a 15-year-old boy collapsed and died after his first day back at football practice when the heat index was 105° F on July 26, even as it appears that all protocols for heat safety were being followed.

We recognize that outdoor workers face devastating consequences from prolonged exertion in the heat and must have safer working conditions.

The elderly and those with long-term medical and mental health conditions are also more vulnerable to heat. The elderly may not have the same warning signs and may not recognize that they are dehydrated until it is too late. In addition, their sweating mechanism weakens, and they may be taking medicines that interfere with their ability to regulate their temperature.

Poverty and inadequate housing are risk factors, especially for those in urban heat islands. For many people, their housing does not have enough cooling to protect them, and they can’t safely get themselves to cooling shelters.

These patterns for the most vulnerable fit for the majority of deaths in Oregon during the late June heat wave. Most victims were older, lived alone, and didn’t have air conditioning. But with climate change, the predictions are that temperatures will go higher and heat waves will last longer.

“There’s probably very few people today that are ‘immune’ to the effects of heat-related stress with climate change. All of us can be put in situations where we are susceptible,” Dr. McCauley said.

Dr. Moseson agreed. Many of her patients fit none of these risk categories – she treated people with no health problems in their 20s in her ICU, and the patient she lost would not traditionally have been thought of as high risk. That 50-something patient had no long-standing medical problems, and lived with family in a newly renovated suburban home that had air conditioning. The only problem was that the air conditioner had broken and there had been no rush to fix it based on past experience with Oregon summers.
 

 

 

Preventing heat deaths

Protecting ourselves and our families means monitoring the “simple things.” The first three rules are to make sure we’re drinking plenty of water – this means drinking whether we feel thirsty or not. If we’re not in an air-conditioned place, we’ve got to look for shade. And we need to take regular rest breaks.

Inside a home without air conditioning, placing ice in front of a fan to cool the air can work, but realistically, if you are in a place without air conditioning and the temperatures are approaching 90° F, it’s safest to find another place to stay, if possible.

For those playing sports, there are usually 1-week to 2-week protocols that allow for acclimatization when the season begins – this means starting slowly, without gear, and ramping up activity. Still, parents and coaches should watch advanced weather reports to make sure it’s safe to practice outside.

How we dress can also help us, so light clothing is key. And if we’re able to schedule activities for times when it is cooler, that can also protect us from overheating.

If anyone shows early signs of heat stress, removing clothing, cooling their bodies with cold water, and getting them out of the heat is critical. Any evidence of heatstroke is an emergency, and 911 should be called without delay. The faster the core temperature can be dropped, the better the chances for recovery.

On the level of communities, access to natural air conditioning in the form of healthy tree canopies, and trees at bus stops to provide shade can help a lot. According to Dr. Hoffman, these investments help almost right away. Reimagining our cities to remove the “hot zones” that we have created is another key to protecting ourselves as our climate changes.
 

Reaching our limits in a changing climate

Already, we are seeing more intense, more frequent, and longer-lasting heat waves throughout the country and across the globe.

Dr. Ebi, a coauthor of a recently released scientific analysis that found that the late June Pacific Northwest heat wave would have been virtually impossible without climate change, herself lived through the scorching temperatures in Seattle. Her work shows that the changing climate is killing us right now.

We are approaching a time where extreme temperatures and humidity will make it almost impossible for people to be outside in many parts of the world. Researchers have found that periods of extreme humid heat have more than doubled since 1979, and some places have already had wet-bulb temperatures at the limits of what scientists think humans can tolerate under ideal conditions, meaning for people in perfect health, completely unclothed, in gale-force winds, performing no activity. Obviously that’s less than ideal for most of us and helps explain why thousands of people die at temperatures much lower than our upper limit.

Dr. Ebi pointed out that the good news is that many local communities with a long history of managing high temperatures have a lot of knowledge to share with regions that are newly dealing with these conditions. This includes how local areas develop early warning and response systems with specific action plans.

But, she cautions, it’s going to take a lot of coordination and a lot of behavior change to stabilize the earth’s climate, understand our weak points, and protect our health.

For Dr. Moseson, this reality has hit home.

“I already spent the year being terrified that I as an ICU doctor was going to be the one who gave my mom COVID. Finally I’m vaccinated, she’s vaccinated. Now I’ve watched someone die because they don’t have AC. And my parents, they’re old-school Oregonians, they don’t have AC.”

A version of this article originally appeared on WebMD.com.

Millions of Americans have been languishing for weeks in the oppressive heat and humidity of a merciless summer. Deadly heat has already taken the lives of hundreds in the Pacific Northwest alone, with numbers likely to grow as the full impact of heat-related deaths eventually comes to light.

In the final week of July, the National Weather Service issued excessive heat warnings for 17 states, stretching from the West Coast, across the Midwest, down south into Louisiana and Georgia. Temperatures 10° to 15° F above average threaten the lives and livelihoods of people all across the country.

After a scorching heat wave in late June, residents of the Pacific Northwest are once again likely to see triple-digit temperatures in the coming days. With the heat, hospitals may face another surge of people with heat-related illnesses.

Erika Moseson, MD, a lung and intensive care specialist, witnessed firsthand the life-threatening impacts of soaring temperatures. She happened to be running her 10-bed intensive care unit in a suburban hospital in Gresham, Ore., about 15 miles east of Portland, the weekend of June 26. Within 12 hours, almost half her ICU beds were filled with people found unconscious on the street, in the bushes, or in their own beds, all because their body’s defenses had become overwhelmed by heat.

“It was unidentified person after unidentified person, coming in, same story, temperatures through the roof, comatose,” Dr. Moseson recalled. Young people in their 20s with muscle breakdown markers through the roof, a sign of rhabdomyolysis; people with no other medical problems that would have put them in a high-risk category.

As a lifelong Oregonian, she’d never seen anything like this before. “We’re all trained for it. I know what happens to you if you have heatstroke, I know how to treat it,” she trailed off, still finding it hard to believe. Still reeling from the number of cases in just a few hours. Still shocked that this happened on what’s supposed to be the cooler, rainforest side of Oregon.

Among those she treated and resuscitated, the memory of a patient that she lost continues to gnaw at her.

“I’ve gone back to it day after day since it happened,” she reflected.

Adults, in their 50s, living at home with their children. Just 1 hour prior, they’d all said goodnight. Then 1 hour later, when a child came to check in, both parents were unconscious.

Dr. Moseson shared how her team tried everything in their power for 18 hours to save the parent that was brought to her ICU. But like hundreds of others who went through the heat wave that weekend, her patient didn’t survive.

It was too late. From Dr. Moseson’s experience, it’s what happens “if you’re cooking a human.”
 

How heat kills

Regardless of where we live on the planet, humans maintain a consistent internal temperature around 98° F for our systems to function properly. 

Our bodies have an entire temperature-regulating system to balance heat gain with heat loss so we don’t stray too far from our ideal range. The hypothalamus functions as the thermostat, communicating with heat sensors in our skin, muscles, and spinal cord. Based on signals about our core body temperature, our nervous system makes many decisions for us – opening up blood vessels in the peripheral parts of our body, pushing more blood toward the skin, and activating sweat glands to produce more sweat.  

Sweat is one of the most powerful tools we have to maintain a safe internal temperature. Of course, there are some things under our control, such as removing clothing, drinking more water, and finding shade (or preferably air conditioning). But beyond that, it’s our ability to sweat that keeps us cool. When sweat evaporates into the air, heat from our skin goes with it, cooling us off.

Over time, our sweat response can work better as we get used to warmer environments, a process that’s known as acclimatization. Over the period of a few days to weeks, the sweat glands of acclimated people can start making sweat at lower temperatures, produce more sweat, and absorb more salt back into our system, all to make us more efficient “sweaters.”

While someone who’s not used to the heat may only produce 1 liter of sweat per hour, people who have become acclimated can produce 2-3 liters every hour, allowing evaporation to eliminate more than two times the amount of heat.   

Because the process of acclimatization can take some time, typically it’s the first throes of summer, or heat waves in places where people don’t typically see high temperatures, that are the most deadly. And of course, the right infrastructure, like access to air conditioning, also plays a large role in limiting heat-related death and hospitalization.

A 2019 study showed that heat-related hospitalizations peak at different temperatures in different places. For example, hospitalizations typically peak in Texas when the temperature hits 105° F. But they might be highest in the Pacific Northwest at just 81° F.

Even with acclimatization, there are limits to how much our bodies can adapt to heat. When the humidity goes up past 75%, there’s already so much moisture in the air that heat loss through evaporation no longer occurs.

It’s this connection between heat and humidity that can be deadly. This is why the heat index (a measure that takes into account temperature and relative humidity) and wet bulb globe temperature (a measure commonly used by the military and competitive athletes that takes into account temperature, humidity, wind speed, sun angle, and cloud cover) are both better at showing how dangerous the heat may be for our health, compared to temperature alone.

Kristie L. Ebi, PhD, a professor in the Center for Health and the Global Environment at the University of Washington, Seattle, has been studying the effects of heat and other climate-sensitive conditions on health for over 20 years. She stresses that it’s not just the recorded temperatures, but the prolonged exposure that kills.

If you never get a chance to bring down that core body temperature, if your internal temperatures stay above the range where your cells and your organs can work well for a long time, that’s when you can have the most dangerous effects of heat.

“It depends then on your age, your fitness, your individual physiology, underlying medical conditions, to how quickly that could affect the functioning of those organs. There’s lots of variability in there,” Dr. Ebi said.

Our hearts take on the brunt of the early response, working harder to pump blood toward the skin. Water and salt loss through our skin can start to cause electrolyte changes that can cause heat cramps and heat exhaustion. We feel tired, nauseated, dizzy. With enough water loss, we may become dehydrated, limiting the blood flow to our brains, causing us to pass out.

These early signs are like a car’s check engine light – systems are already being damaged, but resting, refueling, and, most importantly, turning off the heat are critical steps to prevent fatal injury.

If hazardous heat exposure continues and our internal temperatures continue to rise, nerves stop talking to each other, the proteins in our body unfold and lose their shape, and the cells of our organs disintegrate. This in turn sets off a fire alarm in our blood vessels, where a variety of chemical messengers, including “heat-shock proteins,” are released. The release of these inflammatory proteins, coupled with the loss of blood flow, eventually leads to the death of cells throughout the body, from the brain, to the heart, the muscles, and the kidneys.

This process is referred to as heatstroke. In essence, we melt from the inside.

At a certain point, this cascade can’t be reversed. Just like when you cool a melting block of ice, the parts that have melted will not go back to their original shape. It’s a similar process in our bodies, so delays in cooling and treatment can lead to death rates as high as 80%.

On the outside, we see people who look confused and disoriented, with hot skin and rapid breathing, and they may eventually become unconscious. Core body temperatures over 105° F clinch the diagnosis, but at the first sign of feeling unwell, cooling should be started.

There is no fancier or more effective treatment than that: Cool right away. In emergency rooms in Washington State, doctors used body bags filled with ice and water to cool victims of the heat wave in late June.

“It was all from heat ... that’s the thing, you feel so idiotic ... you’re like, ‘I’ve given you ice’ ... you bring their temperature down. But it’s already set off this cascade that you can’t stop,” Dr. Moseson said.

By the time Dr. Moseson’s patient made it to her, cooling with ice was just the beginning of the attempts to resuscitate and revive. The patient was already showing evidence of a process causing widespread bleeding and clotting, known as disseminated intravascular coagulation, along with damage to the heart and failing kidneys. Over 18 hours, her team cooled the patient, flooded the blood vessels with fluids and blood products, attempted to start dialysis, and inserted a breathing tube – all of the technology that is used to save people from serious cardiovascular collapse from other conditions. But nothing could reverse the melting that had already occurred.

Deaths from heat are 100% preventable. Until they’re not.
 

 

 

No respite

As Dr. Ebi says, the key to preventing heat-related death is to cool down enough to stabilize our internal cells and proteins before the irreversible cascade begins.

But for close to 80% of Americans who live in urban areas, temperatures can be even higher and more intolerable compared to surrounding areas because of the way we’ve designed our cities. In effect, we have unintentionally created hot zones called “urban heat islands.”

Jeremy Hoffman, PhD, chief scientist for the Science Museum of Virginia, explains that things like bricks, asphalt, and parking lots absorb more of the sun’s energy throughout the day and then emit that back into the air as heat throughout the afternoon and into the evening. This raises the air and surface temperatures in cities, relative to rural areas. When temperatures don’t cool enough at night, there’s no way to recover from the day’s heat. You start the next day still depleted, with less reserve to face the heat of a new day.

When you dig even deeper, it turns out that even within the same city, there are huge “thermal inequities,” as Dr. Hoffman calls them. In a 2019 study, he found that wealthier parts of cities had more natural spaces such as parks and tree-lined streets, compared to areas that had been intentionally “redlined,” or systematically deprived of investment. This pattern repeats itself in over 100 urban areas across the country and translates to huge temperature differences on the order of 10-20 degrees Fahrenheit within the same city, at the exact same time during a heat wave.

“In some ways, the way that we’ve decided to plan and build our cities physically turns up the thermostat by several tens of degrees during heat waves in particular neighborhoods,” Dr. Hoffman said.

Dr. Hoffman’s work showed that the city of Portland (where the death toll from the heat wave in late June was the highest) had some of the most intense differences between formerly redlined vs. tree-lined areas out of the more than 100 cities that he studied.  

“Watching it play out, I was really concerned, not only as a climate scientist, but as a human. Understanding the urban heat island effect and the extreme nature of the inequity in our cities, thermally and otherwise, once you start to really recognize it, you can’t forget it.”
 

The most vulnerable

When it comes to identifying and protecting the people most vulnerable to heat stress and heat-related death, there is an ever-growing list of those most at risk. Unfortunately, very few recognize when they themselves are at risk, often until it’s too late.

According to Linda McCauley, PhD, dean of the Emory University School of Nursing in Atlanta, “the scope of who is vulnerable is quickly increasing.”

For example, we’re used to recognizing that pregnant women and young children are at risk. Public health campaigns have long advised us not to leave young children and pets in hot cars. We know that adolescents who play sports during hot summer months are at high risk for heat-related events and even death.

In Georgia, a 15-year-old boy collapsed and died after his first day back at football practice when the heat index was 105° F on July 26, even as it appears that all protocols for heat safety were being followed.

We recognize that outdoor workers face devastating consequences from prolonged exertion in the heat and must have safer working conditions.

The elderly and those with long-term medical and mental health conditions are also more vulnerable to heat. The elderly may not have the same warning signs and may not recognize that they are dehydrated until it is too late. In addition, their sweating mechanism weakens, and they may be taking medicines that interfere with their ability to regulate their temperature.

Poverty and inadequate housing are risk factors, especially for those in urban heat islands. For many people, their housing does not have enough cooling to protect them, and they can’t safely get themselves to cooling shelters.

These patterns for the most vulnerable fit for the majority of deaths in Oregon during the late June heat wave. Most victims were older, lived alone, and didn’t have air conditioning. But with climate change, the predictions are that temperatures will go higher and heat waves will last longer.

“There’s probably very few people today that are ‘immune’ to the effects of heat-related stress with climate change. All of us can be put in situations where we are susceptible,” Dr. McCauley said.

Dr. Moseson agreed. Many of her patients fit none of these risk categories – she treated people with no health problems in their 20s in her ICU, and the patient she lost would not traditionally have been thought of as high risk. That 50-something patient had no long-standing medical problems, and lived with family in a newly renovated suburban home that had air conditioning. The only problem was that the air conditioner had broken and there had been no rush to fix it based on past experience with Oregon summers.
 

 

 

Preventing heat deaths

Protecting ourselves and our families means monitoring the “simple things.” The first three rules are to make sure we’re drinking plenty of water – this means drinking whether we feel thirsty or not. If we’re not in an air-conditioned place, we’ve got to look for shade. And we need to take regular rest breaks.

Inside a home without air conditioning, placing ice in front of a fan to cool the air can work, but realistically, if you are in a place without air conditioning and the temperatures are approaching 90° F, it’s safest to find another place to stay, if possible.

For those playing sports, there are usually 1-week to 2-week protocols that allow for acclimatization when the season begins – this means starting slowly, without gear, and ramping up activity. Still, parents and coaches should watch advanced weather reports to make sure it’s safe to practice outside.

How we dress can also help us, so light clothing is key. And if we’re able to schedule activities for times when it is cooler, that can also protect us from overheating.

If anyone shows early signs of heat stress, removing clothing, cooling their bodies with cold water, and getting them out of the heat is critical. Any evidence of heatstroke is an emergency, and 911 should be called without delay. The faster the core temperature can be dropped, the better the chances for recovery.

On the level of communities, access to natural air conditioning in the form of healthy tree canopies, and trees at bus stops to provide shade can help a lot. According to Dr. Hoffman, these investments help almost right away. Reimagining our cities to remove the “hot zones” that we have created is another key to protecting ourselves as our climate changes.
 

Reaching our limits in a changing climate

Already, we are seeing more intense, more frequent, and longer-lasting heat waves throughout the country and across the globe.

Dr. Ebi, a coauthor of a recently released scientific analysis that found that the late June Pacific Northwest heat wave would have been virtually impossible without climate change, herself lived through the scorching temperatures in Seattle. Her work shows that the changing climate is killing us right now.

We are approaching a time where extreme temperatures and humidity will make it almost impossible for people to be outside in many parts of the world. Researchers have found that periods of extreme humid heat have more than doubled since 1979, and some places have already had wet-bulb temperatures at the limits of what scientists think humans can tolerate under ideal conditions, meaning for people in perfect health, completely unclothed, in gale-force winds, performing no activity. Obviously that’s less than ideal for most of us and helps explain why thousands of people die at temperatures much lower than our upper limit.

Dr. Ebi pointed out that the good news is that many local communities with a long history of managing high temperatures have a lot of knowledge to share with regions that are newly dealing with these conditions. This includes how local areas develop early warning and response systems with specific action plans.

But, she cautions, it’s going to take a lot of coordination and a lot of behavior change to stabilize the earth’s climate, understand our weak points, and protect our health.

For Dr. Moseson, this reality has hit home.

“I already spent the year being terrified that I as an ICU doctor was going to be the one who gave my mom COVID. Finally I’m vaccinated, she’s vaccinated. Now I’ve watched someone die because they don’t have AC. And my parents, they’re old-school Oregonians, they don’t have AC.”

A version of this article originally appeared on WebMD.com.

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Hospitalists and medical malpractice

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Wed, 08/04/2021 - 11:37

A look at some sobering trends

Among the pressures felt by hospitalists are concerns about being subject to a malpractice claim. Anxiety about malpractice influences the way hospitalists practice, giving rise to defensive medicine.

Dr. Adam C. Schaffer, attending physician in the Hospital Medicine Unit at Brigham and Women's Hospital, instructor at Harvard Medical School, senior clinical analytics specialist at CRICO/Risk Management Foundation of the Harvard Medical Institutions.
Dr. Adam C. Schaffer

One survey, which asked hospitalists to retrospectively rate which of their orders represented defensive medicine, found that 28% of orders were deemed defensive.1 Defensive medicine can lead to low-value medical care, drive up health care costs, and potentially subject patients to unnecessary testing.2,3

Encouragingly, medical malpractice claims rates have, overall, been downtrending. An analysis of data from the National Practitioner Data Bank, which is a repository of all paid malpractice claims against individual physicians, found that malpractice claims rates decreased by 55.7% from 1992 to 2014 among all specialties, and by 46.1% for internal medicine physicians.4 The data used in this analysis did not separate hospitalists from other internal medicine physicians. An older study of malpractice claims against hospitalists found that hospitalists had significantly lower claims rates than non-hospitalist internal medicine physicians.5

Current malpractice environment for hospitalists

Seeking to shed light on the current malpractice environment faced by hospitalists, a recent study examined claims against hospitalists using the Comparative Benchmarking System (CBS), a national database of malpractice claims containing approximately 30% of all U.S. malpractice claims, which is maintained by CRICO, the malpractice insurer for the Harvard-affiliated medical institutions.6

Claims in the CBS database are examined by trained nurse coders who review the claims, along with the associated medical and legal records, to understand the contributing factors behind the adverse event leading to the claim.

Contrary to the trends for nearly all other physician specialties, the malpractice claims rates of hospitalists were not downtrending, going from 1.77 claims per 100 physician-years from 2009-2013 to 2.08 claims per 100 physician-years from 2014-2018. The overall claims rate for hospitalists was significantly higher than that for internal medicine subspecialists (though roughly the same as the claims rate for non-hospitalist general internal medicine physicians). These sobering findings raise the important question of why hospitalists claims rates are heading in the wrong direction.

One possible answer relates the ever-broadening scope of hospitalist practice. Hospitalists are being asked to care for surgical patients and other patient populations that they may have less familiarity with, increasing the risk of medical errors. Among the other specialties most commonly also named in hospitalist claims, general surgery and orthopedic surgery are in the top five. The extraordinary growth in the field of hospital medicine has meant a need to hire an increasing number of hospitalists, leading to less-experienced physicians entering the field.
 

Making hospital medicine safer

A more urgent question than what is driving the trends in hospitalist claims rates is what can be done to avoid adverse events and make hospital medicine safer. One potential answer is thoughtful collaboration arrangements with the surgical and other specialties with whom hospitalists may be co-managing patients.

Questions about who responds to what types of clinical issues that might arise and specific domains of responsibility should be defined in advance, so that a lack of role clarity does not negatively impact patient care. Given that hospitalists will be less comfortable addressing more technical surgical issues, expectations about surgeons’ availability should be established. Nocturnists may be tasked with overnight cross-coverage of patients on services, such as oncology and cardiology, that subspecialty physicians have responsibility for during the day. Agreeing upon triggers for when the nocturnist should contact the daytime subspecialty attending (for example, if a rapid response is called on their patient) should be considered, so that nocturnists are not left deciding, in the moment, whether to call the daytime attending. Measures such as this ensure that everyone’s expectations are aligned. In addition, new hospitalists need to be offered support, in the form of training and mentorship.

CBS malpractice data, which includes the contributing factors underlying what went wrong, illuminates potential targets for programs designed to enhance patient safety. In the recent hospitalist malpractice study, the two contributing factors that were the best predictors of a hospitalist malpractice claim closing with payment to the claimant were clinical judgment errors and communication breakdowns. Identifying measures that are effective in promoting patient safety by refining the clinical judgement of clinicians is a challenge, and there are limited data demonstrating what programs are effective in this area.

Clinical decision support (CDS) systems have shown promise in promoting guideline-concordant care.7 However, the role of CDS in aiding the higher-stakes clinical decisions that may be called into question after an adverse outcome is not well defined. Alerts that a patient may be developing sepsis is one type of CDS that has been extensively studied and has been shown to be of some benefit.8 The importance of clinical judgment to whether payment is made on a malpractice claim can inform risk management strategies. Hospitalists should document the thought process behind their decision making in the chart, especially for important clinical decisions. A note showing that the clinician was thoughtfully weighing the risks and benefits using the data available at the time will help make a case defensible if an adverse outcome occurs.

The effect of communication breakdowns on hospitalist case outcomes highlights the importance of measures to improve and systematize communication among clinicians, particularly at vulnerable junctures – such as handoffs from the day team to the night team, and transitions from one care setting to another. An example of an intervention to improve handoffs with cogent evidence to support it is I-PASS, which is an approach to handoffs between teams in which information about the patient’s illness severity, clinical background, and contingencies is conveyed and synthesized in a structured manner. A study of the effect of implementation of I-PASS among nine pediatric residency programs demonstrated a 30% reduction in preventable adverse events.9

 

 

Applying insights from malpractice claims analysis to clinical practice

The systematic review of malpractice cases to determine the contributing factors and other case attributes is an important source of patient safety insights. The process breakdowns described by the contributing factors can inform the design of patient safety initiatives. In addition, malpractice data provides information on which specialties and what types of clinicians are being named together in malpractice claims.

In the hospitalist malpractice study, in addition to general surgery and orthopedic surgery, the other clinical services most commonly subject to claims along with hospitalists were nursing, emergency medicine, and cardiology. Another observation was that physician assistants and nurse practitioners are increasingly being named in hospitalist claims. This information is crucial to guiding who needs to be in the room with hospitalists when efforts are undertaken to enhance patient safety within hospital medicine.

An understandable response to the finding that hospitalist claims rates are not decreasing is for hospitalists to seek ways to lower their risk of being named in a malpractice claim. Of course, avoiding adverse events by providing the safest possible care is paramount. Even when patients do suffer adverse events due to a physician negligence, only rarely, less than 5% of the time, does this result in a malpractice claim.10 Important lessons in risk management can be learned from examining why patients decide to sue when mistakes lead to bad outcomes.

An analysis of plaintiffs’ depositions found that the key reasons that patients decided to file a malpractice claim include a poor relationship with the physician – specifically, a lack of empathy from the physician, feeling deserted by the physician, and feeling devalued by the physician.11 These findings support the use of programs that assist physicians in compassionately disclosing adverse events to patients. Among inpatient physicians, patient satisfaction survey questions about the time the physician spent with the patient and the physician’s concern for the patient are better predictors of the physicians’ risk management performance than is the question about the skill of the physician.12 In the aftermath of an adverse event, focusing on maintaining a strong patient-physician relationship is not only the right the thing to do, the data tell us that it is also a sensible approach to reducing medicolegal risk.
 

Dr. Schaffer practices as a member of the Hospital Medicine Unit at Brigham and Women’s Hospital, Boston, where he serves as an attending physician on the inpatient general medicine services. An instructor at Harvard Medical School, his academic interests include research using large medical malpractice databases to examine temporal trends in medical malpractice.

References

1. Rothberg MB, et al. The cost of defensive medicine on 3 hospital medicine services. JAMA Intern Med. 2014;174(11):1867-1868. doi:10.1001/jamainternmed.2014.4649.

2. Kachalia A, et al. Overuse of testing in preoperative evaluation and syncope: A survey of hospitalists. Ann Intern Med. 2015;162(2):100-108. doi: 10.7326/M14-0694.

3. Mello MM, et al. National costs of the medical liability system. Health Aff (Millwood). 2010;29(9):1569-1577. doi: 10.1377/hlthaff.2009.0807.

4. Schaffer AC, et al. Rates and characteristics of paid malpractice claims among U.S. physicians by specialty, 1992-2014. JAMA Intern Med. 2017;177(5):710-718. doi:10.1001/jamainternmed.2017.0311.

5. Schaffer AC, et al. Liability impact of the hospitalist model of care. J Hosp Med. 2014;9(12):750-755. doi: 10.1002/jhm.2244.

6. Schaffer AC, et al. Rates and characteristics of medical malpractice claims against hospitalists. J Hosp Med. 2021 Jul;16(7):390-396. doi: 10.12788/jhm.3557.

7. Poon EG. Clinical decision support: a tool of the hospital trade. J Hosp Med. 2015;10(1):60-61. doi: 10.1002/jhm.2295.

8. Makam AN, Nguyen OK, Auerbach AD. Diagnostic accuracy and effectiveness of automated electronic sepsis alert systems: A systematic review. J Hosp Med. 2015;10(6):396-402. doi: 10.1002/jhm.2347.

9. Starmer AJ, et al. Changes in medical errors after implementation of a handoff program. N Engl J Med. 2014;371(19):1803-1812. doi: 10.1056/NEJMsa1405556.

10. Localio AR, et al. Relation between malpractice claims and adverse events due to negligence. Results of the Harvard Medical Practice Study III. N Engl J Med. 1991;325(4):245-251. doi: 10.1056/NEJM199107253250405.

11. Beckman HB, et al. The doctor-patient relationship and malpractice. Lessons from plaintiff depositions. Arch Intern Med. 1994;154(12):1365-1370. doi:10.1001/archinte.1994.00420120093010.

12. Stelfox HT, et al. The relation of patient satisfaction with complaints against physicians and malpractice lawsuits. Am J Med. 2005;118(10):1126-1133. doi: 10.1016/j.amjmed.2005.01.060.

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A look at some sobering trends

A look at some sobering trends

Among the pressures felt by hospitalists are concerns about being subject to a malpractice claim. Anxiety about malpractice influences the way hospitalists practice, giving rise to defensive medicine.

Dr. Adam C. Schaffer, attending physician in the Hospital Medicine Unit at Brigham and Women's Hospital, instructor at Harvard Medical School, senior clinical analytics specialist at CRICO/Risk Management Foundation of the Harvard Medical Institutions.
Dr. Adam C. Schaffer

One survey, which asked hospitalists to retrospectively rate which of their orders represented defensive medicine, found that 28% of orders were deemed defensive.1 Defensive medicine can lead to low-value medical care, drive up health care costs, and potentially subject patients to unnecessary testing.2,3

Encouragingly, medical malpractice claims rates have, overall, been downtrending. An analysis of data from the National Practitioner Data Bank, which is a repository of all paid malpractice claims against individual physicians, found that malpractice claims rates decreased by 55.7% from 1992 to 2014 among all specialties, and by 46.1% for internal medicine physicians.4 The data used in this analysis did not separate hospitalists from other internal medicine physicians. An older study of malpractice claims against hospitalists found that hospitalists had significantly lower claims rates than non-hospitalist internal medicine physicians.5

Current malpractice environment for hospitalists

Seeking to shed light on the current malpractice environment faced by hospitalists, a recent study examined claims against hospitalists using the Comparative Benchmarking System (CBS), a national database of malpractice claims containing approximately 30% of all U.S. malpractice claims, which is maintained by CRICO, the malpractice insurer for the Harvard-affiliated medical institutions.6

Claims in the CBS database are examined by trained nurse coders who review the claims, along with the associated medical and legal records, to understand the contributing factors behind the adverse event leading to the claim.

Contrary to the trends for nearly all other physician specialties, the malpractice claims rates of hospitalists were not downtrending, going from 1.77 claims per 100 physician-years from 2009-2013 to 2.08 claims per 100 physician-years from 2014-2018. The overall claims rate for hospitalists was significantly higher than that for internal medicine subspecialists (though roughly the same as the claims rate for non-hospitalist general internal medicine physicians). These sobering findings raise the important question of why hospitalists claims rates are heading in the wrong direction.

One possible answer relates the ever-broadening scope of hospitalist practice. Hospitalists are being asked to care for surgical patients and other patient populations that they may have less familiarity with, increasing the risk of medical errors. Among the other specialties most commonly also named in hospitalist claims, general surgery and orthopedic surgery are in the top five. The extraordinary growth in the field of hospital medicine has meant a need to hire an increasing number of hospitalists, leading to less-experienced physicians entering the field.
 

Making hospital medicine safer

A more urgent question than what is driving the trends in hospitalist claims rates is what can be done to avoid adverse events and make hospital medicine safer. One potential answer is thoughtful collaboration arrangements with the surgical and other specialties with whom hospitalists may be co-managing patients.

Questions about who responds to what types of clinical issues that might arise and specific domains of responsibility should be defined in advance, so that a lack of role clarity does not negatively impact patient care. Given that hospitalists will be less comfortable addressing more technical surgical issues, expectations about surgeons’ availability should be established. Nocturnists may be tasked with overnight cross-coverage of patients on services, such as oncology and cardiology, that subspecialty physicians have responsibility for during the day. Agreeing upon triggers for when the nocturnist should contact the daytime subspecialty attending (for example, if a rapid response is called on their patient) should be considered, so that nocturnists are not left deciding, in the moment, whether to call the daytime attending. Measures such as this ensure that everyone’s expectations are aligned. In addition, new hospitalists need to be offered support, in the form of training and mentorship.

CBS malpractice data, which includes the contributing factors underlying what went wrong, illuminates potential targets for programs designed to enhance patient safety. In the recent hospitalist malpractice study, the two contributing factors that were the best predictors of a hospitalist malpractice claim closing with payment to the claimant were clinical judgment errors and communication breakdowns. Identifying measures that are effective in promoting patient safety by refining the clinical judgement of clinicians is a challenge, and there are limited data demonstrating what programs are effective in this area.

Clinical decision support (CDS) systems have shown promise in promoting guideline-concordant care.7 However, the role of CDS in aiding the higher-stakes clinical decisions that may be called into question after an adverse outcome is not well defined. Alerts that a patient may be developing sepsis is one type of CDS that has been extensively studied and has been shown to be of some benefit.8 The importance of clinical judgment to whether payment is made on a malpractice claim can inform risk management strategies. Hospitalists should document the thought process behind their decision making in the chart, especially for important clinical decisions. A note showing that the clinician was thoughtfully weighing the risks and benefits using the data available at the time will help make a case defensible if an adverse outcome occurs.

The effect of communication breakdowns on hospitalist case outcomes highlights the importance of measures to improve and systematize communication among clinicians, particularly at vulnerable junctures – such as handoffs from the day team to the night team, and transitions from one care setting to another. An example of an intervention to improve handoffs with cogent evidence to support it is I-PASS, which is an approach to handoffs between teams in which information about the patient’s illness severity, clinical background, and contingencies is conveyed and synthesized in a structured manner. A study of the effect of implementation of I-PASS among nine pediatric residency programs demonstrated a 30% reduction in preventable adverse events.9

 

 

Applying insights from malpractice claims analysis to clinical practice

The systematic review of malpractice cases to determine the contributing factors and other case attributes is an important source of patient safety insights. The process breakdowns described by the contributing factors can inform the design of patient safety initiatives. In addition, malpractice data provides information on which specialties and what types of clinicians are being named together in malpractice claims.

In the hospitalist malpractice study, in addition to general surgery and orthopedic surgery, the other clinical services most commonly subject to claims along with hospitalists were nursing, emergency medicine, and cardiology. Another observation was that physician assistants and nurse practitioners are increasingly being named in hospitalist claims. This information is crucial to guiding who needs to be in the room with hospitalists when efforts are undertaken to enhance patient safety within hospital medicine.

An understandable response to the finding that hospitalist claims rates are not decreasing is for hospitalists to seek ways to lower their risk of being named in a malpractice claim. Of course, avoiding adverse events by providing the safest possible care is paramount. Even when patients do suffer adverse events due to a physician negligence, only rarely, less than 5% of the time, does this result in a malpractice claim.10 Important lessons in risk management can be learned from examining why patients decide to sue when mistakes lead to bad outcomes.

An analysis of plaintiffs’ depositions found that the key reasons that patients decided to file a malpractice claim include a poor relationship with the physician – specifically, a lack of empathy from the physician, feeling deserted by the physician, and feeling devalued by the physician.11 These findings support the use of programs that assist physicians in compassionately disclosing adverse events to patients. Among inpatient physicians, patient satisfaction survey questions about the time the physician spent with the patient and the physician’s concern for the patient are better predictors of the physicians’ risk management performance than is the question about the skill of the physician.12 In the aftermath of an adverse event, focusing on maintaining a strong patient-physician relationship is not only the right the thing to do, the data tell us that it is also a sensible approach to reducing medicolegal risk.
 

Dr. Schaffer practices as a member of the Hospital Medicine Unit at Brigham and Women’s Hospital, Boston, where he serves as an attending physician on the inpatient general medicine services. An instructor at Harvard Medical School, his academic interests include research using large medical malpractice databases to examine temporal trends in medical malpractice.

References

1. Rothberg MB, et al. The cost of defensive medicine on 3 hospital medicine services. JAMA Intern Med. 2014;174(11):1867-1868. doi:10.1001/jamainternmed.2014.4649.

2. Kachalia A, et al. Overuse of testing in preoperative evaluation and syncope: A survey of hospitalists. Ann Intern Med. 2015;162(2):100-108. doi: 10.7326/M14-0694.

3. Mello MM, et al. National costs of the medical liability system. Health Aff (Millwood). 2010;29(9):1569-1577. doi: 10.1377/hlthaff.2009.0807.

4. Schaffer AC, et al. Rates and characteristics of paid malpractice claims among U.S. physicians by specialty, 1992-2014. JAMA Intern Med. 2017;177(5):710-718. doi:10.1001/jamainternmed.2017.0311.

5. Schaffer AC, et al. Liability impact of the hospitalist model of care. J Hosp Med. 2014;9(12):750-755. doi: 10.1002/jhm.2244.

6. Schaffer AC, et al. Rates and characteristics of medical malpractice claims against hospitalists. J Hosp Med. 2021 Jul;16(7):390-396. doi: 10.12788/jhm.3557.

7. Poon EG. Clinical decision support: a tool of the hospital trade. J Hosp Med. 2015;10(1):60-61. doi: 10.1002/jhm.2295.

8. Makam AN, Nguyen OK, Auerbach AD. Diagnostic accuracy and effectiveness of automated electronic sepsis alert systems: A systematic review. J Hosp Med. 2015;10(6):396-402. doi: 10.1002/jhm.2347.

9. Starmer AJ, et al. Changes in medical errors after implementation of a handoff program. N Engl J Med. 2014;371(19):1803-1812. doi: 10.1056/NEJMsa1405556.

10. Localio AR, et al. Relation between malpractice claims and adverse events due to negligence. Results of the Harvard Medical Practice Study III. N Engl J Med. 1991;325(4):245-251. doi: 10.1056/NEJM199107253250405.

11. Beckman HB, et al. The doctor-patient relationship and malpractice. Lessons from plaintiff depositions. Arch Intern Med. 1994;154(12):1365-1370. doi:10.1001/archinte.1994.00420120093010.

12. Stelfox HT, et al. The relation of patient satisfaction with complaints against physicians and malpractice lawsuits. Am J Med. 2005;118(10):1126-1133. doi: 10.1016/j.amjmed.2005.01.060.

Among the pressures felt by hospitalists are concerns about being subject to a malpractice claim. Anxiety about malpractice influences the way hospitalists practice, giving rise to defensive medicine.

Dr. Adam C. Schaffer, attending physician in the Hospital Medicine Unit at Brigham and Women's Hospital, instructor at Harvard Medical School, senior clinical analytics specialist at CRICO/Risk Management Foundation of the Harvard Medical Institutions.
Dr. Adam C. Schaffer

One survey, which asked hospitalists to retrospectively rate which of their orders represented defensive medicine, found that 28% of orders were deemed defensive.1 Defensive medicine can lead to low-value medical care, drive up health care costs, and potentially subject patients to unnecessary testing.2,3

Encouragingly, medical malpractice claims rates have, overall, been downtrending. An analysis of data from the National Practitioner Data Bank, which is a repository of all paid malpractice claims against individual physicians, found that malpractice claims rates decreased by 55.7% from 1992 to 2014 among all specialties, and by 46.1% for internal medicine physicians.4 The data used in this analysis did not separate hospitalists from other internal medicine physicians. An older study of malpractice claims against hospitalists found that hospitalists had significantly lower claims rates than non-hospitalist internal medicine physicians.5

Current malpractice environment for hospitalists

Seeking to shed light on the current malpractice environment faced by hospitalists, a recent study examined claims against hospitalists using the Comparative Benchmarking System (CBS), a national database of malpractice claims containing approximately 30% of all U.S. malpractice claims, which is maintained by CRICO, the malpractice insurer for the Harvard-affiliated medical institutions.6

Claims in the CBS database are examined by trained nurse coders who review the claims, along with the associated medical and legal records, to understand the contributing factors behind the adverse event leading to the claim.

Contrary to the trends for nearly all other physician specialties, the malpractice claims rates of hospitalists were not downtrending, going from 1.77 claims per 100 physician-years from 2009-2013 to 2.08 claims per 100 physician-years from 2014-2018. The overall claims rate for hospitalists was significantly higher than that for internal medicine subspecialists (though roughly the same as the claims rate for non-hospitalist general internal medicine physicians). These sobering findings raise the important question of why hospitalists claims rates are heading in the wrong direction.

One possible answer relates the ever-broadening scope of hospitalist practice. Hospitalists are being asked to care for surgical patients and other patient populations that they may have less familiarity with, increasing the risk of medical errors. Among the other specialties most commonly also named in hospitalist claims, general surgery and orthopedic surgery are in the top five. The extraordinary growth in the field of hospital medicine has meant a need to hire an increasing number of hospitalists, leading to less-experienced physicians entering the field.
 

Making hospital medicine safer

A more urgent question than what is driving the trends in hospitalist claims rates is what can be done to avoid adverse events and make hospital medicine safer. One potential answer is thoughtful collaboration arrangements with the surgical and other specialties with whom hospitalists may be co-managing patients.

Questions about who responds to what types of clinical issues that might arise and specific domains of responsibility should be defined in advance, so that a lack of role clarity does not negatively impact patient care. Given that hospitalists will be less comfortable addressing more technical surgical issues, expectations about surgeons’ availability should be established. Nocturnists may be tasked with overnight cross-coverage of patients on services, such as oncology and cardiology, that subspecialty physicians have responsibility for during the day. Agreeing upon triggers for when the nocturnist should contact the daytime subspecialty attending (for example, if a rapid response is called on their patient) should be considered, so that nocturnists are not left deciding, in the moment, whether to call the daytime attending. Measures such as this ensure that everyone’s expectations are aligned. In addition, new hospitalists need to be offered support, in the form of training and mentorship.

CBS malpractice data, which includes the contributing factors underlying what went wrong, illuminates potential targets for programs designed to enhance patient safety. In the recent hospitalist malpractice study, the two contributing factors that were the best predictors of a hospitalist malpractice claim closing with payment to the claimant were clinical judgment errors and communication breakdowns. Identifying measures that are effective in promoting patient safety by refining the clinical judgement of clinicians is a challenge, and there are limited data demonstrating what programs are effective in this area.

Clinical decision support (CDS) systems have shown promise in promoting guideline-concordant care.7 However, the role of CDS in aiding the higher-stakes clinical decisions that may be called into question after an adverse outcome is not well defined. Alerts that a patient may be developing sepsis is one type of CDS that has been extensively studied and has been shown to be of some benefit.8 The importance of clinical judgment to whether payment is made on a malpractice claim can inform risk management strategies. Hospitalists should document the thought process behind their decision making in the chart, especially for important clinical decisions. A note showing that the clinician was thoughtfully weighing the risks and benefits using the data available at the time will help make a case defensible if an adverse outcome occurs.

The effect of communication breakdowns on hospitalist case outcomes highlights the importance of measures to improve and systematize communication among clinicians, particularly at vulnerable junctures – such as handoffs from the day team to the night team, and transitions from one care setting to another. An example of an intervention to improve handoffs with cogent evidence to support it is I-PASS, which is an approach to handoffs between teams in which information about the patient’s illness severity, clinical background, and contingencies is conveyed and synthesized in a structured manner. A study of the effect of implementation of I-PASS among nine pediatric residency programs demonstrated a 30% reduction in preventable adverse events.9

 

 

Applying insights from malpractice claims analysis to clinical practice

The systematic review of malpractice cases to determine the contributing factors and other case attributes is an important source of patient safety insights. The process breakdowns described by the contributing factors can inform the design of patient safety initiatives. In addition, malpractice data provides information on which specialties and what types of clinicians are being named together in malpractice claims.

In the hospitalist malpractice study, in addition to general surgery and orthopedic surgery, the other clinical services most commonly subject to claims along with hospitalists were nursing, emergency medicine, and cardiology. Another observation was that physician assistants and nurse practitioners are increasingly being named in hospitalist claims. This information is crucial to guiding who needs to be in the room with hospitalists when efforts are undertaken to enhance patient safety within hospital medicine.

An understandable response to the finding that hospitalist claims rates are not decreasing is for hospitalists to seek ways to lower their risk of being named in a malpractice claim. Of course, avoiding adverse events by providing the safest possible care is paramount. Even when patients do suffer adverse events due to a physician negligence, only rarely, less than 5% of the time, does this result in a malpractice claim.10 Important lessons in risk management can be learned from examining why patients decide to sue when mistakes lead to bad outcomes.

An analysis of plaintiffs’ depositions found that the key reasons that patients decided to file a malpractice claim include a poor relationship with the physician – specifically, a lack of empathy from the physician, feeling deserted by the physician, and feeling devalued by the physician.11 These findings support the use of programs that assist physicians in compassionately disclosing adverse events to patients. Among inpatient physicians, patient satisfaction survey questions about the time the physician spent with the patient and the physician’s concern for the patient are better predictors of the physicians’ risk management performance than is the question about the skill of the physician.12 In the aftermath of an adverse event, focusing on maintaining a strong patient-physician relationship is not only the right the thing to do, the data tell us that it is also a sensible approach to reducing medicolegal risk.
 

Dr. Schaffer practices as a member of the Hospital Medicine Unit at Brigham and Women’s Hospital, Boston, where he serves as an attending physician on the inpatient general medicine services. An instructor at Harvard Medical School, his academic interests include research using large medical malpractice databases to examine temporal trends in medical malpractice.

References

1. Rothberg MB, et al. The cost of defensive medicine on 3 hospital medicine services. JAMA Intern Med. 2014;174(11):1867-1868. doi:10.1001/jamainternmed.2014.4649.

2. Kachalia A, et al. Overuse of testing in preoperative evaluation and syncope: A survey of hospitalists. Ann Intern Med. 2015;162(2):100-108. doi: 10.7326/M14-0694.

3. Mello MM, et al. National costs of the medical liability system. Health Aff (Millwood). 2010;29(9):1569-1577. doi: 10.1377/hlthaff.2009.0807.

4. Schaffer AC, et al. Rates and characteristics of paid malpractice claims among U.S. physicians by specialty, 1992-2014. JAMA Intern Med. 2017;177(5):710-718. doi:10.1001/jamainternmed.2017.0311.

5. Schaffer AC, et al. Liability impact of the hospitalist model of care. J Hosp Med. 2014;9(12):750-755. doi: 10.1002/jhm.2244.

6. Schaffer AC, et al. Rates and characteristics of medical malpractice claims against hospitalists. J Hosp Med. 2021 Jul;16(7):390-396. doi: 10.12788/jhm.3557.

7. Poon EG. Clinical decision support: a tool of the hospital trade. J Hosp Med. 2015;10(1):60-61. doi: 10.1002/jhm.2295.

8. Makam AN, Nguyen OK, Auerbach AD. Diagnostic accuracy and effectiveness of automated electronic sepsis alert systems: A systematic review. J Hosp Med. 2015;10(6):396-402. doi: 10.1002/jhm.2347.

9. Starmer AJ, et al. Changes in medical errors after implementation of a handoff program. N Engl J Med. 2014;371(19):1803-1812. doi: 10.1056/NEJMsa1405556.

10. Localio AR, et al. Relation between malpractice claims and adverse events due to negligence. Results of the Harvard Medical Practice Study III. N Engl J Med. 1991;325(4):245-251. doi: 10.1056/NEJM199107253250405.

11. Beckman HB, et al. The doctor-patient relationship and malpractice. Lessons from plaintiff depositions. Arch Intern Med. 1994;154(12):1365-1370. doi:10.1001/archinte.1994.00420120093010.

12. Stelfox HT, et al. The relation of patient satisfaction with complaints against physicians and malpractice lawsuits. Am J Med. 2005;118(10):1126-1133. doi: 10.1016/j.amjmed.2005.01.060.

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Shorter antibiotic course okay for UTIs in men with no fever

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Changed
Wed, 08/04/2021 - 10:15

A week of antibiotics appears just as effective as 2 weeks in treating afebrile men with urinary tract infections (UTIs), researchers say.

Shortening the course of treatment could spare patients side effects from the medications and reduce the risk that bacteria will develop resistance to the drugs, said Dimitri Drekonja, MD, chief of infectious diseases at the Minneapolis VA Medical Center.

“You’d like to be on these drugs for as short [an] amount of time as gets the job done,” he told this news organization. The study was published online July 28 in JAMA.

Researchers have recently found that shorter courses of antimicrobials are effective in the treatment of other types of infection and for UTIs in women. However, UTIs in men are thought to be more complicated because the male urethra is longer.

To see whether reducing length of treatment could be effective in men as well, Dr. Drekonja and colleagues compared 7-day and 14-day regimens in men treated at U.S. Veterans Affairs medical centers in Minnesota and Texas.

They recruited 272 men who had symptoms of UTI and were willing to participate. All the men received trimethoprim/sulfamethoxazole or ciprofloxacin for 7 days. Half the men were randomly assigned to continue this treatment for an additional 7 days; the other half received placebo pills for an additional 7 days.

The average age of the men was 69 years. Urine samples were cultured from 87.9% of the men. In 60.7% of these samples, the researchers found more than 100,000 CFU/mL; in 16.3%, they found lower colony counts; and in 23.0%, they found no growth of bacteria. The most common organism they isolated was Escherchia coli.

Results for the two groups were similar. Symptoms resolved 14 days after completion of the course of treatment in 90.4% of those who received 14 days of antibiotics, versus 91.9% of those who received 7 days of antibiotics plus 7 days of placebo pills. At 1.5%, the difference between the two arms was within the predetermined boundary for noninferiority.

The percentage of those who experienced recurrence of symptoms within 28 days of stopping medication was also similar between the two groups. Among those who received 7 days of antibiotics, 10.3% experienced recurrence of symptoms, compared to 16.9% of those assigned to 14 days of antibiotics.

There was no significant difference in the resolution of UTI symptoms between the two groups by type of antibiotic, pretreatment bacteriuria count, or study site.

Adverse events were also similar in the two groups, occurring in 20.6% of the men who received 7 days of antibiotics, versus 24.3% of the men who received 14 days of treatment. In both groups, 8.8% of patients had diarrhea, which was the most common adverse event.

Clinicians should not worry that antibiotic resistance is more likely to develop or that symptoms will recur when patients don’t finish a prescribed course of treatment, Dr. Drekonja said. “That is an old piece of guidance that has persisted for such a long time,” he said. “And it makes all of us in the infectious disease field cringe.”

Rather, the current thinking is that the more antibiotics patients take, the more resistance bacteria will develop, he said.

The success of the 7-day regimen raises the question of whether an even shorter course would work equally well. It’s not clear how short a course of antibiotics will do the trick. Research in certain populations, such as patients with spinal cord injuries, has suggested that recurrences are more frequent with 3 days of antibiotics than with 14, “so there could be a floor that you do need to go beyond,” Dr. Drekonja said.

“We’re not really sure how much people need,” agreed Daniel Morgan, MD, a professor of epidemiology and public health and medicine at the University of Maryland, Baltimore, which is why this study is important. “It really defined that 1 week is better than 2 weeks,” he said in an interview.

Another way that clinicians can reduce the use of antibiotics by men with UTIs is to consider alternative diagnoses and to culture urine samples when UTI seems like the most likely cause of their symptoms, said Dr. Morgan, who co-authored an accompanying editorial.

He pointed out that the U.S. Food and Drug Administration has issued a black box warning on fluoroquinolones, including ciprofloxacin, because they increase the risk for tendinitis and tendon rupture. Nitrofurantoin and amoxicillin-clavulanate are better alternatives for UTIs, he said.

Even some men with fevers and UTIs may need no more than 7 days of antibiotics, said Dr. Morgan. Dr. Drekonja said he generally prescribes at least 10 days antibiotics for these men.

The study was funded by the VA Merit Review Program. Dr. Drekonja and Dr. Morgan have disclosed no relevant financial relationships.

A version of this article first appeared on Medscape.com.

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A week of antibiotics appears just as effective as 2 weeks in treating afebrile men with urinary tract infections (UTIs), researchers say.

Shortening the course of treatment could spare patients side effects from the medications and reduce the risk that bacteria will develop resistance to the drugs, said Dimitri Drekonja, MD, chief of infectious diseases at the Minneapolis VA Medical Center.

“You’d like to be on these drugs for as short [an] amount of time as gets the job done,” he told this news organization. The study was published online July 28 in JAMA.

Researchers have recently found that shorter courses of antimicrobials are effective in the treatment of other types of infection and for UTIs in women. However, UTIs in men are thought to be more complicated because the male urethra is longer.

To see whether reducing length of treatment could be effective in men as well, Dr. Drekonja and colleagues compared 7-day and 14-day regimens in men treated at U.S. Veterans Affairs medical centers in Minnesota and Texas.

They recruited 272 men who had symptoms of UTI and were willing to participate. All the men received trimethoprim/sulfamethoxazole or ciprofloxacin for 7 days. Half the men were randomly assigned to continue this treatment for an additional 7 days; the other half received placebo pills for an additional 7 days.

The average age of the men was 69 years. Urine samples were cultured from 87.9% of the men. In 60.7% of these samples, the researchers found more than 100,000 CFU/mL; in 16.3%, they found lower colony counts; and in 23.0%, they found no growth of bacteria. The most common organism they isolated was Escherchia coli.

Results for the two groups were similar. Symptoms resolved 14 days after completion of the course of treatment in 90.4% of those who received 14 days of antibiotics, versus 91.9% of those who received 7 days of antibiotics plus 7 days of placebo pills. At 1.5%, the difference between the two arms was within the predetermined boundary for noninferiority.

The percentage of those who experienced recurrence of symptoms within 28 days of stopping medication was also similar between the two groups. Among those who received 7 days of antibiotics, 10.3% experienced recurrence of symptoms, compared to 16.9% of those assigned to 14 days of antibiotics.

There was no significant difference in the resolution of UTI symptoms between the two groups by type of antibiotic, pretreatment bacteriuria count, or study site.

Adverse events were also similar in the two groups, occurring in 20.6% of the men who received 7 days of antibiotics, versus 24.3% of the men who received 14 days of treatment. In both groups, 8.8% of patients had diarrhea, which was the most common adverse event.

Clinicians should not worry that antibiotic resistance is more likely to develop or that symptoms will recur when patients don’t finish a prescribed course of treatment, Dr. Drekonja said. “That is an old piece of guidance that has persisted for such a long time,” he said. “And it makes all of us in the infectious disease field cringe.”

Rather, the current thinking is that the more antibiotics patients take, the more resistance bacteria will develop, he said.

The success of the 7-day regimen raises the question of whether an even shorter course would work equally well. It’s not clear how short a course of antibiotics will do the trick. Research in certain populations, such as patients with spinal cord injuries, has suggested that recurrences are more frequent with 3 days of antibiotics than with 14, “so there could be a floor that you do need to go beyond,” Dr. Drekonja said.

“We’re not really sure how much people need,” agreed Daniel Morgan, MD, a professor of epidemiology and public health and medicine at the University of Maryland, Baltimore, which is why this study is important. “It really defined that 1 week is better than 2 weeks,” he said in an interview.

Another way that clinicians can reduce the use of antibiotics by men with UTIs is to consider alternative diagnoses and to culture urine samples when UTI seems like the most likely cause of their symptoms, said Dr. Morgan, who co-authored an accompanying editorial.

He pointed out that the U.S. Food and Drug Administration has issued a black box warning on fluoroquinolones, including ciprofloxacin, because they increase the risk for tendinitis and tendon rupture. Nitrofurantoin and amoxicillin-clavulanate are better alternatives for UTIs, he said.

Even some men with fevers and UTIs may need no more than 7 days of antibiotics, said Dr. Morgan. Dr. Drekonja said he generally prescribes at least 10 days antibiotics for these men.

The study was funded by the VA Merit Review Program. Dr. Drekonja and Dr. Morgan have disclosed no relevant financial relationships.

A version of this article first appeared on Medscape.com.

A week of antibiotics appears just as effective as 2 weeks in treating afebrile men with urinary tract infections (UTIs), researchers say.

Shortening the course of treatment could spare patients side effects from the medications and reduce the risk that bacteria will develop resistance to the drugs, said Dimitri Drekonja, MD, chief of infectious diseases at the Minneapolis VA Medical Center.

“You’d like to be on these drugs for as short [an] amount of time as gets the job done,” he told this news organization. The study was published online July 28 in JAMA.

Researchers have recently found that shorter courses of antimicrobials are effective in the treatment of other types of infection and for UTIs in women. However, UTIs in men are thought to be more complicated because the male urethra is longer.

To see whether reducing length of treatment could be effective in men as well, Dr. Drekonja and colleagues compared 7-day and 14-day regimens in men treated at U.S. Veterans Affairs medical centers in Minnesota and Texas.

They recruited 272 men who had symptoms of UTI and were willing to participate. All the men received trimethoprim/sulfamethoxazole or ciprofloxacin for 7 days. Half the men were randomly assigned to continue this treatment for an additional 7 days; the other half received placebo pills for an additional 7 days.

The average age of the men was 69 years. Urine samples were cultured from 87.9% of the men. In 60.7% of these samples, the researchers found more than 100,000 CFU/mL; in 16.3%, they found lower colony counts; and in 23.0%, they found no growth of bacteria. The most common organism they isolated was Escherchia coli.

Results for the two groups were similar. Symptoms resolved 14 days after completion of the course of treatment in 90.4% of those who received 14 days of antibiotics, versus 91.9% of those who received 7 days of antibiotics plus 7 days of placebo pills. At 1.5%, the difference between the two arms was within the predetermined boundary for noninferiority.

The percentage of those who experienced recurrence of symptoms within 28 days of stopping medication was also similar between the two groups. Among those who received 7 days of antibiotics, 10.3% experienced recurrence of symptoms, compared to 16.9% of those assigned to 14 days of antibiotics.

There was no significant difference in the resolution of UTI symptoms between the two groups by type of antibiotic, pretreatment bacteriuria count, or study site.

Adverse events were also similar in the two groups, occurring in 20.6% of the men who received 7 days of antibiotics, versus 24.3% of the men who received 14 days of treatment. In both groups, 8.8% of patients had diarrhea, which was the most common adverse event.

Clinicians should not worry that antibiotic resistance is more likely to develop or that symptoms will recur when patients don’t finish a prescribed course of treatment, Dr. Drekonja said. “That is an old piece of guidance that has persisted for such a long time,” he said. “And it makes all of us in the infectious disease field cringe.”

Rather, the current thinking is that the more antibiotics patients take, the more resistance bacteria will develop, he said.

The success of the 7-day regimen raises the question of whether an even shorter course would work equally well. It’s not clear how short a course of antibiotics will do the trick. Research in certain populations, such as patients with spinal cord injuries, has suggested that recurrences are more frequent with 3 days of antibiotics than with 14, “so there could be a floor that you do need to go beyond,” Dr. Drekonja said.

“We’re not really sure how much people need,” agreed Daniel Morgan, MD, a professor of epidemiology and public health and medicine at the University of Maryland, Baltimore, which is why this study is important. “It really defined that 1 week is better than 2 weeks,” he said in an interview.

Another way that clinicians can reduce the use of antibiotics by men with UTIs is to consider alternative diagnoses and to culture urine samples when UTI seems like the most likely cause of their symptoms, said Dr. Morgan, who co-authored an accompanying editorial.

He pointed out that the U.S. Food and Drug Administration has issued a black box warning on fluoroquinolones, including ciprofloxacin, because they increase the risk for tendinitis and tendon rupture. Nitrofurantoin and amoxicillin-clavulanate are better alternatives for UTIs, he said.

Even some men with fevers and UTIs may need no more than 7 days of antibiotics, said Dr. Morgan. Dr. Drekonja said he generally prescribes at least 10 days antibiotics for these men.

The study was funded by the VA Merit Review Program. Dr. Drekonja and Dr. Morgan have disclosed no relevant financial relationships.

A version of this article first appeared on Medscape.com.

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Midodrine reduces fainting in young patients

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Thu, 08/05/2021 - 10:50

 

Taking midodrine can reduce vasovagal syncope in younger healthy patients, according to a new study.

Vasovagal syncope is the most common cause of fainting and is often triggered by dehydration and upright posture, according to Johns Hopkins Medicine. But it can also be caused by stimuli like the sight of blood or sudden emotional distress. The stimulus causes the heart rate and blood pressure to drop rapidly, according to the Mayo Clinic.

The randomized, placebo-controlled, double-blind trial included 133 patients with recurrent vasovagal syncope and was published in Annals of Internal Medicine. Those that received midodrine were less likely to have one syncope episode (28 of 66 [42%]), compared with those that took the placebo (41 of 67 [61%]). The absolute risk reduction for vasovagal syncope was 19 percentage points (95% confidence interval, 2-36 percentage points).

The study included patients from 25 university hospitals in Canada, the United States, Mexico, and the United Kingdom, who were followed for 12 months. The trial participants were highly symptomatic for vasovagal syncope, having experienced a median of 23 episodes in their lifetime and 5 syncope episodes in the last year, and they had no comorbid conditions.

“We don’t have many arrows in our quiver,” said Robert Sheldon, MD, PhD, a cardiologist at University of Calgary (Alta.) and lead author of the study, referring to the lack of evidence-based treatments for syncope.

For 20 years Dr. Sheldon’s lab has been testing drugs that showed some potential. While a previous study of fludrocortisone (Florinef ) showed some benefit, “[midodrine] was the first to be unequivocally, slam-dunk positive,” he said in an interview.

Earlier trials of midodrine

Other studies have shown midodrine to prevent syncope on tilt tests. There have been two randomized trials where midodrine significantly reduced vasovagal syncope, but one of these was short and in children, and the other one was open label with no placebo control.

“Risk reduction was very high in previous studies,” Dr. Sheldon said in an interview. But, because they were open label, there was a huge placebo effect, he noted.

“There were no adequately done, adequately powered [studies] that have been positive,” Dr. Sheldon added.

New study methods and outcomes

The study published in Annals of Internal Medicine this week included patients over 18 years of age with a Calgary Syncope Symptom Score of at least 2. All were educated on lifestyle measures that can prevent syncopes before beginning to take 5 mg of study drug or placebo three times daily, 4 hours apart.

In these cases, the study authors wrote, “taking medication three times a day seems worth the effort.” But in patients with a lower frequency of episodes, midodrine might not have an adequate payoff.

These results are “impressive,” said Roopinder K. Sandhu, MD, MPH, clinical electrophysiologist at Cedar-Sinai in Los Angeles. “This study demonstrated that midodrine is the first medical therapy, in addition to education and lifestyle measures, to unequivocally pass the scrutiny of an international, placebo-controlled, RCT to show a significant reduction in syncope recurrence in a younger population with frequent syncope events.”

“[Taking midodrine] doesn’t carry the long-term consequence of pacemakers,” she added.

 

 

Study limitations

Limitations of the new study include its small size and short observation period, the authors wrote. Additionally, a large proportion of patients enrolled were also from a single center in Calgary that specializes in syncope care. Twenty-seven patients in the trial stopped taking their assigned medication during the year observation period, but the authors concluded these participants “likely would bias the results against midodrine.”

For doctors considering midodrine for their patients, it’s critical to confirm the diagnosis and to try patient education first, Dr. Sheldon advised.

Lifestyle factors like hydration, adequate sodium intake, and squatting or lying down when the syncope is coming on can sufficiently suppress syncopes in two-thirds of patients, he noted.

This is a treatment for young people, Dr. Sandhu said. The median age in the trial was 35, so patients taking midodrine should be younger than 50. Midodrine is also not effective in patients with high blood pressure or heart failure, she said.

“[Midodrine] is easy to use but kind of a pain at first,” Dr. Sheldon noted. Every patient should start out taking 5 mg doses, three times a day – during waking hours. But then you have to adjust the dosage, “and it’s tricky,” he said.

If a patient experiences goosebumps or the sensation of worms crawling in the hair, the dose might be too much, Dr. Sheldon noted.

If the patient is still fainting, first consider when they are fainting, he said. If it’s around the time they should take another dose, it might be trough effect.

Dr. Sandhu was not involved in the study, but Cedar Sinai was a participating center, and she considers Dr. Sheldon to be a mentor. Dr. Sandhu also noted that she has published papers with Dr. Sheldon, who reported no conflicts.

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Taking midodrine can reduce vasovagal syncope in younger healthy patients, according to a new study.

Vasovagal syncope is the most common cause of fainting and is often triggered by dehydration and upright posture, according to Johns Hopkins Medicine. But it can also be caused by stimuli like the sight of blood or sudden emotional distress. The stimulus causes the heart rate and blood pressure to drop rapidly, according to the Mayo Clinic.

The randomized, placebo-controlled, double-blind trial included 133 patients with recurrent vasovagal syncope and was published in Annals of Internal Medicine. Those that received midodrine were less likely to have one syncope episode (28 of 66 [42%]), compared with those that took the placebo (41 of 67 [61%]). The absolute risk reduction for vasovagal syncope was 19 percentage points (95% confidence interval, 2-36 percentage points).

The study included patients from 25 university hospitals in Canada, the United States, Mexico, and the United Kingdom, who were followed for 12 months. The trial participants were highly symptomatic for vasovagal syncope, having experienced a median of 23 episodes in their lifetime and 5 syncope episodes in the last year, and they had no comorbid conditions.

“We don’t have many arrows in our quiver,” said Robert Sheldon, MD, PhD, a cardiologist at University of Calgary (Alta.) and lead author of the study, referring to the lack of evidence-based treatments for syncope.

For 20 years Dr. Sheldon’s lab has been testing drugs that showed some potential. While a previous study of fludrocortisone (Florinef ) showed some benefit, “[midodrine] was the first to be unequivocally, slam-dunk positive,” he said in an interview.

Earlier trials of midodrine

Other studies have shown midodrine to prevent syncope on tilt tests. There have been two randomized trials where midodrine significantly reduced vasovagal syncope, but one of these was short and in children, and the other one was open label with no placebo control.

“Risk reduction was very high in previous studies,” Dr. Sheldon said in an interview. But, because they were open label, there was a huge placebo effect, he noted.

“There were no adequately done, adequately powered [studies] that have been positive,” Dr. Sheldon added.

New study methods and outcomes

The study published in Annals of Internal Medicine this week included patients over 18 years of age with a Calgary Syncope Symptom Score of at least 2. All were educated on lifestyle measures that can prevent syncopes before beginning to take 5 mg of study drug or placebo three times daily, 4 hours apart.

In these cases, the study authors wrote, “taking medication three times a day seems worth the effort.” But in patients with a lower frequency of episodes, midodrine might not have an adequate payoff.

These results are “impressive,” said Roopinder K. Sandhu, MD, MPH, clinical electrophysiologist at Cedar-Sinai in Los Angeles. “This study demonstrated that midodrine is the first medical therapy, in addition to education and lifestyle measures, to unequivocally pass the scrutiny of an international, placebo-controlled, RCT to show a significant reduction in syncope recurrence in a younger population with frequent syncope events.”

“[Taking midodrine] doesn’t carry the long-term consequence of pacemakers,” she added.

 

 

Study limitations

Limitations of the new study include its small size and short observation period, the authors wrote. Additionally, a large proportion of patients enrolled were also from a single center in Calgary that specializes in syncope care. Twenty-seven patients in the trial stopped taking their assigned medication during the year observation period, but the authors concluded these participants “likely would bias the results against midodrine.”

For doctors considering midodrine for their patients, it’s critical to confirm the diagnosis and to try patient education first, Dr. Sheldon advised.

Lifestyle factors like hydration, adequate sodium intake, and squatting or lying down when the syncope is coming on can sufficiently suppress syncopes in two-thirds of patients, he noted.

This is a treatment for young people, Dr. Sandhu said. The median age in the trial was 35, so patients taking midodrine should be younger than 50. Midodrine is also not effective in patients with high blood pressure or heart failure, she said.

“[Midodrine] is easy to use but kind of a pain at first,” Dr. Sheldon noted. Every patient should start out taking 5 mg doses, three times a day – during waking hours. But then you have to adjust the dosage, “and it’s tricky,” he said.

If a patient experiences goosebumps or the sensation of worms crawling in the hair, the dose might be too much, Dr. Sheldon noted.

If the patient is still fainting, first consider when they are fainting, he said. If it’s around the time they should take another dose, it might be trough effect.

Dr. Sandhu was not involved in the study, but Cedar Sinai was a participating center, and she considers Dr. Sheldon to be a mentor. Dr. Sandhu also noted that she has published papers with Dr. Sheldon, who reported no conflicts.

 

Taking midodrine can reduce vasovagal syncope in younger healthy patients, according to a new study.

Vasovagal syncope is the most common cause of fainting and is often triggered by dehydration and upright posture, according to Johns Hopkins Medicine. But it can also be caused by stimuli like the sight of blood or sudden emotional distress. The stimulus causes the heart rate and blood pressure to drop rapidly, according to the Mayo Clinic.

The randomized, placebo-controlled, double-blind trial included 133 patients with recurrent vasovagal syncope and was published in Annals of Internal Medicine. Those that received midodrine were less likely to have one syncope episode (28 of 66 [42%]), compared with those that took the placebo (41 of 67 [61%]). The absolute risk reduction for vasovagal syncope was 19 percentage points (95% confidence interval, 2-36 percentage points).

The study included patients from 25 university hospitals in Canada, the United States, Mexico, and the United Kingdom, who were followed for 12 months. The trial participants were highly symptomatic for vasovagal syncope, having experienced a median of 23 episodes in their lifetime and 5 syncope episodes in the last year, and they had no comorbid conditions.

“We don’t have many arrows in our quiver,” said Robert Sheldon, MD, PhD, a cardiologist at University of Calgary (Alta.) and lead author of the study, referring to the lack of evidence-based treatments for syncope.

For 20 years Dr. Sheldon’s lab has been testing drugs that showed some potential. While a previous study of fludrocortisone (Florinef ) showed some benefit, “[midodrine] was the first to be unequivocally, slam-dunk positive,” he said in an interview.

Earlier trials of midodrine

Other studies have shown midodrine to prevent syncope on tilt tests. There have been two randomized trials where midodrine significantly reduced vasovagal syncope, but one of these was short and in children, and the other one was open label with no placebo control.

“Risk reduction was very high in previous studies,” Dr. Sheldon said in an interview. But, because they were open label, there was a huge placebo effect, he noted.

“There were no adequately done, adequately powered [studies] that have been positive,” Dr. Sheldon added.

New study methods and outcomes

The study published in Annals of Internal Medicine this week included patients over 18 years of age with a Calgary Syncope Symptom Score of at least 2. All were educated on lifestyle measures that can prevent syncopes before beginning to take 5 mg of study drug or placebo three times daily, 4 hours apart.

In these cases, the study authors wrote, “taking medication three times a day seems worth the effort.” But in patients with a lower frequency of episodes, midodrine might not have an adequate payoff.

These results are “impressive,” said Roopinder K. Sandhu, MD, MPH, clinical electrophysiologist at Cedar-Sinai in Los Angeles. “This study demonstrated that midodrine is the first medical therapy, in addition to education and lifestyle measures, to unequivocally pass the scrutiny of an international, placebo-controlled, RCT to show a significant reduction in syncope recurrence in a younger population with frequent syncope events.”

“[Taking midodrine] doesn’t carry the long-term consequence of pacemakers,” she added.

 

 

Study limitations

Limitations of the new study include its small size and short observation period, the authors wrote. Additionally, a large proportion of patients enrolled were also from a single center in Calgary that specializes in syncope care. Twenty-seven patients in the trial stopped taking their assigned medication during the year observation period, but the authors concluded these participants “likely would bias the results against midodrine.”

For doctors considering midodrine for their patients, it’s critical to confirm the diagnosis and to try patient education first, Dr. Sheldon advised.

Lifestyle factors like hydration, adequate sodium intake, and squatting or lying down when the syncope is coming on can sufficiently suppress syncopes in two-thirds of patients, he noted.

This is a treatment for young people, Dr. Sandhu said. The median age in the trial was 35, so patients taking midodrine should be younger than 50. Midodrine is also not effective in patients with high blood pressure or heart failure, she said.

“[Midodrine] is easy to use but kind of a pain at first,” Dr. Sheldon noted. Every patient should start out taking 5 mg doses, three times a day – during waking hours. But then you have to adjust the dosage, “and it’s tricky,” he said.

If a patient experiences goosebumps or the sensation of worms crawling in the hair, the dose might be too much, Dr. Sheldon noted.

If the patient is still fainting, first consider when they are fainting, he said. If it’s around the time they should take another dose, it might be trough effect.

Dr. Sandhu was not involved in the study, but Cedar Sinai was a participating center, and she considers Dr. Sheldon to be a mentor. Dr. Sandhu also noted that she has published papers with Dr. Sheldon, who reported no conflicts.

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Never prouder to be a hospitalist

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Thu, 08/26/2021 - 15:43

I have been a proud hospitalist for more than 20 years, and yet I have never been prouder to be a hospitalist than now. The pandemic has been brutal, killing more than 600,000 Americans as of this writing. It has stretched the health care system, its doctors, nurses, and other providers to the limit. Yet we will get through it, we are getting through it, and hospitalists deserve a huge portion of the credit.

Dr. Eric E. Howell

According to the CDC, there have been over 2.3 million COVID-19 hospitalizations. In my home state of Maryland, between two-thirds and three-quarters of hospitalized COVID patients are cared for on general medical floors, the domain of hospitalists. When hospitals needed COVID units, hospitalists stepped up to design and staff them. When our ICU colleagues needed support, especially in those early dark days, hospitalists stepped in. When our outpatient colleagues were called into the hospital, hospitalists were there to help them on board. When the House of Medicine was in chaos due to COVID-19, hospitalists ran towards that fire. Our previous 20+ years of collective experience made us the ideal specialty to manage the inpatient challenges over the last 18 months.

Need a new clinical schedule by Sunday? Check.

Need help with new clinical protocols? Check.

Need to help other colleagues? Check.

Need to reprogram the EMR? Check.

Need a new way to teach residents and students on the wards? Check.

Need a whole new unit – no, wait – a new hospital wing? No, scratch that – a whole new COVID hospital in a few weeks? Check. (I personally did that last one at the Baltimore Convention Center!)

For me and many hospitalists like me, it is as if the last 20 years were prep work for the pandemic.

Here at SHM, we know the pandemic is hard work – exhausting, even. SHM has been actively focused on supporting hospitalists during this crisis so that hospitalists can focus on patients. Early in the pandemic, SHM quickly pivoted to supply hospitalists with COVID-19 resources in their fight against the coronavirus. Numerous COVID-19 webinars, a COVID addendum to the State of Hospital Medicine Report, and a dedicated COVID issue of the Journal of Hospital Medicine were early and successful information dissemination strategies.

As the world – and hospitalists – dug in for a multi-year pandemic, SHM continued to advance the care of patients by opening our library of educational content for free to anyone. Our Public Policy Committee was active around both COVID-19- and hospitalist-related topics: immigration, telehealth, wellbeing, and financial impacts, to name a few.

As the pandemic slogged on, our Wellbeing Task Force came up with innovative support measures, including a check-in guide for hospitalists and fellow health care workers and dedicated wellness sessions complete with a licensed therapist for members. All the while, despite the restrictions and hurdles the pandemic has thrown our way, SHM members keep meeting and collaborating through virtual chapter events, committee work, special interest groups, and our annual conference, SHM Converge. Thank you to the countless members who donated their time to SHM, so that SHM could support hospitalists and their patients.

Now, we are transitioning into a new phase of the pandemic. The medical miracles that are the COVID-19 vaccines have made that possible. Fully vaccinated, I no longer worry that every time someone sneezes, or when I care for patients with a fever, that I am playing a high stakes poker game with my life. Don’t get me wrong; as I write, the Delta variant has a hold on the nation, and I know it’s not over yet. But it does appear as if the medical war on COVID is shifting from national to regional (or even local) responses.

During this new phase, we must rebuild our personal and professional lives. If you haven’t read Retired Lieutenant General Mark Hertling’s perspective piece in the August issue of the Journal of Hospital Medicine, I strongly encourage you to do so. He shares profound lessons on transitioning from active combat that are directly applicable to hospitalists who have been “deployed” battling COVID-19.

SHM will continue to pivot to meet our members’ needs too. We are already gearing up for more in-person education and networking. Chapters are starting to meet in person, and SHM is happy to provide visiting faculty. I will visit members from Florida to Maine and places in between starting this fall! Our Board of Directors and other SHM leaders are also starting to meet with members in person. Our own Leadership Academy will take place at Amelia Island in Florida in October, where we can learn, network, and even decompress. We also can’t wait for SHM Converge 2022 in Nashville, where we hope to reunite with many of you after 2 years of virtual conferences.

Our response to the pandemic, a once in a century crisis where our own safety was at risk, where doing the right thing might mean death or harming loved ones, our response of running into the fire to save lives is truly inspiring. The power of care – for our patients, for our family and friends, and for our hospital medicine community and the community at large – is evident more now than ever.

There have always been good reasons to be proud of being a hospitalist: taking care of the acutely ill, helping hospitals improve, teaching young doctors, and watching my specialty grow by leaps and bounds, to name just a few. But I’ve never been prouder than I am now.

Dr. Howell is the CEO of the Society of Hospital Medicine.

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I have been a proud hospitalist for more than 20 years, and yet I have never been prouder to be a hospitalist than now. The pandemic has been brutal, killing more than 600,000 Americans as of this writing. It has stretched the health care system, its doctors, nurses, and other providers to the limit. Yet we will get through it, we are getting through it, and hospitalists deserve a huge portion of the credit.

Dr. Eric E. Howell

According to the CDC, there have been over 2.3 million COVID-19 hospitalizations. In my home state of Maryland, between two-thirds and three-quarters of hospitalized COVID patients are cared for on general medical floors, the domain of hospitalists. When hospitals needed COVID units, hospitalists stepped up to design and staff them. When our ICU colleagues needed support, especially in those early dark days, hospitalists stepped in. When our outpatient colleagues were called into the hospital, hospitalists were there to help them on board. When the House of Medicine was in chaos due to COVID-19, hospitalists ran towards that fire. Our previous 20+ years of collective experience made us the ideal specialty to manage the inpatient challenges over the last 18 months.

Need a new clinical schedule by Sunday? Check.

Need help with new clinical protocols? Check.

Need to help other colleagues? Check.

Need to reprogram the EMR? Check.

Need a new way to teach residents and students on the wards? Check.

Need a whole new unit – no, wait – a new hospital wing? No, scratch that – a whole new COVID hospital in a few weeks? Check. (I personally did that last one at the Baltimore Convention Center!)

For me and many hospitalists like me, it is as if the last 20 years were prep work for the pandemic.

Here at SHM, we know the pandemic is hard work – exhausting, even. SHM has been actively focused on supporting hospitalists during this crisis so that hospitalists can focus on patients. Early in the pandemic, SHM quickly pivoted to supply hospitalists with COVID-19 resources in their fight against the coronavirus. Numerous COVID-19 webinars, a COVID addendum to the State of Hospital Medicine Report, and a dedicated COVID issue of the Journal of Hospital Medicine were early and successful information dissemination strategies.

As the world – and hospitalists – dug in for a multi-year pandemic, SHM continued to advance the care of patients by opening our library of educational content for free to anyone. Our Public Policy Committee was active around both COVID-19- and hospitalist-related topics: immigration, telehealth, wellbeing, and financial impacts, to name a few.

As the pandemic slogged on, our Wellbeing Task Force came up with innovative support measures, including a check-in guide for hospitalists and fellow health care workers and dedicated wellness sessions complete with a licensed therapist for members. All the while, despite the restrictions and hurdles the pandemic has thrown our way, SHM members keep meeting and collaborating through virtual chapter events, committee work, special interest groups, and our annual conference, SHM Converge. Thank you to the countless members who donated their time to SHM, so that SHM could support hospitalists and their patients.

Now, we are transitioning into a new phase of the pandemic. The medical miracles that are the COVID-19 vaccines have made that possible. Fully vaccinated, I no longer worry that every time someone sneezes, or when I care for patients with a fever, that I am playing a high stakes poker game with my life. Don’t get me wrong; as I write, the Delta variant has a hold on the nation, and I know it’s not over yet. But it does appear as if the medical war on COVID is shifting from national to regional (or even local) responses.

During this new phase, we must rebuild our personal and professional lives. If you haven’t read Retired Lieutenant General Mark Hertling’s perspective piece in the August issue of the Journal of Hospital Medicine, I strongly encourage you to do so. He shares profound lessons on transitioning from active combat that are directly applicable to hospitalists who have been “deployed” battling COVID-19.

SHM will continue to pivot to meet our members’ needs too. We are already gearing up for more in-person education and networking. Chapters are starting to meet in person, and SHM is happy to provide visiting faculty. I will visit members from Florida to Maine and places in between starting this fall! Our Board of Directors and other SHM leaders are also starting to meet with members in person. Our own Leadership Academy will take place at Amelia Island in Florida in October, where we can learn, network, and even decompress. We also can’t wait for SHM Converge 2022 in Nashville, where we hope to reunite with many of you after 2 years of virtual conferences.

Our response to the pandemic, a once in a century crisis where our own safety was at risk, where doing the right thing might mean death or harming loved ones, our response of running into the fire to save lives is truly inspiring. The power of care – for our patients, for our family and friends, and for our hospital medicine community and the community at large – is evident more now than ever.

There have always been good reasons to be proud of being a hospitalist: taking care of the acutely ill, helping hospitals improve, teaching young doctors, and watching my specialty grow by leaps and bounds, to name just a few. But I’ve never been prouder than I am now.

Dr. Howell is the CEO of the Society of Hospital Medicine.

I have been a proud hospitalist for more than 20 years, and yet I have never been prouder to be a hospitalist than now. The pandemic has been brutal, killing more than 600,000 Americans as of this writing. It has stretched the health care system, its doctors, nurses, and other providers to the limit. Yet we will get through it, we are getting through it, and hospitalists deserve a huge portion of the credit.

Dr. Eric E. Howell

According to the CDC, there have been over 2.3 million COVID-19 hospitalizations. In my home state of Maryland, between two-thirds and three-quarters of hospitalized COVID patients are cared for on general medical floors, the domain of hospitalists. When hospitals needed COVID units, hospitalists stepped up to design and staff them. When our ICU colleagues needed support, especially in those early dark days, hospitalists stepped in. When our outpatient colleagues were called into the hospital, hospitalists were there to help them on board. When the House of Medicine was in chaos due to COVID-19, hospitalists ran towards that fire. Our previous 20+ years of collective experience made us the ideal specialty to manage the inpatient challenges over the last 18 months.

Need a new clinical schedule by Sunday? Check.

Need help with new clinical protocols? Check.

Need to help other colleagues? Check.

Need to reprogram the EMR? Check.

Need a new way to teach residents and students on the wards? Check.

Need a whole new unit – no, wait – a new hospital wing? No, scratch that – a whole new COVID hospital in a few weeks? Check. (I personally did that last one at the Baltimore Convention Center!)

For me and many hospitalists like me, it is as if the last 20 years were prep work for the pandemic.

Here at SHM, we know the pandemic is hard work – exhausting, even. SHM has been actively focused on supporting hospitalists during this crisis so that hospitalists can focus on patients. Early in the pandemic, SHM quickly pivoted to supply hospitalists with COVID-19 resources in their fight against the coronavirus. Numerous COVID-19 webinars, a COVID addendum to the State of Hospital Medicine Report, and a dedicated COVID issue of the Journal of Hospital Medicine were early and successful information dissemination strategies.

As the world – and hospitalists – dug in for a multi-year pandemic, SHM continued to advance the care of patients by opening our library of educational content for free to anyone. Our Public Policy Committee was active around both COVID-19- and hospitalist-related topics: immigration, telehealth, wellbeing, and financial impacts, to name a few.

As the pandemic slogged on, our Wellbeing Task Force came up with innovative support measures, including a check-in guide for hospitalists and fellow health care workers and dedicated wellness sessions complete with a licensed therapist for members. All the while, despite the restrictions and hurdles the pandemic has thrown our way, SHM members keep meeting and collaborating through virtual chapter events, committee work, special interest groups, and our annual conference, SHM Converge. Thank you to the countless members who donated their time to SHM, so that SHM could support hospitalists and their patients.

Now, we are transitioning into a new phase of the pandemic. The medical miracles that are the COVID-19 vaccines have made that possible. Fully vaccinated, I no longer worry that every time someone sneezes, or when I care for patients with a fever, that I am playing a high stakes poker game with my life. Don’t get me wrong; as I write, the Delta variant has a hold on the nation, and I know it’s not over yet. But it does appear as if the medical war on COVID is shifting from national to regional (or even local) responses.

During this new phase, we must rebuild our personal and professional lives. If you haven’t read Retired Lieutenant General Mark Hertling’s perspective piece in the August issue of the Journal of Hospital Medicine, I strongly encourage you to do so. He shares profound lessons on transitioning from active combat that are directly applicable to hospitalists who have been “deployed” battling COVID-19.

SHM will continue to pivot to meet our members’ needs too. We are already gearing up for more in-person education and networking. Chapters are starting to meet in person, and SHM is happy to provide visiting faculty. I will visit members from Florida to Maine and places in between starting this fall! Our Board of Directors and other SHM leaders are also starting to meet with members in person. Our own Leadership Academy will take place at Amelia Island in Florida in October, where we can learn, network, and even decompress. We also can’t wait for SHM Converge 2022 in Nashville, where we hope to reunite with many of you after 2 years of virtual conferences.

Our response to the pandemic, a once in a century crisis where our own safety was at risk, where doing the right thing might mean death or harming loved ones, our response of running into the fire to save lives is truly inspiring. The power of care – for our patients, for our family and friends, and for our hospital medicine community and the community at large – is evident more now than ever.

There have always been good reasons to be proud of being a hospitalist: taking care of the acutely ill, helping hospitals improve, teaching young doctors, and watching my specialty grow by leaps and bounds, to name just a few. But I’ve never been prouder than I am now.

Dr. Howell is the CEO of the Society of Hospital Medicine.

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Catching up with ourselves

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Sun, 08/01/2021 - 00:15

August is a month that we traditionally reserved for rest and recovery. But unfortunately, there seems to be little of either as we recover from COVID-19, deal with the care that has been delayed, try to understand issues of health inequity, and manage our hybrid reimbursement landscape. So let’s set those issues aside for a bit and get back to science.

Dr. John I. Allen

In this month’s cover stories, we can read about some astounding accomplishments. A fantastic study comes from Dana-Farber Cancer Institute, Boston, where researchers found 900 colorectal cancers from nurses who had participated in the long-running Nurse’s Health Studies. The researchers completed a whole-exome sequence on both normal and tumor tissue and then linked findings to the nutritional information contained in the Health Studies. With this information, they connected a tumor-associated mutation to the ingestion of red meat, which may suggest a causal link for the known association between red meat and CRC.

AGA has published a detailed clinical practice update about endoscopic management of postsurgical complications after bariatric/metabolic surgery. Bariatric therapy is an area in which gastroenterologists should play an increasingly prominent role, in conjunction with our surgical and metabolic colleagues.

Finally, read about a novel oral therapy that may provide substantial relief for celiac patients. This randomized trial of a transglutaminase inhibitor was published in the New England Journal of Medicine and may provide new hope for this difficult condition.

October marks the end of my term as Editor-in-Chief. Megan Adams, MD, JD, MSc, will take over and provide insights and opinions beyond my past missives. I thank Christopher Palmer and the excellent Frontline staff who find topics and compose articles for us. Finally, the publication department at the American Gastroenterological Association is unparalleled, led by Erin Landis with Jillian Schweitzer managing the GI & Hepatology News area. I am fortunate to return to the AGA Governing Board as Secretary/Treasurer and work with our new president, John Inadomi, as well as Tom Serena, a great friend and AGA CEO.

John I Allen, MD, MBA, AGAF
Editor in Chief

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August is a month that we traditionally reserved for rest and recovery. But unfortunately, there seems to be little of either as we recover from COVID-19, deal with the care that has been delayed, try to understand issues of health inequity, and manage our hybrid reimbursement landscape. So let’s set those issues aside for a bit and get back to science.

Dr. John I. Allen

In this month’s cover stories, we can read about some astounding accomplishments. A fantastic study comes from Dana-Farber Cancer Institute, Boston, where researchers found 900 colorectal cancers from nurses who had participated in the long-running Nurse’s Health Studies. The researchers completed a whole-exome sequence on both normal and tumor tissue and then linked findings to the nutritional information contained in the Health Studies. With this information, they connected a tumor-associated mutation to the ingestion of red meat, which may suggest a causal link for the known association between red meat and CRC.

AGA has published a detailed clinical practice update about endoscopic management of postsurgical complications after bariatric/metabolic surgery. Bariatric therapy is an area in which gastroenterologists should play an increasingly prominent role, in conjunction with our surgical and metabolic colleagues.

Finally, read about a novel oral therapy that may provide substantial relief for celiac patients. This randomized trial of a transglutaminase inhibitor was published in the New England Journal of Medicine and may provide new hope for this difficult condition.

October marks the end of my term as Editor-in-Chief. Megan Adams, MD, JD, MSc, will take over and provide insights and opinions beyond my past missives. I thank Christopher Palmer and the excellent Frontline staff who find topics and compose articles for us. Finally, the publication department at the American Gastroenterological Association is unparalleled, led by Erin Landis with Jillian Schweitzer managing the GI & Hepatology News area. I am fortunate to return to the AGA Governing Board as Secretary/Treasurer and work with our new president, John Inadomi, as well as Tom Serena, a great friend and AGA CEO.

John I Allen, MD, MBA, AGAF
Editor in Chief

August is a month that we traditionally reserved for rest and recovery. But unfortunately, there seems to be little of either as we recover from COVID-19, deal with the care that has been delayed, try to understand issues of health inequity, and manage our hybrid reimbursement landscape. So let’s set those issues aside for a bit and get back to science.

Dr. John I. Allen

In this month’s cover stories, we can read about some astounding accomplishments. A fantastic study comes from Dana-Farber Cancer Institute, Boston, where researchers found 900 colorectal cancers from nurses who had participated in the long-running Nurse’s Health Studies. The researchers completed a whole-exome sequence on both normal and tumor tissue and then linked findings to the nutritional information contained in the Health Studies. With this information, they connected a tumor-associated mutation to the ingestion of red meat, which may suggest a causal link for the known association between red meat and CRC.

AGA has published a detailed clinical practice update about endoscopic management of postsurgical complications after bariatric/metabolic surgery. Bariatric therapy is an area in which gastroenterologists should play an increasingly prominent role, in conjunction with our surgical and metabolic colleagues.

Finally, read about a novel oral therapy that may provide substantial relief for celiac patients. This randomized trial of a transglutaminase inhibitor was published in the New England Journal of Medicine and may provide new hope for this difficult condition.

October marks the end of my term as Editor-in-Chief. Megan Adams, MD, JD, MSc, will take over and provide insights and opinions beyond my past missives. I thank Christopher Palmer and the excellent Frontline staff who find topics and compose articles for us. Finally, the publication department at the American Gastroenterological Association is unparalleled, led by Erin Landis with Jillian Schweitzer managing the GI & Hepatology News area. I am fortunate to return to the AGA Governing Board as Secretary/Treasurer and work with our new president, John Inadomi, as well as Tom Serena, a great friend and AGA CEO.

John I Allen, MD, MBA, AGAF
Editor in Chief

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