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CDC panel recommends Pfizer’s COVID-19 vaccine for people 16 and over
stating they found it was safe and effective.
The agency said it will quickly issue guidance to clinicians so they can determine when and when not to give the vaccine, and to help them communicate the risks and benefits to patients.
CDC staff gave a preview of those clinical considerations at the agency’s Advisory Committee on Immunization Practices (ACIP) meeting on December 12 and said it would be holding calls with clinicians on December 13 and 14.
The CDC will also issue guidance December 13 on how organizations can handle the workforce problems that might arise as health care workers experience side effects from vaccination.
ACIP voted 11-0, with three recusals, to recommend use of the Pfizer-BioNTech mRNA vaccine in individuals 16 years or older according to the guidelines of the Food and Drug Administration’s (FDA’s) emergency use authorization issued December 11.
The panel also voted unanimously to include the vaccine in 2021 immunization schedules. All panel members said the recommendation should go hand-in-hand with ACIP’s previous recommendation on December 1 that allocation of the vaccine be phased-in, with health care workers and residents and staff of long-term care facilities in phase 1a.
Allergies, pregnant women?
ACIP panelists said clinicians need more guidance on whether to use the vaccine in pregnant or breastfeeding women, the immunocompromised, or those who have a history of allergies.
The FDA health care provider information sheet said there is not enough data to recommend vaccinating those women or the immunocompromised, and also advises against giving the vaccine to individuals who have a history of serious allergic reaction to any component of the vaccine.
Peter Marks, MD, PhD, director of the FDA’s Center for Biologic Evaluation and Research (CBER) clarified this in a briefing on December 12, noting that women who are pregnant or lactating can make the decision in consultation with their physician. And, he said, patients with any other history of allergy should be able to safely get the vaccine.
The CDC — in its soon-to-be-released guidance — will make the same recommendations. For any woman considering vaccination, she should consider the level of COVID-19 in the community, her personal risk of contracting the virus, the risks to her or her fetus of developing the disease, and the vaccine’s known side effects, Sarah Mbaeyi, MD, MPH, a medical officer at the agency, said during the panel meeting December 12.
She added that the CDC will also urge physicians to advise women to take acetaminophen if they develop a fever after vaccination — to protect the developing fetus from fever.
Sandra Fryhofer, MD, representing the American Medical Association, commended the CDC for these recommendations. But she also called on Pfizer, the FDA, and the CDC to make data from the developmental and reproductive toxicity (DART) studies public as soon as possible.
“We really need to put those results on warp speed and get them out there to give our physicians and pregnant women more information,” said Fryhofer, an adjunct associate professor of medicine at Emory University School of Medicine in Atlanta, Georgia.
The American College of Obstetricians and Gynecologists (ACOG) will also soon release guidance for vaccinating pregnant and breastfeeding women, said Linda Eckert, MD, FACOG, an ACOG representative on the panel.
ACOG and the CDC met the morning of December 12 to discuss risks and benefits with experts in immunology, placental pathology, and vaccine kinetics, she said.
“The overall complete consensus was that we don’t see biological plausibility at this time for placental transfer of the mRNA and that we see that direct fetal exposure or the possibility of fetal inflammatory response is extremely unlikely,” said Eckert, professor of obstetrics and gynecology at the University of Washington, Seattle. “Clearly we are waiting on the data.”
A Pfizer official told the ACIP panel that preliminary data “show no indication of either developmental or reproductive toxicity,” and that the company plans to send the final DART data to the FDA at the end of December.
On the potential for allergic reactions, the CDC concurred with the FDA that the vaccine should not be given to people with a history of serious reactions. The agency added that the category should include anyone who has had a reaction to any vaccine or injectable drug product because injectables may contain the same ingredients as the Pfizer vaccine, said Mbaeyi.
The CDC will also urge clinicians to observe patients with a history of anaphylaxis for 30 minutes after vaccination and all patients for at least 15 minutes afterward.
Should teens be a special population?
At least one ACIP panel member — Henry Bernstein, DO, MHCM, FAAP — said he was concerned that backing use of the vaccine in 16- and 17-year-olds was a leap of faith, given that Pfizer had extremely limited data on this cohort.
Bernstein, professor of pediatrics at the Zucker School of Medicine at Hofstra/Northwell in Hempstead, New York, also said that systemic reactions were more common in that age group.
He argued for making the 16- and 17-year-olds a “special population” that would get specific attention and guidance for vaccination from the federal agencies and professional societies.
Bernstein said he did not want to sow any more doubts in parents’ minds about vaccination, noting that hesitancy was a growing concern. “A successful pediatric vaccination program depends on creating and sustaining parental confidence in both the safety and effectiveness of this vaccine,” he said.
Many panelists, however, noted that there has been no evidence to suggest that the vaccine is not safe or less effective in that younger age group.
Yvonne Maldonado, MD, the American Academy of Pediatrics representative on the panel, said that this age group should not be denied the vaccine as they often have essential or front-line jobs that put them at higher risk for infection.
“I am very concerned about this message being sent out that this vaccine will not be safe in children,” said Maldonado, professor of pediatrics and health research and policy at Stanford University School of Medicine in California.
“We currently have no evidence that that is the case,” she said, adding there is also no indication younger children are biologically or physiologically different in their response or safety risk than 18-year-olds.
Vaccine = hope
Committee members breathed a sigh of relief at the end of the 2-day meeting, saying that although the Pfizer vaccine is not perfect, it represents a scientific milestone and a significant advance against the continuing march of the SARS-CoV-2 pandemic.
“This vaccine and future vaccines do provide a promise for a lot of progress in the future,” said panelist Beth P. Bell, MD, MPH, clinical professor of global health at the University of Washington School of Public Health in Seattle.
Peter Szilagyi, MD, MPH, executive vice-chair and vice-chair for research at the University of California, Los Angeles pediatrics department, said, “I’m really hopeful that this is the beginning of the end of the coronavirus pandemic.”
“The need for this vaccine is profound,” said Veronica McNally, president and CEO of the Franny Strong Foundation in West Bloomfield, Michigan.
The ACIP panel also made the argument that while the at least $10 billion spent on vaccine development by the federal government’s Operation Warp Speed alone has been a good investment, more spending is needed to actually get Americans vaccinated.
The imbalance between the two is “shocking and needs to be corrected,” said Bell. “We are not going to be able to protect the American public if we don’t have a way to deliver the vaccine to them.”
This article first appeared on Medscape.com.
stating they found it was safe and effective.
The agency said it will quickly issue guidance to clinicians so they can determine when and when not to give the vaccine, and to help them communicate the risks and benefits to patients.
CDC staff gave a preview of those clinical considerations at the agency’s Advisory Committee on Immunization Practices (ACIP) meeting on December 12 and said it would be holding calls with clinicians on December 13 and 14.
The CDC will also issue guidance December 13 on how organizations can handle the workforce problems that might arise as health care workers experience side effects from vaccination.
ACIP voted 11-0, with three recusals, to recommend use of the Pfizer-BioNTech mRNA vaccine in individuals 16 years or older according to the guidelines of the Food and Drug Administration’s (FDA’s) emergency use authorization issued December 11.
The panel also voted unanimously to include the vaccine in 2021 immunization schedules. All panel members said the recommendation should go hand-in-hand with ACIP’s previous recommendation on December 1 that allocation of the vaccine be phased-in, with health care workers and residents and staff of long-term care facilities in phase 1a.
Allergies, pregnant women?
ACIP panelists said clinicians need more guidance on whether to use the vaccine in pregnant or breastfeeding women, the immunocompromised, or those who have a history of allergies.
The FDA health care provider information sheet said there is not enough data to recommend vaccinating those women or the immunocompromised, and also advises against giving the vaccine to individuals who have a history of serious allergic reaction to any component of the vaccine.
Peter Marks, MD, PhD, director of the FDA’s Center for Biologic Evaluation and Research (CBER) clarified this in a briefing on December 12, noting that women who are pregnant or lactating can make the decision in consultation with their physician. And, he said, patients with any other history of allergy should be able to safely get the vaccine.
The CDC — in its soon-to-be-released guidance — will make the same recommendations. For any woman considering vaccination, she should consider the level of COVID-19 in the community, her personal risk of contracting the virus, the risks to her or her fetus of developing the disease, and the vaccine’s known side effects, Sarah Mbaeyi, MD, MPH, a medical officer at the agency, said during the panel meeting December 12.
She added that the CDC will also urge physicians to advise women to take acetaminophen if they develop a fever after vaccination — to protect the developing fetus from fever.
Sandra Fryhofer, MD, representing the American Medical Association, commended the CDC for these recommendations. But she also called on Pfizer, the FDA, and the CDC to make data from the developmental and reproductive toxicity (DART) studies public as soon as possible.
“We really need to put those results on warp speed and get them out there to give our physicians and pregnant women more information,” said Fryhofer, an adjunct associate professor of medicine at Emory University School of Medicine in Atlanta, Georgia.
The American College of Obstetricians and Gynecologists (ACOG) will also soon release guidance for vaccinating pregnant and breastfeeding women, said Linda Eckert, MD, FACOG, an ACOG representative on the panel.
ACOG and the CDC met the morning of December 12 to discuss risks and benefits with experts in immunology, placental pathology, and vaccine kinetics, she said.
“The overall complete consensus was that we don’t see biological plausibility at this time for placental transfer of the mRNA and that we see that direct fetal exposure or the possibility of fetal inflammatory response is extremely unlikely,” said Eckert, professor of obstetrics and gynecology at the University of Washington, Seattle. “Clearly we are waiting on the data.”
A Pfizer official told the ACIP panel that preliminary data “show no indication of either developmental or reproductive toxicity,” and that the company plans to send the final DART data to the FDA at the end of December.
On the potential for allergic reactions, the CDC concurred with the FDA that the vaccine should not be given to people with a history of serious reactions. The agency added that the category should include anyone who has had a reaction to any vaccine or injectable drug product because injectables may contain the same ingredients as the Pfizer vaccine, said Mbaeyi.
The CDC will also urge clinicians to observe patients with a history of anaphylaxis for 30 minutes after vaccination and all patients for at least 15 minutes afterward.
Should teens be a special population?
At least one ACIP panel member — Henry Bernstein, DO, MHCM, FAAP — said he was concerned that backing use of the vaccine in 16- and 17-year-olds was a leap of faith, given that Pfizer had extremely limited data on this cohort.
Bernstein, professor of pediatrics at the Zucker School of Medicine at Hofstra/Northwell in Hempstead, New York, also said that systemic reactions were more common in that age group.
He argued for making the 16- and 17-year-olds a “special population” that would get specific attention and guidance for vaccination from the federal agencies and professional societies.
Bernstein said he did not want to sow any more doubts in parents’ minds about vaccination, noting that hesitancy was a growing concern. “A successful pediatric vaccination program depends on creating and sustaining parental confidence in both the safety and effectiveness of this vaccine,” he said.
Many panelists, however, noted that there has been no evidence to suggest that the vaccine is not safe or less effective in that younger age group.
Yvonne Maldonado, MD, the American Academy of Pediatrics representative on the panel, said that this age group should not be denied the vaccine as they often have essential or front-line jobs that put them at higher risk for infection.
“I am very concerned about this message being sent out that this vaccine will not be safe in children,” said Maldonado, professor of pediatrics and health research and policy at Stanford University School of Medicine in California.
“We currently have no evidence that that is the case,” she said, adding there is also no indication younger children are biologically or physiologically different in their response or safety risk than 18-year-olds.
Vaccine = hope
Committee members breathed a sigh of relief at the end of the 2-day meeting, saying that although the Pfizer vaccine is not perfect, it represents a scientific milestone and a significant advance against the continuing march of the SARS-CoV-2 pandemic.
“This vaccine and future vaccines do provide a promise for a lot of progress in the future,” said panelist Beth P. Bell, MD, MPH, clinical professor of global health at the University of Washington School of Public Health in Seattle.
Peter Szilagyi, MD, MPH, executive vice-chair and vice-chair for research at the University of California, Los Angeles pediatrics department, said, “I’m really hopeful that this is the beginning of the end of the coronavirus pandemic.”
“The need for this vaccine is profound,” said Veronica McNally, president and CEO of the Franny Strong Foundation in West Bloomfield, Michigan.
The ACIP panel also made the argument that while the at least $10 billion spent on vaccine development by the federal government’s Operation Warp Speed alone has been a good investment, more spending is needed to actually get Americans vaccinated.
The imbalance between the two is “shocking and needs to be corrected,” said Bell. “We are not going to be able to protect the American public if we don’t have a way to deliver the vaccine to them.”
This article first appeared on Medscape.com.
stating they found it was safe and effective.
The agency said it will quickly issue guidance to clinicians so they can determine when and when not to give the vaccine, and to help them communicate the risks and benefits to patients.
CDC staff gave a preview of those clinical considerations at the agency’s Advisory Committee on Immunization Practices (ACIP) meeting on December 12 and said it would be holding calls with clinicians on December 13 and 14.
The CDC will also issue guidance December 13 on how organizations can handle the workforce problems that might arise as health care workers experience side effects from vaccination.
ACIP voted 11-0, with three recusals, to recommend use of the Pfizer-BioNTech mRNA vaccine in individuals 16 years or older according to the guidelines of the Food and Drug Administration’s (FDA’s) emergency use authorization issued December 11.
The panel also voted unanimously to include the vaccine in 2021 immunization schedules. All panel members said the recommendation should go hand-in-hand with ACIP’s previous recommendation on December 1 that allocation of the vaccine be phased-in, with health care workers and residents and staff of long-term care facilities in phase 1a.
Allergies, pregnant women?
ACIP panelists said clinicians need more guidance on whether to use the vaccine in pregnant or breastfeeding women, the immunocompromised, or those who have a history of allergies.
The FDA health care provider information sheet said there is not enough data to recommend vaccinating those women or the immunocompromised, and also advises against giving the vaccine to individuals who have a history of serious allergic reaction to any component of the vaccine.
Peter Marks, MD, PhD, director of the FDA’s Center for Biologic Evaluation and Research (CBER) clarified this in a briefing on December 12, noting that women who are pregnant or lactating can make the decision in consultation with their physician. And, he said, patients with any other history of allergy should be able to safely get the vaccine.
The CDC — in its soon-to-be-released guidance — will make the same recommendations. For any woman considering vaccination, she should consider the level of COVID-19 in the community, her personal risk of contracting the virus, the risks to her or her fetus of developing the disease, and the vaccine’s known side effects, Sarah Mbaeyi, MD, MPH, a medical officer at the agency, said during the panel meeting December 12.
She added that the CDC will also urge physicians to advise women to take acetaminophen if they develop a fever after vaccination — to protect the developing fetus from fever.
Sandra Fryhofer, MD, representing the American Medical Association, commended the CDC for these recommendations. But she also called on Pfizer, the FDA, and the CDC to make data from the developmental and reproductive toxicity (DART) studies public as soon as possible.
“We really need to put those results on warp speed and get them out there to give our physicians and pregnant women more information,” said Fryhofer, an adjunct associate professor of medicine at Emory University School of Medicine in Atlanta, Georgia.
The American College of Obstetricians and Gynecologists (ACOG) will also soon release guidance for vaccinating pregnant and breastfeeding women, said Linda Eckert, MD, FACOG, an ACOG representative on the panel.
ACOG and the CDC met the morning of December 12 to discuss risks and benefits with experts in immunology, placental pathology, and vaccine kinetics, she said.
“The overall complete consensus was that we don’t see biological plausibility at this time for placental transfer of the mRNA and that we see that direct fetal exposure or the possibility of fetal inflammatory response is extremely unlikely,” said Eckert, professor of obstetrics and gynecology at the University of Washington, Seattle. “Clearly we are waiting on the data.”
A Pfizer official told the ACIP panel that preliminary data “show no indication of either developmental or reproductive toxicity,” and that the company plans to send the final DART data to the FDA at the end of December.
On the potential for allergic reactions, the CDC concurred with the FDA that the vaccine should not be given to people with a history of serious reactions. The agency added that the category should include anyone who has had a reaction to any vaccine or injectable drug product because injectables may contain the same ingredients as the Pfizer vaccine, said Mbaeyi.
The CDC will also urge clinicians to observe patients with a history of anaphylaxis for 30 minutes after vaccination and all patients for at least 15 minutes afterward.
Should teens be a special population?
At least one ACIP panel member — Henry Bernstein, DO, MHCM, FAAP — said he was concerned that backing use of the vaccine in 16- and 17-year-olds was a leap of faith, given that Pfizer had extremely limited data on this cohort.
Bernstein, professor of pediatrics at the Zucker School of Medicine at Hofstra/Northwell in Hempstead, New York, also said that systemic reactions were more common in that age group.
He argued for making the 16- and 17-year-olds a “special population” that would get specific attention and guidance for vaccination from the federal agencies and professional societies.
Bernstein said he did not want to sow any more doubts in parents’ minds about vaccination, noting that hesitancy was a growing concern. “A successful pediatric vaccination program depends on creating and sustaining parental confidence in both the safety and effectiveness of this vaccine,” he said.
Many panelists, however, noted that there has been no evidence to suggest that the vaccine is not safe or less effective in that younger age group.
Yvonne Maldonado, MD, the American Academy of Pediatrics representative on the panel, said that this age group should not be denied the vaccine as they often have essential or front-line jobs that put them at higher risk for infection.
“I am very concerned about this message being sent out that this vaccine will not be safe in children,” said Maldonado, professor of pediatrics and health research and policy at Stanford University School of Medicine in California.
“We currently have no evidence that that is the case,” she said, adding there is also no indication younger children are biologically or physiologically different in their response or safety risk than 18-year-olds.
Vaccine = hope
Committee members breathed a sigh of relief at the end of the 2-day meeting, saying that although the Pfizer vaccine is not perfect, it represents a scientific milestone and a significant advance against the continuing march of the SARS-CoV-2 pandemic.
“This vaccine and future vaccines do provide a promise for a lot of progress in the future,” said panelist Beth P. Bell, MD, MPH, clinical professor of global health at the University of Washington School of Public Health in Seattle.
Peter Szilagyi, MD, MPH, executive vice-chair and vice-chair for research at the University of California, Los Angeles pediatrics department, said, “I’m really hopeful that this is the beginning of the end of the coronavirus pandemic.”
“The need for this vaccine is profound,” said Veronica McNally, president and CEO of the Franny Strong Foundation in West Bloomfield, Michigan.
The ACIP panel also made the argument that while the at least $10 billion spent on vaccine development by the federal government’s Operation Warp Speed alone has been a good investment, more spending is needed to actually get Americans vaccinated.
The imbalance between the two is “shocking and needs to be corrected,” said Bell. “We are not going to be able to protect the American public if we don’t have a way to deliver the vaccine to them.”
This article first appeared on Medscape.com.
FDA OKs emergency use of Pfizer COVID-19 vaccine
The much-anticipated emergency use authorization (EUA) of this vaccine — the first such approval in the United States — was greeted with optimism by infectious disease and pulmonary experts, although unanswered questions remain regarding use in people with allergic hypersensitivity, safety in pregnant women, and how smooth distribution will be.
“I am delighted. This is a first, firm step on a long path to getting this COVID pandemic under control,” William Schaffner, MD, professor of infectious diseases at the Vanderbilt University School of Medicine in Nashville, Tennessee, said in an interview.
The FDA gave the green light after the December 10 recommendation from the agency’s Vaccines and Related Biological Products Advisory Committee (VRBPAC) meeting. The committee voted 17-4 in favor of the emergency authorization.
The COVID-19 vaccine is “going to have a major impact here in the US. I’m very optimistic about it,” Dial Hewlett, MD, a spokesperson for the Infectious Diseases Society of American (IDSA), told this news organization.
Daniel Culver, DO, chair of medicine at the Cleveland Clinic in Ohio, is likewise hopeful. “My understanding is that supplies of the vaccine are already in place in hubs and will be shipped relatively quickly. The hope would be we can start vaccinating people as early as next week.”
Allergic reactions reported in the UK
After vaccinations with the Pfizer vaccine began in the UK on December 8, reports surfaced of two healthcare workers who experienced allergic reactions. They have since recovered, but officials warned that people with a history of severe allergic reactions should not receive the Pfizer vaccine at this time.
“For the moment, they are asking people who have had notable allergic reactions to step aside while this is investigated. It shows you that the system is working,” Schaffner said.
Both vaccine recipients who experienced anaphylaxis carried EpiPens, as they were at high risk for allergic reactions, Hewlett said. Also, if other COVID-19 vaccines are approved for use in the future, people allergic to the Pfizer vaccine might have another option, he added.
Reassuring role models
Schaffner supports the CDC Advisory Committee on Immunization Practices (ACIP) decision to start vaccinations with healthcare workers and residents of long-term care facilities.
“Vaccinating healthcare workers, in particular, will be a model for the general public,” said Schaffner, who is also a former member of the IDSA board of directors. “If they see those of us in white coats and blue scrubs lining up for the vaccine, that will provide confidence.”
To further increase acceptance of the COVID-19 vaccine, public health officials need to provide information and reassure the general public, Schaffner said.
Hewlett agreed. “I know there are a lot of people in the population who are very hesitant about vaccines. As infection disease specialists and people in public health, we are trying to allay a lot of concerns people have.”
Reassurance will be especially important in minority communities. “They have been disproportionately affected by the virus, and they have a traditional history of not being optimally vaccinated,” Schaffner said. “We need to reach them in particular with good information and reassurance…so they can make good decisions for themselves and their families.”
No vaccine is 100% effective or completely free of side effects. “There is always a chance there can be adverse reactions, but we think for the most part this is going to be a safe and effective vaccine,” said Hewlett, medical director at the Division of Disease Control and deputy to commissioner of health at the Westchester County Department of Health in White Plains, New York.
Distribution: Smooth or full of strife?
In addition to the concern that some people will not take advantage of vaccination against COVID-19, there could be vaccine supply issues down the road, Schaffner said.
Culver agreed. “In the early phases, I expect that there will be some kinks to work out, but because the numbers are relatively small, this should be okay,” he said.
“I think when we start to get into larger-scale vaccination programs — the supply chain, transport, and storage will be a Herculean undertaking,” Culver added. “It will take careful coordination between healthcare providers, distributors, suppliers, and public health officials to pull this off.”
Planning and distribution also should focus beyond US borders. Any issues in vaccine distribution or administration in the United States “will only be multiplied in several other parts of the world,” Culver said. Because COVID-19 is a pandemic, “we need to think about vaccinating globally.”
Investigating adverse events
Adverse events common to vaccinations in general — injection site pain, headaches, and fever — would not be unexpected with the COVID-19 vaccines. However, experts remain concerned that other, unrelated adverse events might be erroneously attributed to vaccination. For example, if a fall, heart attack, or death occurs within days of immunization, some might immediately blame the vaccine product.
“It’s important to remember that any new, highly touted medical therapy like this will receive a lot of scrutiny, so it would be unusual not to hear about something happening to somebody,” Culver said. Vaccine companies and health agencies will be carefully evaluating any reported adverse events to ensure no safety signal was missed in the trials.
“Fortunately, there are systems in place to investigate these events immediately,” Schaffner said.
Pregnancy recommendations pending
One question still looms: Is the COVID-19 vaccination safe for pregnant women? This isn’t just a question for the general public, either, Schaffner said. He estimated that about 70 percent of healthcare workers are women, and data suggests about 300,000 of these healthcare workers are pregnant.
“The CDC’s Advisory Committee on Immunization Practices will speak to that just as soon as the EUA is issued,” he added.
Patients are asking Culver about the priority order for vaccination. He said it’s difficult to provide firm guidance at this point.
People also have “lingering skepticism” about whether vaccine development was done in a prudent way, Culver said. Some people question whether the Pfizer vaccine and others were rushed to market. “So we try to spend time with the patients, reassuring them that all the usual safety evaluations were carefully done,” he said.
Another concern is whether mRNA vaccines can interact with human DNA. “The quick, short, and definitive answer is no,” Schaffner said. The m stands for messenger — the vaccines transmit information. "Once it gets into a cell, the mRNA does not go anywhere near the DNA, and once it transmits its information to the cell appropriately, it gets metabolized, and we excrete all the remnants."
Hewlett pointed out that investigations and surveillance will continue. Because this is an EUA and not full approval, “that essentially means they will still be obligated to collect a lot more data than they would ordinarily,” he said.
How long immunoprotection will last also remains an unknown. “The big question left on the table now is the durability,” Culver said. “Of course, we won’t know the answer to that for quite some time.”
Schaffner and Culver have disclosed no relevant financial relationships. Hewlett was an employee of Pfizer until mid-2019. His previous work as Pfizer’s senior medical director of global medical product evaluation was not associated with development of the COVID-19 vaccine.
This article first appeared on Medscape.com.
The much-anticipated emergency use authorization (EUA) of this vaccine — the first such approval in the United States — was greeted with optimism by infectious disease and pulmonary experts, although unanswered questions remain regarding use in people with allergic hypersensitivity, safety in pregnant women, and how smooth distribution will be.
“I am delighted. This is a first, firm step on a long path to getting this COVID pandemic under control,” William Schaffner, MD, professor of infectious diseases at the Vanderbilt University School of Medicine in Nashville, Tennessee, said in an interview.
The FDA gave the green light after the December 10 recommendation from the agency’s Vaccines and Related Biological Products Advisory Committee (VRBPAC) meeting. The committee voted 17-4 in favor of the emergency authorization.
The COVID-19 vaccine is “going to have a major impact here in the US. I’m very optimistic about it,” Dial Hewlett, MD, a spokesperson for the Infectious Diseases Society of American (IDSA), told this news organization.
Daniel Culver, DO, chair of medicine at the Cleveland Clinic in Ohio, is likewise hopeful. “My understanding is that supplies of the vaccine are already in place in hubs and will be shipped relatively quickly. The hope would be we can start vaccinating people as early as next week.”
Allergic reactions reported in the UK
After vaccinations with the Pfizer vaccine began in the UK on December 8, reports surfaced of two healthcare workers who experienced allergic reactions. They have since recovered, but officials warned that people with a history of severe allergic reactions should not receive the Pfizer vaccine at this time.
“For the moment, they are asking people who have had notable allergic reactions to step aside while this is investigated. It shows you that the system is working,” Schaffner said.
Both vaccine recipients who experienced anaphylaxis carried EpiPens, as they were at high risk for allergic reactions, Hewlett said. Also, if other COVID-19 vaccines are approved for use in the future, people allergic to the Pfizer vaccine might have another option, he added.
Reassuring role models
Schaffner supports the CDC Advisory Committee on Immunization Practices (ACIP) decision to start vaccinations with healthcare workers and residents of long-term care facilities.
“Vaccinating healthcare workers, in particular, will be a model for the general public,” said Schaffner, who is also a former member of the IDSA board of directors. “If they see those of us in white coats and blue scrubs lining up for the vaccine, that will provide confidence.”
To further increase acceptance of the COVID-19 vaccine, public health officials need to provide information and reassure the general public, Schaffner said.
Hewlett agreed. “I know there are a lot of people in the population who are very hesitant about vaccines. As infection disease specialists and people in public health, we are trying to allay a lot of concerns people have.”
Reassurance will be especially important in minority communities. “They have been disproportionately affected by the virus, and they have a traditional history of not being optimally vaccinated,” Schaffner said. “We need to reach them in particular with good information and reassurance…so they can make good decisions for themselves and their families.”
No vaccine is 100% effective or completely free of side effects. “There is always a chance there can be adverse reactions, but we think for the most part this is going to be a safe and effective vaccine,” said Hewlett, medical director at the Division of Disease Control and deputy to commissioner of health at the Westchester County Department of Health in White Plains, New York.
Distribution: Smooth or full of strife?
In addition to the concern that some people will not take advantage of vaccination against COVID-19, there could be vaccine supply issues down the road, Schaffner said.
Culver agreed. “In the early phases, I expect that there will be some kinks to work out, but because the numbers are relatively small, this should be okay,” he said.
“I think when we start to get into larger-scale vaccination programs — the supply chain, transport, and storage will be a Herculean undertaking,” Culver added. “It will take careful coordination between healthcare providers, distributors, suppliers, and public health officials to pull this off.”
Planning and distribution also should focus beyond US borders. Any issues in vaccine distribution or administration in the United States “will only be multiplied in several other parts of the world,” Culver said. Because COVID-19 is a pandemic, “we need to think about vaccinating globally.”
Investigating adverse events
Adverse events common to vaccinations in general — injection site pain, headaches, and fever — would not be unexpected with the COVID-19 vaccines. However, experts remain concerned that other, unrelated adverse events might be erroneously attributed to vaccination. For example, if a fall, heart attack, or death occurs within days of immunization, some might immediately blame the vaccine product.
“It’s important to remember that any new, highly touted medical therapy like this will receive a lot of scrutiny, so it would be unusual not to hear about something happening to somebody,” Culver said. Vaccine companies and health agencies will be carefully evaluating any reported adverse events to ensure no safety signal was missed in the trials.
“Fortunately, there are systems in place to investigate these events immediately,” Schaffner said.
Pregnancy recommendations pending
One question still looms: Is the COVID-19 vaccination safe for pregnant women? This isn’t just a question for the general public, either, Schaffner said. He estimated that about 70 percent of healthcare workers are women, and data suggests about 300,000 of these healthcare workers are pregnant.
“The CDC’s Advisory Committee on Immunization Practices will speak to that just as soon as the EUA is issued,” he added.
Patients are asking Culver about the priority order for vaccination. He said it’s difficult to provide firm guidance at this point.
People also have “lingering skepticism” about whether vaccine development was done in a prudent way, Culver said. Some people question whether the Pfizer vaccine and others were rushed to market. “So we try to spend time with the patients, reassuring them that all the usual safety evaluations were carefully done,” he said.
Another concern is whether mRNA vaccines can interact with human DNA. “The quick, short, and definitive answer is no,” Schaffner said. The m stands for messenger — the vaccines transmit information. "Once it gets into a cell, the mRNA does not go anywhere near the DNA, and once it transmits its information to the cell appropriately, it gets metabolized, and we excrete all the remnants."
Hewlett pointed out that investigations and surveillance will continue. Because this is an EUA and not full approval, “that essentially means they will still be obligated to collect a lot more data than they would ordinarily,” he said.
How long immunoprotection will last also remains an unknown. “The big question left on the table now is the durability,” Culver said. “Of course, we won’t know the answer to that for quite some time.”
Schaffner and Culver have disclosed no relevant financial relationships. Hewlett was an employee of Pfizer until mid-2019. His previous work as Pfizer’s senior medical director of global medical product evaluation was not associated with development of the COVID-19 vaccine.
This article first appeared on Medscape.com.
The much-anticipated emergency use authorization (EUA) of this vaccine — the first such approval in the United States — was greeted with optimism by infectious disease and pulmonary experts, although unanswered questions remain regarding use in people with allergic hypersensitivity, safety in pregnant women, and how smooth distribution will be.
“I am delighted. This is a first, firm step on a long path to getting this COVID pandemic under control,” William Schaffner, MD, professor of infectious diseases at the Vanderbilt University School of Medicine in Nashville, Tennessee, said in an interview.
The FDA gave the green light after the December 10 recommendation from the agency’s Vaccines and Related Biological Products Advisory Committee (VRBPAC) meeting. The committee voted 17-4 in favor of the emergency authorization.
The COVID-19 vaccine is “going to have a major impact here in the US. I’m very optimistic about it,” Dial Hewlett, MD, a spokesperson for the Infectious Diseases Society of American (IDSA), told this news organization.
Daniel Culver, DO, chair of medicine at the Cleveland Clinic in Ohio, is likewise hopeful. “My understanding is that supplies of the vaccine are already in place in hubs and will be shipped relatively quickly. The hope would be we can start vaccinating people as early as next week.”
Allergic reactions reported in the UK
After vaccinations with the Pfizer vaccine began in the UK on December 8, reports surfaced of two healthcare workers who experienced allergic reactions. They have since recovered, but officials warned that people with a history of severe allergic reactions should not receive the Pfizer vaccine at this time.
“For the moment, they are asking people who have had notable allergic reactions to step aside while this is investigated. It shows you that the system is working,” Schaffner said.
Both vaccine recipients who experienced anaphylaxis carried EpiPens, as they were at high risk for allergic reactions, Hewlett said. Also, if other COVID-19 vaccines are approved for use in the future, people allergic to the Pfizer vaccine might have another option, he added.
Reassuring role models
Schaffner supports the CDC Advisory Committee on Immunization Practices (ACIP) decision to start vaccinations with healthcare workers and residents of long-term care facilities.
“Vaccinating healthcare workers, in particular, will be a model for the general public,” said Schaffner, who is also a former member of the IDSA board of directors. “If they see those of us in white coats and blue scrubs lining up for the vaccine, that will provide confidence.”
To further increase acceptance of the COVID-19 vaccine, public health officials need to provide information and reassure the general public, Schaffner said.
Hewlett agreed. “I know there are a lot of people in the population who are very hesitant about vaccines. As infection disease specialists and people in public health, we are trying to allay a lot of concerns people have.”
Reassurance will be especially important in minority communities. “They have been disproportionately affected by the virus, and they have a traditional history of not being optimally vaccinated,” Schaffner said. “We need to reach them in particular with good information and reassurance…so they can make good decisions for themselves and their families.”
No vaccine is 100% effective or completely free of side effects. “There is always a chance there can be adverse reactions, but we think for the most part this is going to be a safe and effective vaccine,” said Hewlett, medical director at the Division of Disease Control and deputy to commissioner of health at the Westchester County Department of Health in White Plains, New York.
Distribution: Smooth or full of strife?
In addition to the concern that some people will not take advantage of vaccination against COVID-19, there could be vaccine supply issues down the road, Schaffner said.
Culver agreed. “In the early phases, I expect that there will be some kinks to work out, but because the numbers are relatively small, this should be okay,” he said.
“I think when we start to get into larger-scale vaccination programs — the supply chain, transport, and storage will be a Herculean undertaking,” Culver added. “It will take careful coordination between healthcare providers, distributors, suppliers, and public health officials to pull this off.”
Planning and distribution also should focus beyond US borders. Any issues in vaccine distribution or administration in the United States “will only be multiplied in several other parts of the world,” Culver said. Because COVID-19 is a pandemic, “we need to think about vaccinating globally.”
Investigating adverse events
Adverse events common to vaccinations in general — injection site pain, headaches, and fever — would not be unexpected with the COVID-19 vaccines. However, experts remain concerned that other, unrelated adverse events might be erroneously attributed to vaccination. For example, if a fall, heart attack, or death occurs within days of immunization, some might immediately blame the vaccine product.
“It’s important to remember that any new, highly touted medical therapy like this will receive a lot of scrutiny, so it would be unusual not to hear about something happening to somebody,” Culver said. Vaccine companies and health agencies will be carefully evaluating any reported adverse events to ensure no safety signal was missed in the trials.
“Fortunately, there are systems in place to investigate these events immediately,” Schaffner said.
Pregnancy recommendations pending
One question still looms: Is the COVID-19 vaccination safe for pregnant women? This isn’t just a question for the general public, either, Schaffner said. He estimated that about 70 percent of healthcare workers are women, and data suggests about 300,000 of these healthcare workers are pregnant.
“The CDC’s Advisory Committee on Immunization Practices will speak to that just as soon as the EUA is issued,” he added.
Patients are asking Culver about the priority order for vaccination. He said it’s difficult to provide firm guidance at this point.
People also have “lingering skepticism” about whether vaccine development was done in a prudent way, Culver said. Some people question whether the Pfizer vaccine and others were rushed to market. “So we try to spend time with the patients, reassuring them that all the usual safety evaluations were carefully done,” he said.
Another concern is whether mRNA vaccines can interact with human DNA. “The quick, short, and definitive answer is no,” Schaffner said. The m stands for messenger — the vaccines transmit information. "Once it gets into a cell, the mRNA does not go anywhere near the DNA, and once it transmits its information to the cell appropriately, it gets metabolized, and we excrete all the remnants."
Hewlett pointed out that investigations and surveillance will continue. Because this is an EUA and not full approval, “that essentially means they will still be obligated to collect a lot more data than they would ordinarily,” he said.
How long immunoprotection will last also remains an unknown. “The big question left on the table now is the durability,” Culver said. “Of course, we won’t know the answer to that for quite some time.”
Schaffner and Culver have disclosed no relevant financial relationships. Hewlett was an employee of Pfizer until mid-2019. His previous work as Pfizer’s senior medical director of global medical product evaluation was not associated with development of the COVID-19 vaccine.
This article first appeared on Medscape.com.
How to refine your approach to peripheral arterial disease
Peripheral arterial disease (PAD), the progressive disorder that results in ischemia to distal vascular territories as a result of atherosclerosis, spans a wide range of presentations, from minimally symptomatic disease to limb ischemia secondary to acute or chronic occlusion.
The prevalence of PAD is variable, due to differing diagnostic criteria used in studies, but PAD appears to affect 1 in every 22 people older than age 40.1 However, since PAD incidence increases with age, it is increasing in prevalence as the US population ages.1-3
PAD is associated with increased hospitalizations and decreased quality of life.4 Patients with PAD have an estimated 30% 5-year risk for myocardial infarction, stroke, or death from a vascular cause.3
Screening. Although PAD is underdiagnosed and appears to be undertreated,3 population-based screening for PAD in asymptomatic patients is not recommended. A Cochrane review found no studies evaluating the benefit of asymptomatic population-based screening.5 Similarly, in 2018, the USPSTF performed a comprehensive review and found no studies to support routine screening and determined there was insufficient evidence to recommend it.6,7
Risk factors and associated comorbidities
PAD risk factors, like the ones detailed below, have a potentiating effect. The presence of 2 risk factors doubles PAD risk, while 3 or more risk factors increase PAD risk by a factor of 10.1
Increasing age is the greatest single risk factor for PAD.1,2,8,9 Researchers using data from the National Health and Nutrition Examination Survey (NHANES) found that the prevalence of PAD increased from 1.4% in individuals ages 40 to 49 years to almost 17% in those age 70 or older.1
Demographic characteristics. Most studies demonstrate a higher risk for PAD in men.1-3,10 African-American patients have more than twice the risk for PAD, compared with Whites, even after adjustment for the increased prevalence of associated diseases such as hypertension and diabetes in this population.1-3,10
Continue to: Genetics...
Genetics. A study performed by the National Heart Lung and Blood Institute suggested that genetic correlations between twins were more important than environmental factors in the development of PAD.11
Smoking. Most population studies show smoking to be the greatest modifiable risk factor for PAD. An analysis of the NHANES data yielded an odds ratio (OR) of 4.1 for current smokers and of 1.8 for former smokers.1 Risk increases linearly with cumulative years of smoking.1,2,9,10
Diabetes is another significant modifiable risk factor, increasing PAD risk by 2.5 times.2 Diabetes is also associated with increases in functional limitation from claudication, risk for acute coronary syndrome, and progression to amputation.1
Hypertension nearly doubles the risk for PAD, and poor control further increases this risk.2,9,10
Chronic kidney disease (CKD). Patients with CKD have a progressively higher prevalence of PAD with worsening renal function.1 There is also an association between CKD and increased morbidity, revascularization failure, and increased mortality.1
Two additional risk factors that are less well understood are dyslipidemia and chronic inflammation. There is conflicting data regarding the role of individual components of cholesterol and their effect on PAD, although lipoprotein (a) has been shown to be an independent risk factor for both the development and progression of PAD.12 Similarly, chronic inflammation has been shown to play a role in the initiation and progression of the disease, although the role of inflammatory markers in evaluation and treatment is unclear and assessment for these purposes is not currently recommended.12,13
Continue to: Diagnosis...
Diagnosis
Clinical presentation
Lower extremity pain is the hallmark symptom of PAD, but presentation varies. The classic presentation is claudication, pain within a defined muscle group that occurs with exertion and is relieved by rest. Claudication is most common in the calf but also occurs in the buttock/thigh and the foot.
However, most patients with PAD present with pain that does not fit the definition of claudication. Patients with comorbidities, physical inactivity, and neuropathy are more likely to present with atypical pain.14 These patients may demonstrate critical or acute limb ischemia, characterized by pain at rest and most often localized to the forefoot and toes. Patients with critical limb ischemia may also present with nonhealing wounds/ulcers or gangrene.15
Physical exam findings can support the diagnosis of PAD, but none are reliable enough to rule the diagnosis in or out. Findings suggestive of PAD include cool skin, presence of a bruit (iliac, femoral, or popliteal), and palpable pulse abnormality. Multiple abnormal physical exam findings increase the likelihood of PAD, while the absence of a bruit or palpable pulse abnormality makes PAD less likely.16 In patients with PAD, an associated wound/ulcer is most often distal in the foot and usually appears dry.17
The differential diagnosis for intermittent leg pain is broad and includes neurologic, musculoskeletal, and venous etiologies. Table 118 lists some common alternate diagnoses for patients presenting with leg pain or claudication.
Continue to: Diagnostic testing...
Diagnostic testing
An ankle-brachial index (ABI) test should be performed in patients with history or physical exam findings suggestive of PAD. A resting ABI is performed with the patient in the supine position, with measurement of systolic blood pressure in both arms and ankles using a Doppler ultrasound device. Table 213 outlines ABI scoring and interpretation.
An ABI > 1.4 is an invalid measurement, indicating that the arteries are too calcified to be compressed. These highly elevated ABI measurements are common in patients with diabetes and/or advanced CKD. In these patients, a toe-brachial index (TBI) test should be performed, because the digital arteries are almost always compressible.13
Patients with symptomatic PAD who are under consideration for revascularization may benefit from radiologic imaging of the lower extremities with duplex ultrasound, computed tomography angiography, or magnetic resonance angiography to determine the anatomic location and severity of stenosis.13
Management of PAD
Lifestyle interventions
For patients with PAD, lifestyle modifications are an essential—but challenging—component of disease management.
Continue to: Smoking cessation...
Smoking cessation. As with other atherosclerotic diseases, PAD progression is strongly correlated with smoking. A trial involving 204 active smokers with PAD showed that 5-year mortality and amputation rates dropped by more than half in those who quit smoking within a year, with numbers needed to treat (NNT) of 6 for mortality and 5 for amputation.19 Because of this dramatic effect, American College of Cardiology/American Heart Association (ACC/AHA) guidelines encourage providers to address smoking at every visit and use cessation programs and medication to increase quit rates.13
Exercise may be the most important intervention for PAD. A 2017 Cochrane review found that supervised, structured exercise programs increase pain-free and maximal walking distances by at least 20% and also improve physical and mental quality of life.20 In a trial involving 111 patients with aortoiliac PAD, supervised exercise plus medical care led to greater functional improvement than either revascularization plus medical care or medical care alone.21 In a 2018 Cochrane review, neither revascularization or revascularization added to supervised exercise were better than supervised exercise alone.22 ACC/AHA guidelines recommend supervised exercise programs for claudication prior to considering revascularization.13TABLE 313 outlines the components of a structured exercise program.
Unfortunately, the benefit of these programs has been difficult to reproduce without supervision. Another 2018 Cochrane review demonstrated significant improvement with supervised exercise and no clear improvement in patients given home exercise or advice to walk.23 A recent study examined the effect of having patients use a wearable fitness tracker for home exercise and demonstrated no benefit over usual care.24
Diet. There is some evidence that dietary interventions can prevent and possibly improve PAD. A large randomized controlled trial showed that a Mediterranean diet lowered rates of PAD over 1 year compared to a low-fat diet, with an NNT of 336 if supplemented with extra-virgin olive oil and 448 if supplemented with nuts.25 A small trial of 25 patients who consumed non-soy legumes daily for 8 weeks showed average ABI improvement of 6%, although there was no control group.26
Medical therapy to address peripheral and cardiovascular events
Standard medical therapy for coronary artery disease (CAD) is recommended for patients with PAD to reduce cardiovascular and limb events. For example, treatment of hypertension reduces cardiovascular and cerebrovascular events, and studies verify that lowering blood pressure does not worsen claudication or limb perfusion.
13TABLE 413,27-30 outlines the options for medical therapy.
Continue to: Statins...
Statins reduce cardiovascular events in PAD patients. A large study demonstrated that 40 mg of simvastatin has an NNT of 21 to prevent a coronary or cerebrovascular event in PAD, similar to the NNT of 23 seen in treatment of CAD.27 Statins also reduce adverse limb outcomes. A registry of atherosclerosis patients showed that statins have an NNT of 56 to prevent amputation in PAD and an NNT of 28 to prevent worsening claudication, critical limb ischemia, revascularization, or amputation.28
Antiplatelet therapy with low-dose aspirin or clopidogrel is recommended for symptomatic patients and for asymptomatic patients with an ABI ≤ 0.9.13 A Cochrane review demonstrated significantly reduced mortality with nonaspirin antiplatelet agents vs aspirin (NNT = 94) without increase in major bleeding.29 Only British guidelines specifically recommend clopidogrel over aspirin.31
Dual antiplatelet therapy has not shown consistent benefits over aspirin alone. ACC/AHA guidelines state that dual antiplatelet therapy is not well established for PAD but may be reasonable after revascularization.13
Voraxapar is a novel antiplatelet agent that targets the thrombin-binding receptor on platelets. However, trials show no significant coronary benefit, and slight reductions in acute limb ischemia are offset by increases in major bleeding.13
For patients receiving medical therapy, ongoing evaluation and treatment should be based on claudication symptoms and clinical assessment.
Medical therapy for claudication
Several medications have been proposed for symptomatic treatment of intermittent claudication. Cilostazol is a phosphodiesterase inhibitor with the best risk-benefit ratio. A Cochrane review showed improvements in maximal and pain-free walking distances compared to placebo and improvements in quality of life with cilostazol 100 mg taken twice daily.32 Adverse effects included headache, dizziness, palpitations, and diarrhea.29
Continue to: Pentoxifylline...
Pentoxifylline is another phosphodiesterase inhibitor with less evidence of improvement, higher adverse effect rates, and more frequent dosing. It is not recommended for treatment of intermittent claudication.13,33
Supplements. Padma 28, a Tibetan herbal formulation, appears to improve maximal walking distance with adverse effect rates similar to placebo.34 Other supplements, including vitamin E, ginkgo biloba, and omega-3 fatty acids, have no evidence of benefit.35-37
When revascularizationis needed
Patients who develop limb ischemia or lifestyle-limiting claudication despite conservative therapy are candidates for revascularization. Endovascular techniques include angioplasty, stenting, atherectomy, and precise medication delivery. Surgical approaches mainly consist of thrombectomy and bypass grafting. For intermittent claudication despite conservative care, ACC/AHA guidelines state endovascular procedures are appropriate for aortoiliac disease and reasonable for femoropopliteal disease, but unproven for infrapopliteal disease.13
Acute limb ischemia is an emergency requiring immediate intervention. Two trials revealed identical overall and amputation-free survival rates for percutaneous thrombolysis and surgical thrombectomy.38,39 ACC/AHA guidelines recommend anticoagulation with heparin followed by the revascularization technique that will most rapidly restore arterial flow.13
For chronic limb ischemia, a large trial showed angioplasty had lower initial morbidity, length of hospitalization, and cost than surgical repair. However, surgical mortality was lower after 2 years.40 ACC/AHA guidelines recommend either surgery or endovascular procedures and propose initial endovascular treatment followed by surgery if needed.13 After revascularization, the patient should be followed periodically with a clinical evaluation and ABI measurement with further consideration for routine duplex ultrasound surveillance.13
Outcomes
Patients with PAD have variable outcomes. About 70% to 80% of patients with this diagnosis will have a stable disease process with no worsening of symptoms, 10% to 20% will experience worsening symptoms over time, 5% to 10% will require revascularization within 5 years of diagnosis, and 1% to 5% will progress to critical limb ischemia, which has a 5-year amputation rate of 1% to 4%.2 Patients who require amputation have poor outcomes: Within 2 years, 30% are dead and 15% have had further amputations.18
In addition to the morbidity and mortality from its own progression, PAD is an important predictor of CAD and is associated with a significant elevation in morbidity and mortality from CAD. One small but well-designed prospective cohort study found that patients with PAD had a more than 6-fold increased risk of death from CAD than did patients without PAD.41
Acknowledgement
The authors thank Francesca Cimino, MD, FAAFP, for her help in reviewing this manuscript.
CORRESPONDENCE
Dustin K. Smith, DO, 2080 Child Street, Jacksonville, FL 32214; [email protected]
1. Eraso LH, Fukaya E, Mohler ER 3rd, et al. Peripheral arterial disease, prevalence and cumulative risk factor profile analysis. Eur J Prev Cardiol. 2014;21:704-711.
2. Pasternak RC, Criqui MH, Benjamin EJ, et al; American Heart Association. Atherosclerotic Vascular Disease Conference: Writing Group I: epidemiology. Circulation. 2004;109:2605-2612.
3. Hirsch AT, Criqui MH, Treat-Jacobson D, et al. Peripheral arterial disease detection, awareness, and treatment in primary care. JAMA. 2001;286:1317-1324.
4. Olin JW, Sealove BA. Peripheral artery disease: current insight into the disease and its diagnosis and management. Mayo Clin Proc. 2010;85:678-692.
5. Andras A, Ferkert B. Screening for peripheral arterial disease. Cochrane Database Syst Rev. 2014;(4):CD010835.
6. Guirguis-Blake JM, Evans CV, Redmond N, et al. Screening for peripheral artery disease using ankle-brachial index: updated evidence report and systematic review for the US Preventive Services Task Force. JAMA. 2018;320:184-196.
7. US Preventive Services Task Force. Screening for peripheral artery disease and cardiovascular disease risk assessment with ankle-brachial index: US Preventive Services Task Force recommendation statement. JAMA. 2018;230:177-183.
8. American Heart Association Writing Group 2. Atherosclerotic Peripheral Vascular Disease Symposium II: screening for atherosclerotic vascular diseases: should nationwide programs be instituted? Circulation. 2008;118:2830-2836.
9. Berger JS, Hochman J, Lobach I, et al. Modifiable risk factor burden and the prevalence of peripheral artery disease in different vascular territories. J Vasc Surg. 2013;58:673-681.
10. Joosten MM, Pai JK, Bertoia ML, et al. Associations between conventional cardiovascular risk factors and risk of peripheral artery disease in men. JAMA. 2012;308:1660-1667.
11. Carmelli D, Fabsitz RR, Swan GE, et al. Contribution of genetic and environmental influences to ankle-brachial blood pressure index in the NHLBI Twin Study. National Heart, Lung, and Blood Institute. Am J Epidemiol. 2000;151:452-458.
12. Aboyans V, Criqui MH, Denenberg JO, et al. Risk factors for progression of peripheral arterial disease in large and small vessels. Circulation. 2006;113:2623-2629.
13. Gerald-Herman MD, Gornik HL, Barrett C, et al. 2016 AHA/ACC guideline on the management of patients with lower extremity peripheral artery disease: a report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines. Circulation. 2017;135:e726-e779.
14. McDermott MM, Greenland P, Liu K, et al. Leg symptoms in peripheral arterial disease: associated clinical characteristics and functional impairment. JAMA. 2001;286:1599-1606.
15. Cranley JJ. Ischemic rest pain. Arch Surg. 1969;98:187-188.
16. Khan NA, Rahim SA, Anand SS, et al. Does the clinical examination predict lower extremity peripheral arterial disease? JAMA. 2006;295:536-546.
17. Wennberg PW. Approach to the patient with peripheral arterial disease. Circulation. 2013;128:2241-2250.
18. Norgren L, Hiatt WR, Dormandy JA, et al. Inter-society consensus for the management of peripheral arterial disease (TASC II). Eur J Vas Endovasc Surg. 2007;33:S1-S75.
19. Armstrong EJ, Wu J, Singh GD, et al. Smoking cessation is associated with decreased mortality and improved amputation-free survival among patients with symptomatic peripheral artery disease. J Vasc Surg. 2014;60:1565-1571.
20. Lane R, Harwood A, Watson L, et al. Exercise for intermittent claudication. Cochrane Database Syst Rev. 2017;(12):CD000990.
21. Murphy TP, Cutlip DE, Regensteiner JG, et al; CLEVER Study Investigators. Supervised exercise versus primary stenting for claudication resulting from aortoiliac peripheral artery disease: six-month outcomes from the claudication: exercise versus endoluminal revascularization (CLEVER) study. Circulation. 2012;125:130-139.
22. Fakhry F, Fokkenrood HJP, Pronk S, et al. Endovascular revascularization versus conservative management for intermittent claudication. Cochrane Database Syst Rev. 2018;(3):CD010512.
23. Hageman D, Fokkenrood HJ, Gommans LN, et al. Supervised exercise therapy versus home-based exercise therapy versus walking advice for intermittent claudication. Cochrane Database Syst Rev. 2018;(4):CD005263.
24. McDermott MM, Spring B, Berger JS, et al. Effect of a home-based exercise intervention of wearable technology and telephone coaching on walking performance in peripheral artery disease: the HONOR randomized clinical trial. JAMA. 2018;319:1665-1676.
25. Ruiz-Canela M, Estruch R, Corella D, et al. Association of Mediterranean diet with peripheral artery disease: the PREDIMED randomized trial. JAMA. 2014;311:415-417.
26. Zahradka P, Wright B, Weighell W, et al. Daily non-soy legume consumption reverses vascular impairment due to peripheral artery disease. Atherosclerosis. 2013;230:310-314.
27. Heart Protection Study Collaborative Group. Randomized trial of the effects of cholesterol-lowering with simvastatin on peripheral vascular and other major vascular outcomes in 20536 people with peripheral arterial disease and other high-risk conditions. J Vasc Surg. 2007;45:645-655.
28. Kumbhani DJ, Steg G, Cannon CP, et al. Statin therapy and long-term adverse limb outcomes in patients with peripheral artery disease: insights from the REACH registry. Eur Heart J. 2014;35:2864-2872.
29. Wong PF, Chong LY, Mikhailidis DP, et al. Antiplatelet agents for intermittent claudication. Cochrane Database Syst Rev. 2011;(11):CD001272.
30. Critical Leg Ischaemia Prevention Study (CLIPS) Group, Catalano M, Born G, Peto R. Prevention of serious vascular events by aspirin amongst patients with peripheral arterial disease: randomized, double-blind trial. J Intern Med. 2007;261:276-284.
31. Morley RL, Sharma A, Horsch AD, et al. Peripheral artery disease. BMJ. 2018;360:j5842.
32. Bedenis R, Stewart M, Cleanthis M, et al. Cilostazol for intermittent claudication. Cochrane Database Syst Rev. 2014;(10):CD003748.
33. Salhiyyah K, Forster R, Senanayake E, et al. Pentoxifylline for intermittent claudication. Cochrane Database Syst Rev. 2015;(9):CD005262.
34. Stewart M, Morling JR, Maxwell H. Padma 28 for intermittent claudication. Cochrane Database Syst Rev. 2016;(3):CD007371.
35. Kleijnen J, Mackerras D. Vitamin E for intermittent claudication. Cochrane Database Syst Rev. 1998;(1):CD000987.
36. Nicolai SPA, Kruidenior LM, Bendermacher BLW, et al. Ginkgo biloba for intermittent claudication. Cochrane Database Syst Rev. 2013;(6):CD006888.
37. Campbell A, Price J, Hiatt WR. Omega-3 fatty acids for intermittent claudication. Cochrane Database Syst Rev. 2013;(7):CD003833.
38. American Surgical Association, New York Surgical Society, Philadelphia Academy of Surgery, Southern Surgical Association (US), Central Surgical Association. Results of a prospective randomized trial evaluating surgery versus thrombolysis for ischemia of the lower extremity: the STILE trial. Ann Surg. 1994;220:251-268.
39. Ouriel K, Veith FJ, Sasahara AA.
40. Bradbury AW, Ruckley CV, Fowkes FGR, et al. Bypass versus angioplasty in severe ischaemia of the leg (BASIL): multicentre, randomised, controlled trial. Lancet. 2005;366:1925-1934.
41. Criqui MH, Langer RD, Fronek A, et al. Mortality over a period of 10 years in patients with peripheral arterial disease. N Engl J Med. 1992;326:381-386.
Peripheral arterial disease (PAD), the progressive disorder that results in ischemia to distal vascular territories as a result of atherosclerosis, spans a wide range of presentations, from minimally symptomatic disease to limb ischemia secondary to acute or chronic occlusion.
The prevalence of PAD is variable, due to differing diagnostic criteria used in studies, but PAD appears to affect 1 in every 22 people older than age 40.1 However, since PAD incidence increases with age, it is increasing in prevalence as the US population ages.1-3
PAD is associated with increased hospitalizations and decreased quality of life.4 Patients with PAD have an estimated 30% 5-year risk for myocardial infarction, stroke, or death from a vascular cause.3
Screening. Although PAD is underdiagnosed and appears to be undertreated,3 population-based screening for PAD in asymptomatic patients is not recommended. A Cochrane review found no studies evaluating the benefit of asymptomatic population-based screening.5 Similarly, in 2018, the USPSTF performed a comprehensive review and found no studies to support routine screening and determined there was insufficient evidence to recommend it.6,7
Risk factors and associated comorbidities
PAD risk factors, like the ones detailed below, have a potentiating effect. The presence of 2 risk factors doubles PAD risk, while 3 or more risk factors increase PAD risk by a factor of 10.1
Increasing age is the greatest single risk factor for PAD.1,2,8,9 Researchers using data from the National Health and Nutrition Examination Survey (NHANES) found that the prevalence of PAD increased from 1.4% in individuals ages 40 to 49 years to almost 17% in those age 70 or older.1
Demographic characteristics. Most studies demonstrate a higher risk for PAD in men.1-3,10 African-American patients have more than twice the risk for PAD, compared with Whites, even after adjustment for the increased prevalence of associated diseases such as hypertension and diabetes in this population.1-3,10
Continue to: Genetics...
Genetics. A study performed by the National Heart Lung and Blood Institute suggested that genetic correlations between twins were more important than environmental factors in the development of PAD.11
Smoking. Most population studies show smoking to be the greatest modifiable risk factor for PAD. An analysis of the NHANES data yielded an odds ratio (OR) of 4.1 for current smokers and of 1.8 for former smokers.1 Risk increases linearly with cumulative years of smoking.1,2,9,10
Diabetes is another significant modifiable risk factor, increasing PAD risk by 2.5 times.2 Diabetes is also associated with increases in functional limitation from claudication, risk for acute coronary syndrome, and progression to amputation.1
Hypertension nearly doubles the risk for PAD, and poor control further increases this risk.2,9,10
Chronic kidney disease (CKD). Patients with CKD have a progressively higher prevalence of PAD with worsening renal function.1 There is also an association between CKD and increased morbidity, revascularization failure, and increased mortality.1
Two additional risk factors that are less well understood are dyslipidemia and chronic inflammation. There is conflicting data regarding the role of individual components of cholesterol and their effect on PAD, although lipoprotein (a) has been shown to be an independent risk factor for both the development and progression of PAD.12 Similarly, chronic inflammation has been shown to play a role in the initiation and progression of the disease, although the role of inflammatory markers in evaluation and treatment is unclear and assessment for these purposes is not currently recommended.12,13
Continue to: Diagnosis...
Diagnosis
Clinical presentation
Lower extremity pain is the hallmark symptom of PAD, but presentation varies. The classic presentation is claudication, pain within a defined muscle group that occurs with exertion and is relieved by rest. Claudication is most common in the calf but also occurs in the buttock/thigh and the foot.
However, most patients with PAD present with pain that does not fit the definition of claudication. Patients with comorbidities, physical inactivity, and neuropathy are more likely to present with atypical pain.14 These patients may demonstrate critical or acute limb ischemia, characterized by pain at rest and most often localized to the forefoot and toes. Patients with critical limb ischemia may also present with nonhealing wounds/ulcers or gangrene.15
Physical exam findings can support the diagnosis of PAD, but none are reliable enough to rule the diagnosis in or out. Findings suggestive of PAD include cool skin, presence of a bruit (iliac, femoral, or popliteal), and palpable pulse abnormality. Multiple abnormal physical exam findings increase the likelihood of PAD, while the absence of a bruit or palpable pulse abnormality makes PAD less likely.16 In patients with PAD, an associated wound/ulcer is most often distal in the foot and usually appears dry.17
The differential diagnosis for intermittent leg pain is broad and includes neurologic, musculoskeletal, and venous etiologies. Table 118 lists some common alternate diagnoses for patients presenting with leg pain or claudication.
Continue to: Diagnostic testing...
Diagnostic testing
An ankle-brachial index (ABI) test should be performed in patients with history or physical exam findings suggestive of PAD. A resting ABI is performed with the patient in the supine position, with measurement of systolic blood pressure in both arms and ankles using a Doppler ultrasound device. Table 213 outlines ABI scoring and interpretation.
An ABI > 1.4 is an invalid measurement, indicating that the arteries are too calcified to be compressed. These highly elevated ABI measurements are common in patients with diabetes and/or advanced CKD. In these patients, a toe-brachial index (TBI) test should be performed, because the digital arteries are almost always compressible.13
Patients with symptomatic PAD who are under consideration for revascularization may benefit from radiologic imaging of the lower extremities with duplex ultrasound, computed tomography angiography, or magnetic resonance angiography to determine the anatomic location and severity of stenosis.13
Management of PAD
Lifestyle interventions
For patients with PAD, lifestyle modifications are an essential—but challenging—component of disease management.
Continue to: Smoking cessation...
Smoking cessation. As with other atherosclerotic diseases, PAD progression is strongly correlated with smoking. A trial involving 204 active smokers with PAD showed that 5-year mortality and amputation rates dropped by more than half in those who quit smoking within a year, with numbers needed to treat (NNT) of 6 for mortality and 5 for amputation.19 Because of this dramatic effect, American College of Cardiology/American Heart Association (ACC/AHA) guidelines encourage providers to address smoking at every visit and use cessation programs and medication to increase quit rates.13
Exercise may be the most important intervention for PAD. A 2017 Cochrane review found that supervised, structured exercise programs increase pain-free and maximal walking distances by at least 20% and also improve physical and mental quality of life.20 In a trial involving 111 patients with aortoiliac PAD, supervised exercise plus medical care led to greater functional improvement than either revascularization plus medical care or medical care alone.21 In a 2018 Cochrane review, neither revascularization or revascularization added to supervised exercise were better than supervised exercise alone.22 ACC/AHA guidelines recommend supervised exercise programs for claudication prior to considering revascularization.13TABLE 313 outlines the components of a structured exercise program.
Unfortunately, the benefit of these programs has been difficult to reproduce without supervision. Another 2018 Cochrane review demonstrated significant improvement with supervised exercise and no clear improvement in patients given home exercise or advice to walk.23 A recent study examined the effect of having patients use a wearable fitness tracker for home exercise and demonstrated no benefit over usual care.24
Diet. There is some evidence that dietary interventions can prevent and possibly improve PAD. A large randomized controlled trial showed that a Mediterranean diet lowered rates of PAD over 1 year compared to a low-fat diet, with an NNT of 336 if supplemented with extra-virgin olive oil and 448 if supplemented with nuts.25 A small trial of 25 patients who consumed non-soy legumes daily for 8 weeks showed average ABI improvement of 6%, although there was no control group.26
Medical therapy to address peripheral and cardiovascular events
Standard medical therapy for coronary artery disease (CAD) is recommended for patients with PAD to reduce cardiovascular and limb events. For example, treatment of hypertension reduces cardiovascular and cerebrovascular events, and studies verify that lowering blood pressure does not worsen claudication or limb perfusion.
13TABLE 413,27-30 outlines the options for medical therapy.
Continue to: Statins...
Statins reduce cardiovascular events in PAD patients. A large study demonstrated that 40 mg of simvastatin has an NNT of 21 to prevent a coronary or cerebrovascular event in PAD, similar to the NNT of 23 seen in treatment of CAD.27 Statins also reduce adverse limb outcomes. A registry of atherosclerosis patients showed that statins have an NNT of 56 to prevent amputation in PAD and an NNT of 28 to prevent worsening claudication, critical limb ischemia, revascularization, or amputation.28
Antiplatelet therapy with low-dose aspirin or clopidogrel is recommended for symptomatic patients and for asymptomatic patients with an ABI ≤ 0.9.13 A Cochrane review demonstrated significantly reduced mortality with nonaspirin antiplatelet agents vs aspirin (NNT = 94) without increase in major bleeding.29 Only British guidelines specifically recommend clopidogrel over aspirin.31
Dual antiplatelet therapy has not shown consistent benefits over aspirin alone. ACC/AHA guidelines state that dual antiplatelet therapy is not well established for PAD but may be reasonable after revascularization.13
Voraxapar is a novel antiplatelet agent that targets the thrombin-binding receptor on platelets. However, trials show no significant coronary benefit, and slight reductions in acute limb ischemia are offset by increases in major bleeding.13
For patients receiving medical therapy, ongoing evaluation and treatment should be based on claudication symptoms and clinical assessment.
Medical therapy for claudication
Several medications have been proposed for symptomatic treatment of intermittent claudication. Cilostazol is a phosphodiesterase inhibitor with the best risk-benefit ratio. A Cochrane review showed improvements in maximal and pain-free walking distances compared to placebo and improvements in quality of life with cilostazol 100 mg taken twice daily.32 Adverse effects included headache, dizziness, palpitations, and diarrhea.29
Continue to: Pentoxifylline...
Pentoxifylline is another phosphodiesterase inhibitor with less evidence of improvement, higher adverse effect rates, and more frequent dosing. It is not recommended for treatment of intermittent claudication.13,33
Supplements. Padma 28, a Tibetan herbal formulation, appears to improve maximal walking distance with adverse effect rates similar to placebo.34 Other supplements, including vitamin E, ginkgo biloba, and omega-3 fatty acids, have no evidence of benefit.35-37
When revascularizationis needed
Patients who develop limb ischemia or lifestyle-limiting claudication despite conservative therapy are candidates for revascularization. Endovascular techniques include angioplasty, stenting, atherectomy, and precise medication delivery. Surgical approaches mainly consist of thrombectomy and bypass grafting. For intermittent claudication despite conservative care, ACC/AHA guidelines state endovascular procedures are appropriate for aortoiliac disease and reasonable for femoropopliteal disease, but unproven for infrapopliteal disease.13
Acute limb ischemia is an emergency requiring immediate intervention. Two trials revealed identical overall and amputation-free survival rates for percutaneous thrombolysis and surgical thrombectomy.38,39 ACC/AHA guidelines recommend anticoagulation with heparin followed by the revascularization technique that will most rapidly restore arterial flow.13
For chronic limb ischemia, a large trial showed angioplasty had lower initial morbidity, length of hospitalization, and cost than surgical repair. However, surgical mortality was lower after 2 years.40 ACC/AHA guidelines recommend either surgery or endovascular procedures and propose initial endovascular treatment followed by surgery if needed.13 After revascularization, the patient should be followed periodically with a clinical evaluation and ABI measurement with further consideration for routine duplex ultrasound surveillance.13
Outcomes
Patients with PAD have variable outcomes. About 70% to 80% of patients with this diagnosis will have a stable disease process with no worsening of symptoms, 10% to 20% will experience worsening symptoms over time, 5% to 10% will require revascularization within 5 years of diagnosis, and 1% to 5% will progress to critical limb ischemia, which has a 5-year amputation rate of 1% to 4%.2 Patients who require amputation have poor outcomes: Within 2 years, 30% are dead and 15% have had further amputations.18
In addition to the morbidity and mortality from its own progression, PAD is an important predictor of CAD and is associated with a significant elevation in morbidity and mortality from CAD. One small but well-designed prospective cohort study found that patients with PAD had a more than 6-fold increased risk of death from CAD than did patients without PAD.41
Acknowledgement
The authors thank Francesca Cimino, MD, FAAFP, for her help in reviewing this manuscript.
CORRESPONDENCE
Dustin K. Smith, DO, 2080 Child Street, Jacksonville, FL 32214; [email protected]
Peripheral arterial disease (PAD), the progressive disorder that results in ischemia to distal vascular territories as a result of atherosclerosis, spans a wide range of presentations, from minimally symptomatic disease to limb ischemia secondary to acute or chronic occlusion.
The prevalence of PAD is variable, due to differing diagnostic criteria used in studies, but PAD appears to affect 1 in every 22 people older than age 40.1 However, since PAD incidence increases with age, it is increasing in prevalence as the US population ages.1-3
PAD is associated with increased hospitalizations and decreased quality of life.4 Patients with PAD have an estimated 30% 5-year risk for myocardial infarction, stroke, or death from a vascular cause.3
Screening. Although PAD is underdiagnosed and appears to be undertreated,3 population-based screening for PAD in asymptomatic patients is not recommended. A Cochrane review found no studies evaluating the benefit of asymptomatic population-based screening.5 Similarly, in 2018, the USPSTF performed a comprehensive review and found no studies to support routine screening and determined there was insufficient evidence to recommend it.6,7
Risk factors and associated comorbidities
PAD risk factors, like the ones detailed below, have a potentiating effect. The presence of 2 risk factors doubles PAD risk, while 3 or more risk factors increase PAD risk by a factor of 10.1
Increasing age is the greatest single risk factor for PAD.1,2,8,9 Researchers using data from the National Health and Nutrition Examination Survey (NHANES) found that the prevalence of PAD increased from 1.4% in individuals ages 40 to 49 years to almost 17% in those age 70 or older.1
Demographic characteristics. Most studies demonstrate a higher risk for PAD in men.1-3,10 African-American patients have more than twice the risk for PAD, compared with Whites, even after adjustment for the increased prevalence of associated diseases such as hypertension and diabetes in this population.1-3,10
Continue to: Genetics...
Genetics. A study performed by the National Heart Lung and Blood Institute suggested that genetic correlations between twins were more important than environmental factors in the development of PAD.11
Smoking. Most population studies show smoking to be the greatest modifiable risk factor for PAD. An analysis of the NHANES data yielded an odds ratio (OR) of 4.1 for current smokers and of 1.8 for former smokers.1 Risk increases linearly with cumulative years of smoking.1,2,9,10
Diabetes is another significant modifiable risk factor, increasing PAD risk by 2.5 times.2 Diabetes is also associated with increases in functional limitation from claudication, risk for acute coronary syndrome, and progression to amputation.1
Hypertension nearly doubles the risk for PAD, and poor control further increases this risk.2,9,10
Chronic kidney disease (CKD). Patients with CKD have a progressively higher prevalence of PAD with worsening renal function.1 There is also an association between CKD and increased morbidity, revascularization failure, and increased mortality.1
Two additional risk factors that are less well understood are dyslipidemia and chronic inflammation. There is conflicting data regarding the role of individual components of cholesterol and their effect on PAD, although lipoprotein (a) has been shown to be an independent risk factor for both the development and progression of PAD.12 Similarly, chronic inflammation has been shown to play a role in the initiation and progression of the disease, although the role of inflammatory markers in evaluation and treatment is unclear and assessment for these purposes is not currently recommended.12,13
Continue to: Diagnosis...
Diagnosis
Clinical presentation
Lower extremity pain is the hallmark symptom of PAD, but presentation varies. The classic presentation is claudication, pain within a defined muscle group that occurs with exertion and is relieved by rest. Claudication is most common in the calf but also occurs in the buttock/thigh and the foot.
However, most patients with PAD present with pain that does not fit the definition of claudication. Patients with comorbidities, physical inactivity, and neuropathy are more likely to present with atypical pain.14 These patients may demonstrate critical or acute limb ischemia, characterized by pain at rest and most often localized to the forefoot and toes. Patients with critical limb ischemia may also present with nonhealing wounds/ulcers or gangrene.15
Physical exam findings can support the diagnosis of PAD, but none are reliable enough to rule the diagnosis in or out. Findings suggestive of PAD include cool skin, presence of a bruit (iliac, femoral, or popliteal), and palpable pulse abnormality. Multiple abnormal physical exam findings increase the likelihood of PAD, while the absence of a bruit or palpable pulse abnormality makes PAD less likely.16 In patients with PAD, an associated wound/ulcer is most often distal in the foot and usually appears dry.17
The differential diagnosis for intermittent leg pain is broad and includes neurologic, musculoskeletal, and venous etiologies. Table 118 lists some common alternate diagnoses for patients presenting with leg pain or claudication.
Continue to: Diagnostic testing...
Diagnostic testing
An ankle-brachial index (ABI) test should be performed in patients with history or physical exam findings suggestive of PAD. A resting ABI is performed with the patient in the supine position, with measurement of systolic blood pressure in both arms and ankles using a Doppler ultrasound device. Table 213 outlines ABI scoring and interpretation.
An ABI > 1.4 is an invalid measurement, indicating that the arteries are too calcified to be compressed. These highly elevated ABI measurements are common in patients with diabetes and/or advanced CKD. In these patients, a toe-brachial index (TBI) test should be performed, because the digital arteries are almost always compressible.13
Patients with symptomatic PAD who are under consideration for revascularization may benefit from radiologic imaging of the lower extremities with duplex ultrasound, computed tomography angiography, or magnetic resonance angiography to determine the anatomic location and severity of stenosis.13
Management of PAD
Lifestyle interventions
For patients with PAD, lifestyle modifications are an essential—but challenging—component of disease management.
Continue to: Smoking cessation...
Smoking cessation. As with other atherosclerotic diseases, PAD progression is strongly correlated with smoking. A trial involving 204 active smokers with PAD showed that 5-year mortality and amputation rates dropped by more than half in those who quit smoking within a year, with numbers needed to treat (NNT) of 6 for mortality and 5 for amputation.19 Because of this dramatic effect, American College of Cardiology/American Heart Association (ACC/AHA) guidelines encourage providers to address smoking at every visit and use cessation programs and medication to increase quit rates.13
Exercise may be the most important intervention for PAD. A 2017 Cochrane review found that supervised, structured exercise programs increase pain-free and maximal walking distances by at least 20% and also improve physical and mental quality of life.20 In a trial involving 111 patients with aortoiliac PAD, supervised exercise plus medical care led to greater functional improvement than either revascularization plus medical care or medical care alone.21 In a 2018 Cochrane review, neither revascularization or revascularization added to supervised exercise were better than supervised exercise alone.22 ACC/AHA guidelines recommend supervised exercise programs for claudication prior to considering revascularization.13TABLE 313 outlines the components of a structured exercise program.
Unfortunately, the benefit of these programs has been difficult to reproduce without supervision. Another 2018 Cochrane review demonstrated significant improvement with supervised exercise and no clear improvement in patients given home exercise or advice to walk.23 A recent study examined the effect of having patients use a wearable fitness tracker for home exercise and demonstrated no benefit over usual care.24
Diet. There is some evidence that dietary interventions can prevent and possibly improve PAD. A large randomized controlled trial showed that a Mediterranean diet lowered rates of PAD over 1 year compared to a low-fat diet, with an NNT of 336 if supplemented with extra-virgin olive oil and 448 if supplemented with nuts.25 A small trial of 25 patients who consumed non-soy legumes daily for 8 weeks showed average ABI improvement of 6%, although there was no control group.26
Medical therapy to address peripheral and cardiovascular events
Standard medical therapy for coronary artery disease (CAD) is recommended for patients with PAD to reduce cardiovascular and limb events. For example, treatment of hypertension reduces cardiovascular and cerebrovascular events, and studies verify that lowering blood pressure does not worsen claudication or limb perfusion.
13TABLE 413,27-30 outlines the options for medical therapy.
Continue to: Statins...
Statins reduce cardiovascular events in PAD patients. A large study demonstrated that 40 mg of simvastatin has an NNT of 21 to prevent a coronary or cerebrovascular event in PAD, similar to the NNT of 23 seen in treatment of CAD.27 Statins also reduce adverse limb outcomes. A registry of atherosclerosis patients showed that statins have an NNT of 56 to prevent amputation in PAD and an NNT of 28 to prevent worsening claudication, critical limb ischemia, revascularization, or amputation.28
Antiplatelet therapy with low-dose aspirin or clopidogrel is recommended for symptomatic patients and for asymptomatic patients with an ABI ≤ 0.9.13 A Cochrane review demonstrated significantly reduced mortality with nonaspirin antiplatelet agents vs aspirin (NNT = 94) without increase in major bleeding.29 Only British guidelines specifically recommend clopidogrel over aspirin.31
Dual antiplatelet therapy has not shown consistent benefits over aspirin alone. ACC/AHA guidelines state that dual antiplatelet therapy is not well established for PAD but may be reasonable after revascularization.13
Voraxapar is a novel antiplatelet agent that targets the thrombin-binding receptor on platelets. However, trials show no significant coronary benefit, and slight reductions in acute limb ischemia are offset by increases in major bleeding.13
For patients receiving medical therapy, ongoing evaluation and treatment should be based on claudication symptoms and clinical assessment.
Medical therapy for claudication
Several medications have been proposed for symptomatic treatment of intermittent claudication. Cilostazol is a phosphodiesterase inhibitor with the best risk-benefit ratio. A Cochrane review showed improvements in maximal and pain-free walking distances compared to placebo and improvements in quality of life with cilostazol 100 mg taken twice daily.32 Adverse effects included headache, dizziness, palpitations, and diarrhea.29
Continue to: Pentoxifylline...
Pentoxifylline is another phosphodiesterase inhibitor with less evidence of improvement, higher adverse effect rates, and more frequent dosing. It is not recommended for treatment of intermittent claudication.13,33
Supplements. Padma 28, a Tibetan herbal formulation, appears to improve maximal walking distance with adverse effect rates similar to placebo.34 Other supplements, including vitamin E, ginkgo biloba, and omega-3 fatty acids, have no evidence of benefit.35-37
When revascularizationis needed
Patients who develop limb ischemia or lifestyle-limiting claudication despite conservative therapy are candidates for revascularization. Endovascular techniques include angioplasty, stenting, atherectomy, and precise medication delivery. Surgical approaches mainly consist of thrombectomy and bypass grafting. For intermittent claudication despite conservative care, ACC/AHA guidelines state endovascular procedures are appropriate for aortoiliac disease and reasonable for femoropopliteal disease, but unproven for infrapopliteal disease.13
Acute limb ischemia is an emergency requiring immediate intervention. Two trials revealed identical overall and amputation-free survival rates for percutaneous thrombolysis and surgical thrombectomy.38,39 ACC/AHA guidelines recommend anticoagulation with heparin followed by the revascularization technique that will most rapidly restore arterial flow.13
For chronic limb ischemia, a large trial showed angioplasty had lower initial morbidity, length of hospitalization, and cost than surgical repair. However, surgical mortality was lower after 2 years.40 ACC/AHA guidelines recommend either surgery or endovascular procedures and propose initial endovascular treatment followed by surgery if needed.13 After revascularization, the patient should be followed periodically with a clinical evaluation and ABI measurement with further consideration for routine duplex ultrasound surveillance.13
Outcomes
Patients with PAD have variable outcomes. About 70% to 80% of patients with this diagnosis will have a stable disease process with no worsening of symptoms, 10% to 20% will experience worsening symptoms over time, 5% to 10% will require revascularization within 5 years of diagnosis, and 1% to 5% will progress to critical limb ischemia, which has a 5-year amputation rate of 1% to 4%.2 Patients who require amputation have poor outcomes: Within 2 years, 30% are dead and 15% have had further amputations.18
In addition to the morbidity and mortality from its own progression, PAD is an important predictor of CAD and is associated with a significant elevation in morbidity and mortality from CAD. One small but well-designed prospective cohort study found that patients with PAD had a more than 6-fold increased risk of death from CAD than did patients without PAD.41
Acknowledgement
The authors thank Francesca Cimino, MD, FAAFP, for her help in reviewing this manuscript.
CORRESPONDENCE
Dustin K. Smith, DO, 2080 Child Street, Jacksonville, FL 32214; [email protected]
1. Eraso LH, Fukaya E, Mohler ER 3rd, et al. Peripheral arterial disease, prevalence and cumulative risk factor profile analysis. Eur J Prev Cardiol. 2014;21:704-711.
2. Pasternak RC, Criqui MH, Benjamin EJ, et al; American Heart Association. Atherosclerotic Vascular Disease Conference: Writing Group I: epidemiology. Circulation. 2004;109:2605-2612.
3. Hirsch AT, Criqui MH, Treat-Jacobson D, et al. Peripheral arterial disease detection, awareness, and treatment in primary care. JAMA. 2001;286:1317-1324.
4. Olin JW, Sealove BA. Peripheral artery disease: current insight into the disease and its diagnosis and management. Mayo Clin Proc. 2010;85:678-692.
5. Andras A, Ferkert B. Screening for peripheral arterial disease. Cochrane Database Syst Rev. 2014;(4):CD010835.
6. Guirguis-Blake JM, Evans CV, Redmond N, et al. Screening for peripheral artery disease using ankle-brachial index: updated evidence report and systematic review for the US Preventive Services Task Force. JAMA. 2018;320:184-196.
7. US Preventive Services Task Force. Screening for peripheral artery disease and cardiovascular disease risk assessment with ankle-brachial index: US Preventive Services Task Force recommendation statement. JAMA. 2018;230:177-183.
8. American Heart Association Writing Group 2. Atherosclerotic Peripheral Vascular Disease Symposium II: screening for atherosclerotic vascular diseases: should nationwide programs be instituted? Circulation. 2008;118:2830-2836.
9. Berger JS, Hochman J, Lobach I, et al. Modifiable risk factor burden and the prevalence of peripheral artery disease in different vascular territories. J Vasc Surg. 2013;58:673-681.
10. Joosten MM, Pai JK, Bertoia ML, et al. Associations between conventional cardiovascular risk factors and risk of peripheral artery disease in men. JAMA. 2012;308:1660-1667.
11. Carmelli D, Fabsitz RR, Swan GE, et al. Contribution of genetic and environmental influences to ankle-brachial blood pressure index in the NHLBI Twin Study. National Heart, Lung, and Blood Institute. Am J Epidemiol. 2000;151:452-458.
12. Aboyans V, Criqui MH, Denenberg JO, et al. Risk factors for progression of peripheral arterial disease in large and small vessels. Circulation. 2006;113:2623-2629.
13. Gerald-Herman MD, Gornik HL, Barrett C, et al. 2016 AHA/ACC guideline on the management of patients with lower extremity peripheral artery disease: a report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines. Circulation. 2017;135:e726-e779.
14. McDermott MM, Greenland P, Liu K, et al. Leg symptoms in peripheral arterial disease: associated clinical characteristics and functional impairment. JAMA. 2001;286:1599-1606.
15. Cranley JJ. Ischemic rest pain. Arch Surg. 1969;98:187-188.
16. Khan NA, Rahim SA, Anand SS, et al. Does the clinical examination predict lower extremity peripheral arterial disease? JAMA. 2006;295:536-546.
17. Wennberg PW. Approach to the patient with peripheral arterial disease. Circulation. 2013;128:2241-2250.
18. Norgren L, Hiatt WR, Dormandy JA, et al. Inter-society consensus for the management of peripheral arterial disease (TASC II). Eur J Vas Endovasc Surg. 2007;33:S1-S75.
19. Armstrong EJ, Wu J, Singh GD, et al. Smoking cessation is associated with decreased mortality and improved amputation-free survival among patients with symptomatic peripheral artery disease. J Vasc Surg. 2014;60:1565-1571.
20. Lane R, Harwood A, Watson L, et al. Exercise for intermittent claudication. Cochrane Database Syst Rev. 2017;(12):CD000990.
21. Murphy TP, Cutlip DE, Regensteiner JG, et al; CLEVER Study Investigators. Supervised exercise versus primary stenting for claudication resulting from aortoiliac peripheral artery disease: six-month outcomes from the claudication: exercise versus endoluminal revascularization (CLEVER) study. Circulation. 2012;125:130-139.
22. Fakhry F, Fokkenrood HJP, Pronk S, et al. Endovascular revascularization versus conservative management for intermittent claudication. Cochrane Database Syst Rev. 2018;(3):CD010512.
23. Hageman D, Fokkenrood HJ, Gommans LN, et al. Supervised exercise therapy versus home-based exercise therapy versus walking advice for intermittent claudication. Cochrane Database Syst Rev. 2018;(4):CD005263.
24. McDermott MM, Spring B, Berger JS, et al. Effect of a home-based exercise intervention of wearable technology and telephone coaching on walking performance in peripheral artery disease: the HONOR randomized clinical trial. JAMA. 2018;319:1665-1676.
25. Ruiz-Canela M, Estruch R, Corella D, et al. Association of Mediterranean diet with peripheral artery disease: the PREDIMED randomized trial. JAMA. 2014;311:415-417.
26. Zahradka P, Wright B, Weighell W, et al. Daily non-soy legume consumption reverses vascular impairment due to peripheral artery disease. Atherosclerosis. 2013;230:310-314.
27. Heart Protection Study Collaborative Group. Randomized trial of the effects of cholesterol-lowering with simvastatin on peripheral vascular and other major vascular outcomes in 20536 people with peripheral arterial disease and other high-risk conditions. J Vasc Surg. 2007;45:645-655.
28. Kumbhani DJ, Steg G, Cannon CP, et al. Statin therapy and long-term adverse limb outcomes in patients with peripheral artery disease: insights from the REACH registry. Eur Heart J. 2014;35:2864-2872.
29. Wong PF, Chong LY, Mikhailidis DP, et al. Antiplatelet agents for intermittent claudication. Cochrane Database Syst Rev. 2011;(11):CD001272.
30. Critical Leg Ischaemia Prevention Study (CLIPS) Group, Catalano M, Born G, Peto R. Prevention of serious vascular events by aspirin amongst patients with peripheral arterial disease: randomized, double-blind trial. J Intern Med. 2007;261:276-284.
31. Morley RL, Sharma A, Horsch AD, et al. Peripheral artery disease. BMJ. 2018;360:j5842.
32. Bedenis R, Stewart M, Cleanthis M, et al. Cilostazol for intermittent claudication. Cochrane Database Syst Rev. 2014;(10):CD003748.
33. Salhiyyah K, Forster R, Senanayake E, et al. Pentoxifylline for intermittent claudication. Cochrane Database Syst Rev. 2015;(9):CD005262.
34. Stewart M, Morling JR, Maxwell H. Padma 28 for intermittent claudication. Cochrane Database Syst Rev. 2016;(3):CD007371.
35. Kleijnen J, Mackerras D. Vitamin E for intermittent claudication. Cochrane Database Syst Rev. 1998;(1):CD000987.
36. Nicolai SPA, Kruidenior LM, Bendermacher BLW, et al. Ginkgo biloba for intermittent claudication. Cochrane Database Syst Rev. 2013;(6):CD006888.
37. Campbell A, Price J, Hiatt WR. Omega-3 fatty acids for intermittent claudication. Cochrane Database Syst Rev. 2013;(7):CD003833.
38. American Surgical Association, New York Surgical Society, Philadelphia Academy of Surgery, Southern Surgical Association (US), Central Surgical Association. Results of a prospective randomized trial evaluating surgery versus thrombolysis for ischemia of the lower extremity: the STILE trial. Ann Surg. 1994;220:251-268.
39. Ouriel K, Veith FJ, Sasahara AA.
40. Bradbury AW, Ruckley CV, Fowkes FGR, et al. Bypass versus angioplasty in severe ischaemia of the leg (BASIL): multicentre, randomised, controlled trial. Lancet. 2005;366:1925-1934.
41. Criqui MH, Langer RD, Fronek A, et al. Mortality over a period of 10 years in patients with peripheral arterial disease. N Engl J Med. 1992;326:381-386.
1. Eraso LH, Fukaya E, Mohler ER 3rd, et al. Peripheral arterial disease, prevalence and cumulative risk factor profile analysis. Eur J Prev Cardiol. 2014;21:704-711.
2. Pasternak RC, Criqui MH, Benjamin EJ, et al; American Heart Association. Atherosclerotic Vascular Disease Conference: Writing Group I: epidemiology. Circulation. 2004;109:2605-2612.
3. Hirsch AT, Criqui MH, Treat-Jacobson D, et al. Peripheral arterial disease detection, awareness, and treatment in primary care. JAMA. 2001;286:1317-1324.
4. Olin JW, Sealove BA. Peripheral artery disease: current insight into the disease and its diagnosis and management. Mayo Clin Proc. 2010;85:678-692.
5. Andras A, Ferkert B. Screening for peripheral arterial disease. Cochrane Database Syst Rev. 2014;(4):CD010835.
6. Guirguis-Blake JM, Evans CV, Redmond N, et al. Screening for peripheral artery disease using ankle-brachial index: updated evidence report and systematic review for the US Preventive Services Task Force. JAMA. 2018;320:184-196.
7. US Preventive Services Task Force. Screening for peripheral artery disease and cardiovascular disease risk assessment with ankle-brachial index: US Preventive Services Task Force recommendation statement. JAMA. 2018;230:177-183.
8. American Heart Association Writing Group 2. Atherosclerotic Peripheral Vascular Disease Symposium II: screening for atherosclerotic vascular diseases: should nationwide programs be instituted? Circulation. 2008;118:2830-2836.
9. Berger JS, Hochman J, Lobach I, et al. Modifiable risk factor burden and the prevalence of peripheral artery disease in different vascular territories. J Vasc Surg. 2013;58:673-681.
10. Joosten MM, Pai JK, Bertoia ML, et al. Associations between conventional cardiovascular risk factors and risk of peripheral artery disease in men. JAMA. 2012;308:1660-1667.
11. Carmelli D, Fabsitz RR, Swan GE, et al. Contribution of genetic and environmental influences to ankle-brachial blood pressure index in the NHLBI Twin Study. National Heart, Lung, and Blood Institute. Am J Epidemiol. 2000;151:452-458.
12. Aboyans V, Criqui MH, Denenberg JO, et al. Risk factors for progression of peripheral arterial disease in large and small vessels. Circulation. 2006;113:2623-2629.
13. Gerald-Herman MD, Gornik HL, Barrett C, et al. 2016 AHA/ACC guideline on the management of patients with lower extremity peripheral artery disease: a report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines. Circulation. 2017;135:e726-e779.
14. McDermott MM, Greenland P, Liu K, et al. Leg symptoms in peripheral arterial disease: associated clinical characteristics and functional impairment. JAMA. 2001;286:1599-1606.
15. Cranley JJ. Ischemic rest pain. Arch Surg. 1969;98:187-188.
16. Khan NA, Rahim SA, Anand SS, et al. Does the clinical examination predict lower extremity peripheral arterial disease? JAMA. 2006;295:536-546.
17. Wennberg PW. Approach to the patient with peripheral arterial disease. Circulation. 2013;128:2241-2250.
18. Norgren L, Hiatt WR, Dormandy JA, et al. Inter-society consensus for the management of peripheral arterial disease (TASC II). Eur J Vas Endovasc Surg. 2007;33:S1-S75.
19. Armstrong EJ, Wu J, Singh GD, et al. Smoking cessation is associated with decreased mortality and improved amputation-free survival among patients with symptomatic peripheral artery disease. J Vasc Surg. 2014;60:1565-1571.
20. Lane R, Harwood A, Watson L, et al. Exercise for intermittent claudication. Cochrane Database Syst Rev. 2017;(12):CD000990.
21. Murphy TP, Cutlip DE, Regensteiner JG, et al; CLEVER Study Investigators. Supervised exercise versus primary stenting for claudication resulting from aortoiliac peripheral artery disease: six-month outcomes from the claudication: exercise versus endoluminal revascularization (CLEVER) study. Circulation. 2012;125:130-139.
22. Fakhry F, Fokkenrood HJP, Pronk S, et al. Endovascular revascularization versus conservative management for intermittent claudication. Cochrane Database Syst Rev. 2018;(3):CD010512.
23. Hageman D, Fokkenrood HJ, Gommans LN, et al. Supervised exercise therapy versus home-based exercise therapy versus walking advice for intermittent claudication. Cochrane Database Syst Rev. 2018;(4):CD005263.
24. McDermott MM, Spring B, Berger JS, et al. Effect of a home-based exercise intervention of wearable technology and telephone coaching on walking performance in peripheral artery disease: the HONOR randomized clinical trial. JAMA. 2018;319:1665-1676.
25. Ruiz-Canela M, Estruch R, Corella D, et al. Association of Mediterranean diet with peripheral artery disease: the PREDIMED randomized trial. JAMA. 2014;311:415-417.
26. Zahradka P, Wright B, Weighell W, et al. Daily non-soy legume consumption reverses vascular impairment due to peripheral artery disease. Atherosclerosis. 2013;230:310-314.
27. Heart Protection Study Collaborative Group. Randomized trial of the effects of cholesterol-lowering with simvastatin on peripheral vascular and other major vascular outcomes in 20536 people with peripheral arterial disease and other high-risk conditions. J Vasc Surg. 2007;45:645-655.
28. Kumbhani DJ, Steg G, Cannon CP, et al. Statin therapy and long-term adverse limb outcomes in patients with peripheral artery disease: insights from the REACH registry. Eur Heart J. 2014;35:2864-2872.
29. Wong PF, Chong LY, Mikhailidis DP, et al. Antiplatelet agents for intermittent claudication. Cochrane Database Syst Rev. 2011;(11):CD001272.
30. Critical Leg Ischaemia Prevention Study (CLIPS) Group, Catalano M, Born G, Peto R. Prevention of serious vascular events by aspirin amongst patients with peripheral arterial disease: randomized, double-blind trial. J Intern Med. 2007;261:276-284.
31. Morley RL, Sharma A, Horsch AD, et al. Peripheral artery disease. BMJ. 2018;360:j5842.
32. Bedenis R, Stewart M, Cleanthis M, et al. Cilostazol for intermittent claudication. Cochrane Database Syst Rev. 2014;(10):CD003748.
33. Salhiyyah K, Forster R, Senanayake E, et al. Pentoxifylline for intermittent claudication. Cochrane Database Syst Rev. 2015;(9):CD005262.
34. Stewart M, Morling JR, Maxwell H. Padma 28 for intermittent claudication. Cochrane Database Syst Rev. 2016;(3):CD007371.
35. Kleijnen J, Mackerras D. Vitamin E for intermittent claudication. Cochrane Database Syst Rev. 1998;(1):CD000987.
36. Nicolai SPA, Kruidenior LM, Bendermacher BLW, et al. Ginkgo biloba for intermittent claudication. Cochrane Database Syst Rev. 2013;(6):CD006888.
37. Campbell A, Price J, Hiatt WR. Omega-3 fatty acids for intermittent claudication. Cochrane Database Syst Rev. 2013;(7):CD003833.
38. American Surgical Association, New York Surgical Society, Philadelphia Academy of Surgery, Southern Surgical Association (US), Central Surgical Association. Results of a prospective randomized trial evaluating surgery versus thrombolysis for ischemia of the lower extremity: the STILE trial. Ann Surg. 1994;220:251-268.
39. Ouriel K, Veith FJ, Sasahara AA.
40. Bradbury AW, Ruckley CV, Fowkes FGR, et al. Bypass versus angioplasty in severe ischaemia of the leg (BASIL): multicentre, randomised, controlled trial. Lancet. 2005;366:1925-1934.
41. Criqui MH, Langer RD, Fronek A, et al. Mortality over a period of 10 years in patients with peripheral arterial disease. N Engl J Med. 1992;326:381-386.
PRACTICE RECOMMENDATIONS
❯ Use the ankle-brachial index for diagnosis in patients with history/physical exam findings suggestive of peripheral arterial disease (PAD). A
❯ Strongly encourage smoking cessation in patients with PAD as doing so reduces 5-year mortality and amputation rates. B
❯ Use structured exercise programs for patients with intermittent claudication prior to consideration of revascularization; doing so offers similar benefit and lower risks. A
❯ Recommend revascularization for patients who have limb ischemia or lifestyle-limiting claudication despite medical and exercise therapy. B
Strength of recommendation (SOR)
A Good-quality patient-oriented evidence
B Inconsistent or limited-quality patient-oriented evidence
C Consensus, usual practice, opinion, disease-oriented evidence, case series
Consider this Rx for patients with high triglycerides?
ILLUSTRATIVE CASE
A 63-year-old man with a medical history significant for myocardial infarction (MI) 5 years ago presents to you for an annual exam. His medications include a daily aspirin, angiotensin-converting enzyme inhibitor, beta-blocker, and a high-intensity statin for coronary artery disease (CAD). On his fasting lipid panel, his low-density lipoprotein (LDL) level is 70 mg/dL, but his triglycerides remain elevated at 200 mg/dL despite dietary changes.
In addition to lifestyle modifications, what can be done to reduce his risk of another MI?
Patients with known cardiovascular disease (CVD) or multiple risk factors for CVD are at high risk of cardiovascular events, even when taking primary or secondary preventive medications such as statins.2,3 In these patients, elevated triglycerides are an independent risk factor for increased rates of cardiovascular events.4,5
The 2018 American College of Cardiology/American Heart Association (ACC/AHA) guidelines for the treatment of blood cholesterol recommend statin therapy for moderate (175-499 mg/dL) to severe (≥ 500 mg/dL) hypertriglyceridemia in appropriate patients with atherosclerotic CVD risk ≥ 7.5%, after appropriately addressing secondary causes of hypertriglycidemia.6
Previous studies have shown no benefit from combination therapy with triglyceride-lowering medications (eg, extended-release niacin and fibrates) and statins, compared with statin monotherapy.7 A recent meta-analysis concluded that omega-3 fatty acid supplements offer no reduction in cardiovascular morbidity or mortality, whether taken with or without statins.8
Interestingly, the randomized controlled Japan EPA Lipid Intervention Study (JELIS) demonstrated fewer major coronary events in patients with elevated cholesterol, with or without CAD, who took eicosapentaenoic acid (EPA)—a subtype of omega-3 fatty acids—plus a statin, compared with statin monotherapy.9
The REDUCE-IT trial evaluated icosapent ethyl, a highly purified EPA that has been shown to reduce triglycerides and, at the time this study was conducted, was approved for use solely for the reduction of triglyceride levels in adults with severe hypertriglyceridemia.10,11
Continue to: Study Summary
STUDY SUMMARY
Patients with known CVD had fewercardiovascular events on icosapent ethyl
The multicenter, randomized controlled REDUCE-IT trial evaluated the effectiveness of icosapent ethyl, 2 g orally twice daily, on cardiovascular outcomes.1 A total of 8179 patients, ≥ 45 years of age with hypertriglyceridemia and known CVD or ≥ 50 years with diabetes and at least 1 additional risk factor and no known CVD, were enrolled at 473 participating sites in 11 countries, including the United States.
Patients had a triglyceride level of 150 to 499 mg/dL and an LDL cholesterol level of 41 to 100 mg/dL, and were taking a stable dose of a statin for at least 4 weeks. The enrollment protocol was amended to increase the lower limit of triglycerides from 150 to 200 mg/dL about one-third of the way through the study. Among the study population, 70.7% of patients were enrolled for secondary prevention (ie, had established CVD) and 29.3% of patients were enrolled for primary prevention (ie, had diabetes and at least 1 additional risk factor but no known CVD). Exclusion criteria included severe heart failure, active severe liver disease, glycated hemoglobin > 10%, a planned surgical cardiac intervention, history of pancreatitis, or allergies to fish or shellfish products.
Outcomes. The primary end point was a composite outcome of cardiovascular death, nonfatal MI, nonfatal stroke, coronary revascularization, or unstable angina.
Results. The median duration of follow-up was 4.9 years. From baseline to 1 year, the median change in triglycerides was an 18% reduction in the icosapent ethyl group but a 2% increase in the placebo group. Fewer patients in the icosapent ethyl group than the placebo group had a composite outcome event (17% vs 22%, respectively; hazard ratio [HR] = 0.75; 95% confidence interval [CI], 0.68-0.83; number needed to treat [NNT] to avoid 1 primary end point event = 21). Patients with known CVD had fewer composite outcome events in the icosapent ethyl group than the placebo group (19% vs 26%; HR = 0.73; 95% CI, 0.65-0.81; NNT = 14) but not in the primary prevention group vs the placebo group (12% vs 14%; HR = 0.88; 95% CI, 0.70-1.1).
In the entire population, all individual outcomes in the composite were significantly fewer in the icosapent ethyl group (cardiovascular death: HR = 0.8; 95% CI, 0.66-0.98; fatal or nonfatal MI: HR = 0.69; 95% CI, 0.58-0.81; revascularization: HR = 0.65; 95% CI, 0.55-0.78; unstable angina: HR = 0.68; 95% CI, 0.53-0.87; and fatal or nonfatal stroke: HR = 0.72; 95% CI, 0.55-0.93). All-cause mortality did not differ between groups (HR = 0.87; 95% CI, 0.74-1.02).
No significant differences in adverse events leading to discontinuation of the drug were reported between groups. Atrial fibrillation occurred more frequently in the icosapent ethyl group (5.3% vs 3.9%), but anemia (4.7% vs 5.8%) and gastrointestinal adverse events (33% vs 35%) were less common.
Continue to: What's New
WHAT’S NEW
First RCT to demonstrate valueof pairing icosapent ethyl with a statin
Many prior studies on use of omega-3 fatty acid supplements to treat hypertriglyceridemia did not show any benefit, possibly due to a low dose or low ratio of EPA in the study drug.8 One trial (JELIS) with favorable results was an open-label study, limited to patients in Japan. The REDUCE-IT study was the first randomized, placebo-controlled trial to show that icosapent ethyl treatment for hypertriglyceridemia in patients with known CVD who are taking a statin results in fewer cardiovascular events than statin use alone.
Also worth noting: Since publication of the REDUCE-IT study, the FDA has approved an expanded indication for icosapent ethyl for reduction of risk of cardiovascular events in statin-treated patients with hypertriglyceridemia and established CVD or diabetes and ≥ 2 additional cardiovascular risk factors.11
CAVEATS
Drug’s benefit was not linkedto triglyceride level reductions
The cardiovascular benefits of icosapent ethyl were obtained irrespective of triglyceride levels achieved. This raises the question of other potential mechanisms of action of icosapent ethyl in achieving cardiovascular benefit. However, this should not preclude the use of icosapent ethyl for secondary prevention in appropriate patients.
CHALLENGES TO IMPLEMENTATION
Medication is pricey
Icosapent ethyl is an expensive medication, currently priced at an estimated $351/month using a nationally available discount pharmacy plan, although additional manufacturer’s discounts may apply.12,13 The cost of the medication could be a consideration for widespread implementation of this recommendation.
ACKNOWLEDGEMENT
The PURLs Surveillance System was supported in part by Grant Number UL1RR024999 from the National Center For Research Resources, a Clinical Translational Science Award to the University of Chicago. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Center For Research Resources or the National Institutes of Health.
Copyright © 2020. The Family Physicians Inquiries Network. All rights reserved.
1. Bhatt DL, Steg PG, Miller M, et al; REDUCE-IT Investigators. Cardiovascular risk reduction with icosapent ethyl for hypertriglyceridemia. N Engl J Med. 2019;380:11-22.
2. Bhatt DL, Eagle KA, Ohman EM, et al; REACH Registry Investigators. Comparative determinants of 4-year cardiovascular event rates in stable outpatients at risk of or with atherothrombosis. JAMA. 2010;304:1350-1357.
3. Cannon CP, Braunwald E, McCabe CH, et al; Pravastatin or Atorvastatin Evaluation and Infection Therapy–Thrombolysis in Myocardial Infarction 22 Investigators. Intensive versus moderate lipid lowering with statins after acute coronary syndromes [published correction appears in N Engl J Med. 2006;354:778]. N Engl J Med. 2004;350:1495-1504.
4. Klempfner R, Erez A, Sagit BZ, et al. Elevated triglyceride level is independently associated with increased all-cause mortality in patients with established coronary heart disease: twenty-two-year follow-up of the Bezafibrate Infarction Prevention Study and Registry [published correction appears in Circ Cardiovasc Qual Outcomes. 2016;9:613]. Circ Cardiovasc Qual Outcomes. 2016;9:100-108.
5. Nichols GA, Philip S, Reynolds K, Granowitz CB, Fazio S. Increased cardiovascular risk in hypertriglyceridemic patients with statin-controlled LDL cholesterol. J Clin Endocrinol Metab. 2018;103:3019-3027.
6. Grundy SM, Stone NJ, Bailey AL, et al. 2018 AHA/ACC/AACVPR/AAPA/ABC/ACPM/ADA/AGS/APhA/ASPC/NLA/PCNA guideline on the management of blood cholesterol: a report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines [published correction appears in J Am Coll Cardiol. 2019;73:3237-3241]. J Am Coll Cardiol. 2019;73:e285-e350.
7. Ganda OP, Bhatt DL, Mason RP, Miller M, Boden WE. Unmet need for adjunctive dyslipidemia therapy in hypertriglyceridemia management. J Am Coll Cardiol. 2018;72:330-343.
8. Aung T, Halsey J, Kromhout D, et al; Omega-3 Treatment Trialists’ Collaboration. Associations of omega-3 fatty acid supplement use with cardiovascular disease risks: meta-analysis of 10 trials involving 77 917 individuals. JAMA Cardiol. 2018;3:225-234.
9. Yokoyama M, Origasa H, Matsuzaki M, et al; Japan EPA lipid intervention study (JELIS) Investigators. Effects of eicosapentaenoic acid on major coronary events in hypercholesterolaemic patients (JELIS): a randomised open-label, blinded endpoint analysis [published correction appears in Lancet. 2007;370:220]. Lancet. 2007;369:1090-1098.
10. Ballantyne CM, Bays HE, Kastelein JJ, et al. Efficacy and safety of eicosapentaenoic acid ethyl ester (AMR101) therapy in statin-treated patients with persistent high triglycerides (from the ANCHOR study). Am J Cardiol. 2012;110:984-992.
11. FDA approves use of drug to reduce risk of cardiovascular events in certain adult patient groups [news release]. Silver Spring, MD: US Food and Drug Administration; December 13, 2019. www.fda.gov/news-events/press-announcements/fda-approves-use-drug-reduce-risk-cardiovascular-events-certain-adult-patient-groups. Accessed November 30, 2020.
12. Vascepa. GoodRx. www.goodrx.com/vascepa. Accessed November 30, 2020.
13. The VASCEPA Savings Program. www.vascepa.com/getting-started/savings-card/. Accessed November 30, 2020.
ILLUSTRATIVE CASE
A 63-year-old man with a medical history significant for myocardial infarction (MI) 5 years ago presents to you for an annual exam. His medications include a daily aspirin, angiotensin-converting enzyme inhibitor, beta-blocker, and a high-intensity statin for coronary artery disease (CAD). On his fasting lipid panel, his low-density lipoprotein (LDL) level is 70 mg/dL, but his triglycerides remain elevated at 200 mg/dL despite dietary changes.
In addition to lifestyle modifications, what can be done to reduce his risk of another MI?
Patients with known cardiovascular disease (CVD) or multiple risk factors for CVD are at high risk of cardiovascular events, even when taking primary or secondary preventive medications such as statins.2,3 In these patients, elevated triglycerides are an independent risk factor for increased rates of cardiovascular events.4,5
The 2018 American College of Cardiology/American Heart Association (ACC/AHA) guidelines for the treatment of blood cholesterol recommend statin therapy for moderate (175-499 mg/dL) to severe (≥ 500 mg/dL) hypertriglyceridemia in appropriate patients with atherosclerotic CVD risk ≥ 7.5%, after appropriately addressing secondary causes of hypertriglycidemia.6
Previous studies have shown no benefit from combination therapy with triglyceride-lowering medications (eg, extended-release niacin and fibrates) and statins, compared with statin monotherapy.7 A recent meta-analysis concluded that omega-3 fatty acid supplements offer no reduction in cardiovascular morbidity or mortality, whether taken with or without statins.8
Interestingly, the randomized controlled Japan EPA Lipid Intervention Study (JELIS) demonstrated fewer major coronary events in patients with elevated cholesterol, with or without CAD, who took eicosapentaenoic acid (EPA)—a subtype of omega-3 fatty acids—plus a statin, compared with statin monotherapy.9
The REDUCE-IT trial evaluated icosapent ethyl, a highly purified EPA that has been shown to reduce triglycerides and, at the time this study was conducted, was approved for use solely for the reduction of triglyceride levels in adults with severe hypertriglyceridemia.10,11
Continue to: Study Summary
STUDY SUMMARY
Patients with known CVD had fewercardiovascular events on icosapent ethyl
The multicenter, randomized controlled REDUCE-IT trial evaluated the effectiveness of icosapent ethyl, 2 g orally twice daily, on cardiovascular outcomes.1 A total of 8179 patients, ≥ 45 years of age with hypertriglyceridemia and known CVD or ≥ 50 years with diabetes and at least 1 additional risk factor and no known CVD, were enrolled at 473 participating sites in 11 countries, including the United States.
Patients had a triglyceride level of 150 to 499 mg/dL and an LDL cholesterol level of 41 to 100 mg/dL, and were taking a stable dose of a statin for at least 4 weeks. The enrollment protocol was amended to increase the lower limit of triglycerides from 150 to 200 mg/dL about one-third of the way through the study. Among the study population, 70.7% of patients were enrolled for secondary prevention (ie, had established CVD) and 29.3% of patients were enrolled for primary prevention (ie, had diabetes and at least 1 additional risk factor but no known CVD). Exclusion criteria included severe heart failure, active severe liver disease, glycated hemoglobin > 10%, a planned surgical cardiac intervention, history of pancreatitis, or allergies to fish or shellfish products.
Outcomes. The primary end point was a composite outcome of cardiovascular death, nonfatal MI, nonfatal stroke, coronary revascularization, or unstable angina.
Results. The median duration of follow-up was 4.9 years. From baseline to 1 year, the median change in triglycerides was an 18% reduction in the icosapent ethyl group but a 2% increase in the placebo group. Fewer patients in the icosapent ethyl group than the placebo group had a composite outcome event (17% vs 22%, respectively; hazard ratio [HR] = 0.75; 95% confidence interval [CI], 0.68-0.83; number needed to treat [NNT] to avoid 1 primary end point event = 21). Patients with known CVD had fewer composite outcome events in the icosapent ethyl group than the placebo group (19% vs 26%; HR = 0.73; 95% CI, 0.65-0.81; NNT = 14) but not in the primary prevention group vs the placebo group (12% vs 14%; HR = 0.88; 95% CI, 0.70-1.1).
In the entire population, all individual outcomes in the composite were significantly fewer in the icosapent ethyl group (cardiovascular death: HR = 0.8; 95% CI, 0.66-0.98; fatal or nonfatal MI: HR = 0.69; 95% CI, 0.58-0.81; revascularization: HR = 0.65; 95% CI, 0.55-0.78; unstable angina: HR = 0.68; 95% CI, 0.53-0.87; and fatal or nonfatal stroke: HR = 0.72; 95% CI, 0.55-0.93). All-cause mortality did not differ between groups (HR = 0.87; 95% CI, 0.74-1.02).
No significant differences in adverse events leading to discontinuation of the drug were reported between groups. Atrial fibrillation occurred more frequently in the icosapent ethyl group (5.3% vs 3.9%), but anemia (4.7% vs 5.8%) and gastrointestinal adverse events (33% vs 35%) were less common.
Continue to: What's New
WHAT’S NEW
First RCT to demonstrate valueof pairing icosapent ethyl with a statin
Many prior studies on use of omega-3 fatty acid supplements to treat hypertriglyceridemia did not show any benefit, possibly due to a low dose or low ratio of EPA in the study drug.8 One trial (JELIS) with favorable results was an open-label study, limited to patients in Japan. The REDUCE-IT study was the first randomized, placebo-controlled trial to show that icosapent ethyl treatment for hypertriglyceridemia in patients with known CVD who are taking a statin results in fewer cardiovascular events than statin use alone.
Also worth noting: Since publication of the REDUCE-IT study, the FDA has approved an expanded indication for icosapent ethyl for reduction of risk of cardiovascular events in statin-treated patients with hypertriglyceridemia and established CVD or diabetes and ≥ 2 additional cardiovascular risk factors.11
CAVEATS
Drug’s benefit was not linkedto triglyceride level reductions
The cardiovascular benefits of icosapent ethyl were obtained irrespective of triglyceride levels achieved. This raises the question of other potential mechanisms of action of icosapent ethyl in achieving cardiovascular benefit. However, this should not preclude the use of icosapent ethyl for secondary prevention in appropriate patients.
CHALLENGES TO IMPLEMENTATION
Medication is pricey
Icosapent ethyl is an expensive medication, currently priced at an estimated $351/month using a nationally available discount pharmacy plan, although additional manufacturer’s discounts may apply.12,13 The cost of the medication could be a consideration for widespread implementation of this recommendation.
ACKNOWLEDGEMENT
The PURLs Surveillance System was supported in part by Grant Number UL1RR024999 from the National Center For Research Resources, a Clinical Translational Science Award to the University of Chicago. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Center For Research Resources or the National Institutes of Health.
Copyright © 2020. The Family Physicians Inquiries Network. All rights reserved.
ILLUSTRATIVE CASE
A 63-year-old man with a medical history significant for myocardial infarction (MI) 5 years ago presents to you for an annual exam. His medications include a daily aspirin, angiotensin-converting enzyme inhibitor, beta-blocker, and a high-intensity statin for coronary artery disease (CAD). On his fasting lipid panel, his low-density lipoprotein (LDL) level is 70 mg/dL, but his triglycerides remain elevated at 200 mg/dL despite dietary changes.
In addition to lifestyle modifications, what can be done to reduce his risk of another MI?
Patients with known cardiovascular disease (CVD) or multiple risk factors for CVD are at high risk of cardiovascular events, even when taking primary or secondary preventive medications such as statins.2,3 In these patients, elevated triglycerides are an independent risk factor for increased rates of cardiovascular events.4,5
The 2018 American College of Cardiology/American Heart Association (ACC/AHA) guidelines for the treatment of blood cholesterol recommend statin therapy for moderate (175-499 mg/dL) to severe (≥ 500 mg/dL) hypertriglyceridemia in appropriate patients with atherosclerotic CVD risk ≥ 7.5%, after appropriately addressing secondary causes of hypertriglycidemia.6
Previous studies have shown no benefit from combination therapy with triglyceride-lowering medications (eg, extended-release niacin and fibrates) and statins, compared with statin monotherapy.7 A recent meta-analysis concluded that omega-3 fatty acid supplements offer no reduction in cardiovascular morbidity or mortality, whether taken with or without statins.8
Interestingly, the randomized controlled Japan EPA Lipid Intervention Study (JELIS) demonstrated fewer major coronary events in patients with elevated cholesterol, with or without CAD, who took eicosapentaenoic acid (EPA)—a subtype of omega-3 fatty acids—plus a statin, compared with statin monotherapy.9
The REDUCE-IT trial evaluated icosapent ethyl, a highly purified EPA that has been shown to reduce triglycerides and, at the time this study was conducted, was approved for use solely for the reduction of triglyceride levels in adults with severe hypertriglyceridemia.10,11
Continue to: Study Summary
STUDY SUMMARY
Patients with known CVD had fewercardiovascular events on icosapent ethyl
The multicenter, randomized controlled REDUCE-IT trial evaluated the effectiveness of icosapent ethyl, 2 g orally twice daily, on cardiovascular outcomes.1 A total of 8179 patients, ≥ 45 years of age with hypertriglyceridemia and known CVD or ≥ 50 years with diabetes and at least 1 additional risk factor and no known CVD, were enrolled at 473 participating sites in 11 countries, including the United States.
Patients had a triglyceride level of 150 to 499 mg/dL and an LDL cholesterol level of 41 to 100 mg/dL, and were taking a stable dose of a statin for at least 4 weeks. The enrollment protocol was amended to increase the lower limit of triglycerides from 150 to 200 mg/dL about one-third of the way through the study. Among the study population, 70.7% of patients were enrolled for secondary prevention (ie, had established CVD) and 29.3% of patients were enrolled for primary prevention (ie, had diabetes and at least 1 additional risk factor but no known CVD). Exclusion criteria included severe heart failure, active severe liver disease, glycated hemoglobin > 10%, a planned surgical cardiac intervention, history of pancreatitis, or allergies to fish or shellfish products.
Outcomes. The primary end point was a composite outcome of cardiovascular death, nonfatal MI, nonfatal stroke, coronary revascularization, or unstable angina.
Results. The median duration of follow-up was 4.9 years. From baseline to 1 year, the median change in triglycerides was an 18% reduction in the icosapent ethyl group but a 2% increase in the placebo group. Fewer patients in the icosapent ethyl group than the placebo group had a composite outcome event (17% vs 22%, respectively; hazard ratio [HR] = 0.75; 95% confidence interval [CI], 0.68-0.83; number needed to treat [NNT] to avoid 1 primary end point event = 21). Patients with known CVD had fewer composite outcome events in the icosapent ethyl group than the placebo group (19% vs 26%; HR = 0.73; 95% CI, 0.65-0.81; NNT = 14) but not in the primary prevention group vs the placebo group (12% vs 14%; HR = 0.88; 95% CI, 0.70-1.1).
In the entire population, all individual outcomes in the composite were significantly fewer in the icosapent ethyl group (cardiovascular death: HR = 0.8; 95% CI, 0.66-0.98; fatal or nonfatal MI: HR = 0.69; 95% CI, 0.58-0.81; revascularization: HR = 0.65; 95% CI, 0.55-0.78; unstable angina: HR = 0.68; 95% CI, 0.53-0.87; and fatal or nonfatal stroke: HR = 0.72; 95% CI, 0.55-0.93). All-cause mortality did not differ between groups (HR = 0.87; 95% CI, 0.74-1.02).
No significant differences in adverse events leading to discontinuation of the drug were reported between groups. Atrial fibrillation occurred more frequently in the icosapent ethyl group (5.3% vs 3.9%), but anemia (4.7% vs 5.8%) and gastrointestinal adverse events (33% vs 35%) were less common.
Continue to: What's New
WHAT’S NEW
First RCT to demonstrate valueof pairing icosapent ethyl with a statin
Many prior studies on use of omega-3 fatty acid supplements to treat hypertriglyceridemia did not show any benefit, possibly due to a low dose or low ratio of EPA in the study drug.8 One trial (JELIS) with favorable results was an open-label study, limited to patients in Japan. The REDUCE-IT study was the first randomized, placebo-controlled trial to show that icosapent ethyl treatment for hypertriglyceridemia in patients with known CVD who are taking a statin results in fewer cardiovascular events than statin use alone.
Also worth noting: Since publication of the REDUCE-IT study, the FDA has approved an expanded indication for icosapent ethyl for reduction of risk of cardiovascular events in statin-treated patients with hypertriglyceridemia and established CVD or diabetes and ≥ 2 additional cardiovascular risk factors.11
CAVEATS
Drug’s benefit was not linkedto triglyceride level reductions
The cardiovascular benefits of icosapent ethyl were obtained irrespective of triglyceride levels achieved. This raises the question of other potential mechanisms of action of icosapent ethyl in achieving cardiovascular benefit. However, this should not preclude the use of icosapent ethyl for secondary prevention in appropriate patients.
CHALLENGES TO IMPLEMENTATION
Medication is pricey
Icosapent ethyl is an expensive medication, currently priced at an estimated $351/month using a nationally available discount pharmacy plan, although additional manufacturer’s discounts may apply.12,13 The cost of the medication could be a consideration for widespread implementation of this recommendation.
ACKNOWLEDGEMENT
The PURLs Surveillance System was supported in part by Grant Number UL1RR024999 from the National Center For Research Resources, a Clinical Translational Science Award to the University of Chicago. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Center For Research Resources or the National Institutes of Health.
Copyright © 2020. The Family Physicians Inquiries Network. All rights reserved.
1. Bhatt DL, Steg PG, Miller M, et al; REDUCE-IT Investigators. Cardiovascular risk reduction with icosapent ethyl for hypertriglyceridemia. N Engl J Med. 2019;380:11-22.
2. Bhatt DL, Eagle KA, Ohman EM, et al; REACH Registry Investigators. Comparative determinants of 4-year cardiovascular event rates in stable outpatients at risk of or with atherothrombosis. JAMA. 2010;304:1350-1357.
3. Cannon CP, Braunwald E, McCabe CH, et al; Pravastatin or Atorvastatin Evaluation and Infection Therapy–Thrombolysis in Myocardial Infarction 22 Investigators. Intensive versus moderate lipid lowering with statins after acute coronary syndromes [published correction appears in N Engl J Med. 2006;354:778]. N Engl J Med. 2004;350:1495-1504.
4. Klempfner R, Erez A, Sagit BZ, et al. Elevated triglyceride level is independently associated with increased all-cause mortality in patients with established coronary heart disease: twenty-two-year follow-up of the Bezafibrate Infarction Prevention Study and Registry [published correction appears in Circ Cardiovasc Qual Outcomes. 2016;9:613]. Circ Cardiovasc Qual Outcomes. 2016;9:100-108.
5. Nichols GA, Philip S, Reynolds K, Granowitz CB, Fazio S. Increased cardiovascular risk in hypertriglyceridemic patients with statin-controlled LDL cholesterol. J Clin Endocrinol Metab. 2018;103:3019-3027.
6. Grundy SM, Stone NJ, Bailey AL, et al. 2018 AHA/ACC/AACVPR/AAPA/ABC/ACPM/ADA/AGS/APhA/ASPC/NLA/PCNA guideline on the management of blood cholesterol: a report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines [published correction appears in J Am Coll Cardiol. 2019;73:3237-3241]. J Am Coll Cardiol. 2019;73:e285-e350.
7. Ganda OP, Bhatt DL, Mason RP, Miller M, Boden WE. Unmet need for adjunctive dyslipidemia therapy in hypertriglyceridemia management. J Am Coll Cardiol. 2018;72:330-343.
8. Aung T, Halsey J, Kromhout D, et al; Omega-3 Treatment Trialists’ Collaboration. Associations of omega-3 fatty acid supplement use with cardiovascular disease risks: meta-analysis of 10 trials involving 77 917 individuals. JAMA Cardiol. 2018;3:225-234.
9. Yokoyama M, Origasa H, Matsuzaki M, et al; Japan EPA lipid intervention study (JELIS) Investigators. Effects of eicosapentaenoic acid on major coronary events in hypercholesterolaemic patients (JELIS): a randomised open-label, blinded endpoint analysis [published correction appears in Lancet. 2007;370:220]. Lancet. 2007;369:1090-1098.
10. Ballantyne CM, Bays HE, Kastelein JJ, et al. Efficacy and safety of eicosapentaenoic acid ethyl ester (AMR101) therapy in statin-treated patients with persistent high triglycerides (from the ANCHOR study). Am J Cardiol. 2012;110:984-992.
11. FDA approves use of drug to reduce risk of cardiovascular events in certain adult patient groups [news release]. Silver Spring, MD: US Food and Drug Administration; December 13, 2019. www.fda.gov/news-events/press-announcements/fda-approves-use-drug-reduce-risk-cardiovascular-events-certain-adult-patient-groups. Accessed November 30, 2020.
12. Vascepa. GoodRx. www.goodrx.com/vascepa. Accessed November 30, 2020.
13. The VASCEPA Savings Program. www.vascepa.com/getting-started/savings-card/. Accessed November 30, 2020.
1. Bhatt DL, Steg PG, Miller M, et al; REDUCE-IT Investigators. Cardiovascular risk reduction with icosapent ethyl for hypertriglyceridemia. N Engl J Med. 2019;380:11-22.
2. Bhatt DL, Eagle KA, Ohman EM, et al; REACH Registry Investigators. Comparative determinants of 4-year cardiovascular event rates in stable outpatients at risk of or with atherothrombosis. JAMA. 2010;304:1350-1357.
3. Cannon CP, Braunwald E, McCabe CH, et al; Pravastatin or Atorvastatin Evaluation and Infection Therapy–Thrombolysis in Myocardial Infarction 22 Investigators. Intensive versus moderate lipid lowering with statins after acute coronary syndromes [published correction appears in N Engl J Med. 2006;354:778]. N Engl J Med. 2004;350:1495-1504.
4. Klempfner R, Erez A, Sagit BZ, et al. Elevated triglyceride level is independently associated with increased all-cause mortality in patients with established coronary heart disease: twenty-two-year follow-up of the Bezafibrate Infarction Prevention Study and Registry [published correction appears in Circ Cardiovasc Qual Outcomes. 2016;9:613]. Circ Cardiovasc Qual Outcomes. 2016;9:100-108.
5. Nichols GA, Philip S, Reynolds K, Granowitz CB, Fazio S. Increased cardiovascular risk in hypertriglyceridemic patients with statin-controlled LDL cholesterol. J Clin Endocrinol Metab. 2018;103:3019-3027.
6. Grundy SM, Stone NJ, Bailey AL, et al. 2018 AHA/ACC/AACVPR/AAPA/ABC/ACPM/ADA/AGS/APhA/ASPC/NLA/PCNA guideline on the management of blood cholesterol: a report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines [published correction appears in J Am Coll Cardiol. 2019;73:3237-3241]. J Am Coll Cardiol. 2019;73:e285-e350.
7. Ganda OP, Bhatt DL, Mason RP, Miller M, Boden WE. Unmet need for adjunctive dyslipidemia therapy in hypertriglyceridemia management. J Am Coll Cardiol. 2018;72:330-343.
8. Aung T, Halsey J, Kromhout D, et al; Omega-3 Treatment Trialists’ Collaboration. Associations of omega-3 fatty acid supplement use with cardiovascular disease risks: meta-analysis of 10 trials involving 77 917 individuals. JAMA Cardiol. 2018;3:225-234.
9. Yokoyama M, Origasa H, Matsuzaki M, et al; Japan EPA lipid intervention study (JELIS) Investigators. Effects of eicosapentaenoic acid on major coronary events in hypercholesterolaemic patients (JELIS): a randomised open-label, blinded endpoint analysis [published correction appears in Lancet. 2007;370:220]. Lancet. 2007;369:1090-1098.
10. Ballantyne CM, Bays HE, Kastelein JJ, et al. Efficacy and safety of eicosapentaenoic acid ethyl ester (AMR101) therapy in statin-treated patients with persistent high triglycerides (from the ANCHOR study). Am J Cardiol. 2012;110:984-992.
11. FDA approves use of drug to reduce risk of cardiovascular events in certain adult patient groups [news release]. Silver Spring, MD: US Food and Drug Administration; December 13, 2019. www.fda.gov/news-events/press-announcements/fda-approves-use-drug-reduce-risk-cardiovascular-events-certain-adult-patient-groups. Accessed November 30, 2020.
12. Vascepa. GoodRx. www.goodrx.com/vascepa. Accessed November 30, 2020.
13. The VASCEPA Savings Program. www.vascepa.com/getting-started/savings-card/. Accessed November 30, 2020.
PRACTICE CHANGER
Consider icosapent ethyl, 2 g twice daily, for secondary prevention of adverse cardiovascular events in patients with elevated triglycerides who are already taking a statin.
STRENGTH OF RECOMMENDATION
B: Based on a single, good-quality, multicenter, randomized controlled trial. Bhatt DL, Steg PG, Miller M, et al; REDUCE-IT Investigators. Cardiovascular risk reduction with icosapent ethyl for hypertriglyceridemia. N Engl J Med. 2019;380:11-22.1
Bhatt DL, Steg PG, Miller M, et al; REDUCE-IT Investigators. Cardiovascular risk reduction with icosapent ethyl for hypertriglyceridemia. N Engl J Med. 2019;380:11-22.1
USPSTF update on sexually transmitted infections
In August 2020, the US Preventive Services Task Force published an update of its recommendation on preventing sexually transmitted infections (STIs) with behavioral counseling interventions.1
Whom to counsel. The USPSTF continues to recommend behavioral counseling for all sexually active adolescents and for adults at increased risk for STIs. Adults at increased risk include those who have been diagnosed with an STI in the past year, those with multiple sex partners or a sex partner at high risk for an STI, those not using condoms consistently, and those belonging to populations with high prevalence rates of STIs. These populations with high prevalence rates include1
- individuals seeking care at STI clinics,
- sexual and gender minorities, and
- those who are positive for human immunodeficiency virus (HIV), use injection drugs, exchange sex for drugs or money, or have recently been in a correctional facility.
Features of effective counseling. The Task Force recommends that primary care clinicians provide behavioral counseling or refer to counseling services or suggest media-based interventions. The most effective counseling interventions are those that span more than 120 minutes over several sessions. But the Task Force also states that counseling lasting about 30 minutes in a single session can also be effective. Counseling should include information about common STIs and their modes of transmission; encouragement in the use of safer sex practices; and training in proper condom use, how to communicate with partners about safer sex practices, and problem-solving. Various approaches to this counseling can be found at https://uspreventiveservicestaskforce.org/uspstf/recommendation/sexually-transmitted-infections-behavioral-counseling.
This updated recommendation is timely because most STIs in the United States have been increasing in incidence for the past decade or longer.2 Per 100,000 population, the total number of chlamydia cases since 2000 has risen from 251.4 to 539.9 (115%);gonorrhea cases since 2009 have risen from 98.1 to 179.1 (83%).3 And since 2000, the total number of reported syphilis cases per 100,000 has risen from 2.1 to 10.8 (414%).3
Chlamydia affects primarily those ages 15 to 24 years, with highest rates occurring in females (FIGURE 1).2 Gonorrhea affects women and men fairly evenly with slightly higher rates in men; the highest rates are seen in those ages 20 to 29 (FIGURE 2).2 Syphilis predominantly affects men who have sex with men, and the highest rates are in those ages 20 to 34 (FIGURE 3).2 In contrast to these upward trends, the number of HIV cases diagnosed has been relatively steady, with a slight downward trend over the past decade.4Other STIs that can be prevented through behavioral counseling include herpes simplex, human papillomavirus (HPV), hepatitis B virus (HBV) and trichomonas vaginalis.
Continue to: How to integrate STI preventioninto the primary care encounter
How to integrate STI preventioninto the primary care encounter
A key resource for learning to recognize the signs and symptoms of STIs, to correctly diagnose them, and to treat them according to CDC guidelines can be found at www.cdc.gov/std/tg2015/default.htm.5 Equally important is to integrate the prevention of STIs into the clinical routine by using a 4-step approach: risk assessment, risk reduction (counseling and chemoprevention), screening, and vaccination.
Risk assessment. The first step in prevention is taking a sexual history to accurately assess a patient’s risk for STIs. The CDC provides a tool (www.cdc.gov/std/products/provider-pocket-guides.htm) that can assist in gathering information in a nonjudgmental fashion about 5 Ps: partners, practices, protection from STIs, past history of STIs, and prevention of pregnancy.
Risk reduction. Following STI risk assessment, recommend risk-reduction interventions, as appropriate. Notable in the new Task Force recommendation are behavioral counseling methods that work. Additionally, when needed, pre-exposure prophylaxis with effective antiretroviral agents can be offered to those at high risk of HIV.6
Screening. Task Force recommendations for STI screening are described in the TABLE.7-12 Screening for HIV, chlamydia, gonorrhea, syphilis, and HBV are also recommended for pregnant women. And, although pregnant women are not specifically mentioned in the recommendation on chlamydia screening, it is reasonable to include it in prenatal care testing for STIs.
The Task Force has made an “I” statement regarding screening for gonorrhea and chlamydia in males. This does not mean that screening should be avoided, but only that there is insufficient evidence to support a firm statement regarding the harms and benefits in males. Keep in mind that this applies to asymptomatic males, and that testing and preventive treatment are warranted after documented exposure to either infection.
The Task Force recommends against screening for genital herpes, including in pregnant women, because of a lack of evidence of benefit from such screening, the high rate of false-positive tests, and the potential to cause anxiety and harm to personal relationships.
Continue to: Although hepatitis C virus...
Although hepatitis C virus (HCV) is transmitted mainly through intravenous drug use, it can also be transmitted sexually. The Task Force recommends screening for HCV in all adults ages 18 to 79 years.13
Vaccination. Two STIs can be prevented by immunizations: HPV and HBV. The current recommendations by the Advisory Committee on Immunization Practices (ACIP) are to vaccinate all infants with HBV vaccine and all unvaccinated children and adolescents through age 18.14 Unvaccinated adults who are at risk for HBV infection, including those at risk through sexual practices, should also be vaccinated.14
ACIP recommends routine HPV vaccination at age 11 or 12 years, but it can be started as early as 9 years.15 Catch-up vaccination is recommended for males and females through age 26 years.15 The vaccine is approved for use in individuals ages 27 through 45 years, but ACIP has not recommended it for routine use in this age group, and has instead recommended shared clinical decision-making to evaluate whether there is potential individual benefit from the vaccine.15
Public health implications
All STIs are reportable to local or state health departments. This is important for tracking community infection trends and, if resources are available, for contact notification and testing. In most jurisdictions, local health department resources are limited and contact tracing may be restricted to syphilis and HIV infections. When this is the case, it is especially important to instruct patients in whom STIs have been detected to notify their recent sex partners and advise them to be tested or preventively treated.
Expedited partner therapy (EPT)—providing treatment for exposed sexual contacts without a clinical encounter—is allowed in some states and is a tool that can prevent re-infection in the treated patient and suppress spread in the community. This is most useful for partners of those with gonorrhea, chlamydia, or trichomonas. The CDC has published guidance on how to implement EPT in a clinical setting if state law allows it.16
1. Henderson JT, Senger CA, Henninger M, et al. Behavioral counseling interventions to prevent sexually transmitted infections. JAMA. 2020;324:682-699.
2. CDC. Sexually transmitted disease surveillance, 2018. www.cdc.gov/std/stats18/slides.htm. Accessed November 25, 2020.
3. CDC. Sexually transmitted disease surveillance 2018. www.cdc.gov/std/stats18/tables/1.htm. Accessed November 25, 2020.
4. CDC. Estimated HIV incidence and prevalence in the United States (2010-2018). www.cdc.gov/hiv/pdf/library/slidesets/cdc-hiv-surveillance-epidemiology-2018.pdf. Accessed November 25, 2020.
5. CDC. 2015 sexually transmitted disease treatment guidelines. www.cdc.gov/std/tg2015/default.htm. Accessed November 25, 2020.
6. USPSTF. Prevention of human immunodeficiency (HIV) infection: pre-exposure prophylaxis. https://uspreventiveservicestaskforce.org/uspstf/recommendation/prevention-of-human-immunodeficiency-virus-hiv-infection-pre-exposure-prophylaxis. Accessed November 25, 2020.
7. LeFevre ML, U.S. Preventive Services Task Force. Screening for chlamydia and gonorrhea: US Preventive Services Task Force recommendation statement. Ann Intern Med. 2014;161:902-910. 8. USPSTF. Syphilis infection in nonpregnant adults and adolescents: screening. www.uspreventiveservicestaskforce.org/uspstf/recommendation/syphilis-infection-in-nonpregnant-adults-and-adolescents. Accessed November 25, 2020.
9. Curry SJ, Krist AH, Owens DK, et al. Screening for syphilis in pregnant women: US Preventive Services Task Force reaffirmation recommendation statement. JAMA. 2018;320:911-917.
10. Owens DK, Davidson KW, Krist AH, et al; US Preventive Services Task Force. Screening for HIV infection: US Preventive Services Task Force recommendation statement. JAMA. 2019;321:2326-2336.
11. USPSTF. US Preventive Services Task Force issues draft recommendation statement on screening for hepatitis B virus infection in adolescents and adults. www.uspreventiveservicestaskforce.org/uspstf/sites/default/files/file/supporting_documents/hepatitis-b-nonpregnant-adults-draft-rs-bulletin.pdf. Accessed November 25, 2020.
12. Owens DK, Davidson KW, Krist AH, et al. Screening for Hepatitis B Virus Infection in Pregnant Women: US Preventive Services Task Force reaffirmation recommendation statement. JAMA. 2019;322:349-354.
13. USPSTF. Hepatitis C virus infection in adolescents and adults: screening. www.uspreventiveservicestaskforce.org/uspstf/recommendation/hepatitis-c-screening. Accessed November 25, 2020. 14. Schillie S, Vellozzi C, Reingold A, et al. Prevention of hepatitis B virus infection in the United States: recommendations of the Advisory Committee on Immunization Practices. MMWR Recomm Rep. 2018;67;1-31.
15. Meites E, Szilagyi PG, Chesson HW, et al. Human papillomavirus vaccination for adults: updated recommendations of the Advisory Committee on Immunization Practices. MMWR Morb Mortal Wkly Rep. 2019;68:698-702.
16. CDC. Expedited partner therapy in the management of sexually transmitted diseases. www.cdc.gov/std/treatment/eptfinalreport2006.pdf. Accessed November 25, 2020.
In August 2020, the US Preventive Services Task Force published an update of its recommendation on preventing sexually transmitted infections (STIs) with behavioral counseling interventions.1
Whom to counsel. The USPSTF continues to recommend behavioral counseling for all sexually active adolescents and for adults at increased risk for STIs. Adults at increased risk include those who have been diagnosed with an STI in the past year, those with multiple sex partners or a sex partner at high risk for an STI, those not using condoms consistently, and those belonging to populations with high prevalence rates of STIs. These populations with high prevalence rates include1
- individuals seeking care at STI clinics,
- sexual and gender minorities, and
- those who are positive for human immunodeficiency virus (HIV), use injection drugs, exchange sex for drugs or money, or have recently been in a correctional facility.
Features of effective counseling. The Task Force recommends that primary care clinicians provide behavioral counseling or refer to counseling services or suggest media-based interventions. The most effective counseling interventions are those that span more than 120 minutes over several sessions. But the Task Force also states that counseling lasting about 30 minutes in a single session can also be effective. Counseling should include information about common STIs and their modes of transmission; encouragement in the use of safer sex practices; and training in proper condom use, how to communicate with partners about safer sex practices, and problem-solving. Various approaches to this counseling can be found at https://uspreventiveservicestaskforce.org/uspstf/recommendation/sexually-transmitted-infections-behavioral-counseling.
This updated recommendation is timely because most STIs in the United States have been increasing in incidence for the past decade or longer.2 Per 100,000 population, the total number of chlamydia cases since 2000 has risen from 251.4 to 539.9 (115%);gonorrhea cases since 2009 have risen from 98.1 to 179.1 (83%).3 And since 2000, the total number of reported syphilis cases per 100,000 has risen from 2.1 to 10.8 (414%).3
Chlamydia affects primarily those ages 15 to 24 years, with highest rates occurring in females (FIGURE 1).2 Gonorrhea affects women and men fairly evenly with slightly higher rates in men; the highest rates are seen in those ages 20 to 29 (FIGURE 2).2 Syphilis predominantly affects men who have sex with men, and the highest rates are in those ages 20 to 34 (FIGURE 3).2 In contrast to these upward trends, the number of HIV cases diagnosed has been relatively steady, with a slight downward trend over the past decade.4Other STIs that can be prevented through behavioral counseling include herpes simplex, human papillomavirus (HPV), hepatitis B virus (HBV) and trichomonas vaginalis.
Continue to: How to integrate STI preventioninto the primary care encounter
How to integrate STI preventioninto the primary care encounter
A key resource for learning to recognize the signs and symptoms of STIs, to correctly diagnose them, and to treat them according to CDC guidelines can be found at www.cdc.gov/std/tg2015/default.htm.5 Equally important is to integrate the prevention of STIs into the clinical routine by using a 4-step approach: risk assessment, risk reduction (counseling and chemoprevention), screening, and vaccination.
Risk assessment. The first step in prevention is taking a sexual history to accurately assess a patient’s risk for STIs. The CDC provides a tool (www.cdc.gov/std/products/provider-pocket-guides.htm) that can assist in gathering information in a nonjudgmental fashion about 5 Ps: partners, practices, protection from STIs, past history of STIs, and prevention of pregnancy.
Risk reduction. Following STI risk assessment, recommend risk-reduction interventions, as appropriate. Notable in the new Task Force recommendation are behavioral counseling methods that work. Additionally, when needed, pre-exposure prophylaxis with effective antiretroviral agents can be offered to those at high risk of HIV.6
Screening. Task Force recommendations for STI screening are described in the TABLE.7-12 Screening for HIV, chlamydia, gonorrhea, syphilis, and HBV are also recommended for pregnant women. And, although pregnant women are not specifically mentioned in the recommendation on chlamydia screening, it is reasonable to include it in prenatal care testing for STIs.
The Task Force has made an “I” statement regarding screening for gonorrhea and chlamydia in males. This does not mean that screening should be avoided, but only that there is insufficient evidence to support a firm statement regarding the harms and benefits in males. Keep in mind that this applies to asymptomatic males, and that testing and preventive treatment are warranted after documented exposure to either infection.
The Task Force recommends against screening for genital herpes, including in pregnant women, because of a lack of evidence of benefit from such screening, the high rate of false-positive tests, and the potential to cause anxiety and harm to personal relationships.
Continue to: Although hepatitis C virus...
Although hepatitis C virus (HCV) is transmitted mainly through intravenous drug use, it can also be transmitted sexually. The Task Force recommends screening for HCV in all adults ages 18 to 79 years.13
Vaccination. Two STIs can be prevented by immunizations: HPV and HBV. The current recommendations by the Advisory Committee on Immunization Practices (ACIP) are to vaccinate all infants with HBV vaccine and all unvaccinated children and adolescents through age 18.14 Unvaccinated adults who are at risk for HBV infection, including those at risk through sexual practices, should also be vaccinated.14
ACIP recommends routine HPV vaccination at age 11 or 12 years, but it can be started as early as 9 years.15 Catch-up vaccination is recommended for males and females through age 26 years.15 The vaccine is approved for use in individuals ages 27 through 45 years, but ACIP has not recommended it for routine use in this age group, and has instead recommended shared clinical decision-making to evaluate whether there is potential individual benefit from the vaccine.15
Public health implications
All STIs are reportable to local or state health departments. This is important for tracking community infection trends and, if resources are available, for contact notification and testing. In most jurisdictions, local health department resources are limited and contact tracing may be restricted to syphilis and HIV infections. When this is the case, it is especially important to instruct patients in whom STIs have been detected to notify their recent sex partners and advise them to be tested or preventively treated.
Expedited partner therapy (EPT)—providing treatment for exposed sexual contacts without a clinical encounter—is allowed in some states and is a tool that can prevent re-infection in the treated patient and suppress spread in the community. This is most useful for partners of those with gonorrhea, chlamydia, or trichomonas. The CDC has published guidance on how to implement EPT in a clinical setting if state law allows it.16
In August 2020, the US Preventive Services Task Force published an update of its recommendation on preventing sexually transmitted infections (STIs) with behavioral counseling interventions.1
Whom to counsel. The USPSTF continues to recommend behavioral counseling for all sexually active adolescents and for adults at increased risk for STIs. Adults at increased risk include those who have been diagnosed with an STI in the past year, those with multiple sex partners or a sex partner at high risk for an STI, those not using condoms consistently, and those belonging to populations with high prevalence rates of STIs. These populations with high prevalence rates include1
- individuals seeking care at STI clinics,
- sexual and gender minorities, and
- those who are positive for human immunodeficiency virus (HIV), use injection drugs, exchange sex for drugs or money, or have recently been in a correctional facility.
Features of effective counseling. The Task Force recommends that primary care clinicians provide behavioral counseling or refer to counseling services or suggest media-based interventions. The most effective counseling interventions are those that span more than 120 minutes over several sessions. But the Task Force also states that counseling lasting about 30 minutes in a single session can also be effective. Counseling should include information about common STIs and their modes of transmission; encouragement in the use of safer sex practices; and training in proper condom use, how to communicate with partners about safer sex practices, and problem-solving. Various approaches to this counseling can be found at https://uspreventiveservicestaskforce.org/uspstf/recommendation/sexually-transmitted-infections-behavioral-counseling.
This updated recommendation is timely because most STIs in the United States have been increasing in incidence for the past decade or longer.2 Per 100,000 population, the total number of chlamydia cases since 2000 has risen from 251.4 to 539.9 (115%);gonorrhea cases since 2009 have risen from 98.1 to 179.1 (83%).3 And since 2000, the total number of reported syphilis cases per 100,000 has risen from 2.1 to 10.8 (414%).3
Chlamydia affects primarily those ages 15 to 24 years, with highest rates occurring in females (FIGURE 1).2 Gonorrhea affects women and men fairly evenly with slightly higher rates in men; the highest rates are seen in those ages 20 to 29 (FIGURE 2).2 Syphilis predominantly affects men who have sex with men, and the highest rates are in those ages 20 to 34 (FIGURE 3).2 In contrast to these upward trends, the number of HIV cases diagnosed has been relatively steady, with a slight downward trend over the past decade.4Other STIs that can be prevented through behavioral counseling include herpes simplex, human papillomavirus (HPV), hepatitis B virus (HBV) and trichomonas vaginalis.
Continue to: How to integrate STI preventioninto the primary care encounter
How to integrate STI preventioninto the primary care encounter
A key resource for learning to recognize the signs and symptoms of STIs, to correctly diagnose them, and to treat them according to CDC guidelines can be found at www.cdc.gov/std/tg2015/default.htm.5 Equally important is to integrate the prevention of STIs into the clinical routine by using a 4-step approach: risk assessment, risk reduction (counseling and chemoprevention), screening, and vaccination.
Risk assessment. The first step in prevention is taking a sexual history to accurately assess a patient’s risk for STIs. The CDC provides a tool (www.cdc.gov/std/products/provider-pocket-guides.htm) that can assist in gathering information in a nonjudgmental fashion about 5 Ps: partners, practices, protection from STIs, past history of STIs, and prevention of pregnancy.
Risk reduction. Following STI risk assessment, recommend risk-reduction interventions, as appropriate. Notable in the new Task Force recommendation are behavioral counseling methods that work. Additionally, when needed, pre-exposure prophylaxis with effective antiretroviral agents can be offered to those at high risk of HIV.6
Screening. Task Force recommendations for STI screening are described in the TABLE.7-12 Screening for HIV, chlamydia, gonorrhea, syphilis, and HBV are also recommended for pregnant women. And, although pregnant women are not specifically mentioned in the recommendation on chlamydia screening, it is reasonable to include it in prenatal care testing for STIs.
The Task Force has made an “I” statement regarding screening for gonorrhea and chlamydia in males. This does not mean that screening should be avoided, but only that there is insufficient evidence to support a firm statement regarding the harms and benefits in males. Keep in mind that this applies to asymptomatic males, and that testing and preventive treatment are warranted after documented exposure to either infection.
The Task Force recommends against screening for genital herpes, including in pregnant women, because of a lack of evidence of benefit from such screening, the high rate of false-positive tests, and the potential to cause anxiety and harm to personal relationships.
Continue to: Although hepatitis C virus...
Although hepatitis C virus (HCV) is transmitted mainly through intravenous drug use, it can also be transmitted sexually. The Task Force recommends screening for HCV in all adults ages 18 to 79 years.13
Vaccination. Two STIs can be prevented by immunizations: HPV and HBV. The current recommendations by the Advisory Committee on Immunization Practices (ACIP) are to vaccinate all infants with HBV vaccine and all unvaccinated children and adolescents through age 18.14 Unvaccinated adults who are at risk for HBV infection, including those at risk through sexual practices, should also be vaccinated.14
ACIP recommends routine HPV vaccination at age 11 or 12 years, but it can be started as early as 9 years.15 Catch-up vaccination is recommended for males and females through age 26 years.15 The vaccine is approved for use in individuals ages 27 through 45 years, but ACIP has not recommended it for routine use in this age group, and has instead recommended shared clinical decision-making to evaluate whether there is potential individual benefit from the vaccine.15
Public health implications
All STIs are reportable to local or state health departments. This is important for tracking community infection trends and, if resources are available, for contact notification and testing. In most jurisdictions, local health department resources are limited and contact tracing may be restricted to syphilis and HIV infections. When this is the case, it is especially important to instruct patients in whom STIs have been detected to notify their recent sex partners and advise them to be tested or preventively treated.
Expedited partner therapy (EPT)—providing treatment for exposed sexual contacts without a clinical encounter—is allowed in some states and is a tool that can prevent re-infection in the treated patient and suppress spread in the community. This is most useful for partners of those with gonorrhea, chlamydia, or trichomonas. The CDC has published guidance on how to implement EPT in a clinical setting if state law allows it.16
1. Henderson JT, Senger CA, Henninger M, et al. Behavioral counseling interventions to prevent sexually transmitted infections. JAMA. 2020;324:682-699.
2. CDC. Sexually transmitted disease surveillance, 2018. www.cdc.gov/std/stats18/slides.htm. Accessed November 25, 2020.
3. CDC. Sexually transmitted disease surveillance 2018. www.cdc.gov/std/stats18/tables/1.htm. Accessed November 25, 2020.
4. CDC. Estimated HIV incidence and prevalence in the United States (2010-2018). www.cdc.gov/hiv/pdf/library/slidesets/cdc-hiv-surveillance-epidemiology-2018.pdf. Accessed November 25, 2020.
5. CDC. 2015 sexually transmitted disease treatment guidelines. www.cdc.gov/std/tg2015/default.htm. Accessed November 25, 2020.
6. USPSTF. Prevention of human immunodeficiency (HIV) infection: pre-exposure prophylaxis. https://uspreventiveservicestaskforce.org/uspstf/recommendation/prevention-of-human-immunodeficiency-virus-hiv-infection-pre-exposure-prophylaxis. Accessed November 25, 2020.
7. LeFevre ML, U.S. Preventive Services Task Force. Screening for chlamydia and gonorrhea: US Preventive Services Task Force recommendation statement. Ann Intern Med. 2014;161:902-910. 8. USPSTF. Syphilis infection in nonpregnant adults and adolescents: screening. www.uspreventiveservicestaskforce.org/uspstf/recommendation/syphilis-infection-in-nonpregnant-adults-and-adolescents. Accessed November 25, 2020.
9. Curry SJ, Krist AH, Owens DK, et al. Screening for syphilis in pregnant women: US Preventive Services Task Force reaffirmation recommendation statement. JAMA. 2018;320:911-917.
10. Owens DK, Davidson KW, Krist AH, et al; US Preventive Services Task Force. Screening for HIV infection: US Preventive Services Task Force recommendation statement. JAMA. 2019;321:2326-2336.
11. USPSTF. US Preventive Services Task Force issues draft recommendation statement on screening for hepatitis B virus infection in adolescents and adults. www.uspreventiveservicestaskforce.org/uspstf/sites/default/files/file/supporting_documents/hepatitis-b-nonpregnant-adults-draft-rs-bulletin.pdf. Accessed November 25, 2020.
12. Owens DK, Davidson KW, Krist AH, et al. Screening for Hepatitis B Virus Infection in Pregnant Women: US Preventive Services Task Force reaffirmation recommendation statement. JAMA. 2019;322:349-354.
13. USPSTF. Hepatitis C virus infection in adolescents and adults: screening. www.uspreventiveservicestaskforce.org/uspstf/recommendation/hepatitis-c-screening. Accessed November 25, 2020. 14. Schillie S, Vellozzi C, Reingold A, et al. Prevention of hepatitis B virus infection in the United States: recommendations of the Advisory Committee on Immunization Practices. MMWR Recomm Rep. 2018;67;1-31.
15. Meites E, Szilagyi PG, Chesson HW, et al. Human papillomavirus vaccination for adults: updated recommendations of the Advisory Committee on Immunization Practices. MMWR Morb Mortal Wkly Rep. 2019;68:698-702.
16. CDC. Expedited partner therapy in the management of sexually transmitted diseases. www.cdc.gov/std/treatment/eptfinalreport2006.pdf. Accessed November 25, 2020.
1. Henderson JT, Senger CA, Henninger M, et al. Behavioral counseling interventions to prevent sexually transmitted infections. JAMA. 2020;324:682-699.
2. CDC. Sexually transmitted disease surveillance, 2018. www.cdc.gov/std/stats18/slides.htm. Accessed November 25, 2020.
3. CDC. Sexually transmitted disease surveillance 2018. www.cdc.gov/std/stats18/tables/1.htm. Accessed November 25, 2020.
4. CDC. Estimated HIV incidence and prevalence in the United States (2010-2018). www.cdc.gov/hiv/pdf/library/slidesets/cdc-hiv-surveillance-epidemiology-2018.pdf. Accessed November 25, 2020.
5. CDC. 2015 sexually transmitted disease treatment guidelines. www.cdc.gov/std/tg2015/default.htm. Accessed November 25, 2020.
6. USPSTF. Prevention of human immunodeficiency (HIV) infection: pre-exposure prophylaxis. https://uspreventiveservicestaskforce.org/uspstf/recommendation/prevention-of-human-immunodeficiency-virus-hiv-infection-pre-exposure-prophylaxis. Accessed November 25, 2020.
7. LeFevre ML, U.S. Preventive Services Task Force. Screening for chlamydia and gonorrhea: US Preventive Services Task Force recommendation statement. Ann Intern Med. 2014;161:902-910. 8. USPSTF. Syphilis infection in nonpregnant adults and adolescents: screening. www.uspreventiveservicestaskforce.org/uspstf/recommendation/syphilis-infection-in-nonpregnant-adults-and-adolescents. Accessed November 25, 2020.
9. Curry SJ, Krist AH, Owens DK, et al. Screening for syphilis in pregnant women: US Preventive Services Task Force reaffirmation recommendation statement. JAMA. 2018;320:911-917.
10. Owens DK, Davidson KW, Krist AH, et al; US Preventive Services Task Force. Screening for HIV infection: US Preventive Services Task Force recommendation statement. JAMA. 2019;321:2326-2336.
11. USPSTF. US Preventive Services Task Force issues draft recommendation statement on screening for hepatitis B virus infection in adolescents and adults. www.uspreventiveservicestaskforce.org/uspstf/sites/default/files/file/supporting_documents/hepatitis-b-nonpregnant-adults-draft-rs-bulletin.pdf. Accessed November 25, 2020.
12. Owens DK, Davidson KW, Krist AH, et al. Screening for Hepatitis B Virus Infection in Pregnant Women: US Preventive Services Task Force reaffirmation recommendation statement. JAMA. 2019;322:349-354.
13. USPSTF. Hepatitis C virus infection in adolescents and adults: screening. www.uspreventiveservicestaskforce.org/uspstf/recommendation/hepatitis-c-screening. Accessed November 25, 2020. 14. Schillie S, Vellozzi C, Reingold A, et al. Prevention of hepatitis B virus infection in the United States: recommendations of the Advisory Committee on Immunization Practices. MMWR Recomm Rep. 2018;67;1-31.
15. Meites E, Szilagyi PG, Chesson HW, et al. Human papillomavirus vaccination for adults: updated recommendations of the Advisory Committee on Immunization Practices. MMWR Morb Mortal Wkly Rep. 2019;68:698-702.
16. CDC. Expedited partner therapy in the management of sexually transmitted diseases. www.cdc.gov/std/treatment/eptfinalreport2006.pdf. Accessed November 25, 2020.
Worsening skin lesions but no diagnosis
A 50-year-old woman presented to her family physician for a urinary tract infection (UTI) and an itchy rash. She said the rash had developed 2 years earlier and had gotten worse, with additional lesions emerging on her skin as time went on. She noted that other physicians had evaluated the rash but provided no clear diagnosis and had done no testing.
A physical exam revealed scattered erythematous papules with white centers on the patient’s trunk, arms, and legs (FIGURE 1). The patient’s medical history was significant for asthma, obstructive sleep apnea, obesity, gastroesophageal reflux disease, urinary incontinence, and depression. Her medications included montelukast, inhaled fluticasone, albuterol, tolterodine, omeprazole, and fluoxetine.
The patient was prescribed nitrofurantoin, 100 mg twice daily for 5 days, to treat her UTI, and a punch biopsy was performed on one of the patient’s lesions to determine the cause of the rash.
WHAT IS YOUR DIAGNOSIS?
HOW WOULD YOU TREAT THIS PATIENT?
Diagnosis: Atrophic papulosis
Pathology suggested a diagnosis of atrophic papulosis. A consultation with a dermatologist and additional biopsies confirmed the diagnosis. The biopsies showed wedge-shaped areas of superficial dermal sclerosis with thinning of the overlying epidermis. The superficial dermal vessels contained scattered, small thrombi at the periphery of the areas of sclerosis.
Atrophic papulosis (also known as Degos disease or Kölmeier-Degos disease) is a vasculopathy characterized by thrombotic occlusion of small arteries.1 Although rare—with fewer than 200 published case reports in the literature—it is likely underdiagnosed.1 Atrophic papulosis can be distinguished by hallmark skin findings, including 0.5- to 1-cm papular skin lesions with central porcelain-white atrophy and an erythematous, telangiectatic rim.1 It usually manifests between ages 20 to 50 but can occur in infants and children.1 The etiology is unknown, but case evidence suggests the condition is sometimes familial.1,2
Easy to confuse with common conditions
Clinical presentation of atrophic papulosis can vary, but evaluation should rule out systemic lupus erythematosus and other connective tissue diseases.1 In addition, the lesions can easily be confused with other common conditions such as molluscum contagiosum or insect bites.
The hallmark finding of molluscum contagiosum is raised papules with central umbilication, whereas atrophic papulosis lesions are characterized by white centers. While insect bites typically disappear within weeks, atrophic papulosis lesions persist for years or are even lifelong.1
Is it benign or malignant?
Benign atrophic papulosis is limited to the skin.1 The probability of a patient having benign atrophic papulosis is about 70% at the onset of skin lesions and 97% after 7 years without other symptoms.2
Malignant atrophic papulosis—although less common—is systemic and life-threatening. About 30% of patients with atrophic papulosis develop lesions manifesting both on the skin and in internal organs.1,2 Systemic involvement can develop at any time, sometimes years after the appearance of skin lesions, but the risk declines over time.2 In a case series, systemic signs were shown to develop, on average, 1 year after skin lesions.2 Some evidence suggests a mortality rate of 50% within 2 to 3 years of the onset of systemic involvement, making regular follow-up necessary.1
Continue to: Patients with malignant atrophic papulosis...
Patients with malignant atrophic papulosis may have systemic involvement in multiple organ systems. Gastrointestinal (GI) involvement can cause bowel perforation. Central nervous system (CNS) involvement may put the patient at risk for stroke, intracranial bleeding, meningitis, and encephalitis.1,3 There can also be cardiopulmonary involvement that causes pleuritis and pericarditis.1 Ocular involvement can affect the eyelids, conjunctiva, retina, sclera, and choroid plexus.1 Renal involvement has been noted in a few cases.2
In a prospective, single-center cohort study of 39 patients with atrophic papulosis, systemic involvement (malignant atrophic papulosis) was reported in 29% (n = 11) of the patients.2 In these patients, involved organ systems included the GI tract (73%; n = 8), CNS (64%; n = 7), eye (18%; n = 2), heart (18%; n = 2), and lungs (9%; n = 1); 64% (n = 7) had multiorgan involvement. Mortality was reported in 73% of the patients with systemic disease.
Ongoing testing is required
For a patient presenting with atrophic papulosis, initial and follow-up visits should include evaluation for systemic manifestations through a full skin examination, fecal occult blood test, and ocular fundus examination.1,2 If the patient shows any symptoms that suggest systemic involvement, further testing is advised, including evaluation of renal function, colonoscopy, endoscopy, magnetic resonance imaging of the brain, an echocardiogram, and chest computed tomography.
Because internal organ involvement in malignant atrophic papulosis can develop within years of (benign) cutaneous manifestations, regular follow-up is recommended.1 Research suggests evaluation of patients with benign atrophic papulosis every 6 months for the first 7 years after disease onset and then yearly between 7 and 10 years after onset.2
Treatment options are limited
Antiplatelet agents (aspirin, pentoxifylline, dipyridamole, and ticlodipine) and anticoagulants (heparin) have led to partial regression of skin lesions in case reports.1 Some lesions seem to disappear after treatment, but due to limited evidence, it is difficult to determine whether treatment leads to a reduction of future lesions.
When it comes to malignant atrophic papulosis, there is no uniformly effective treatment. Antiplatelet agents and anticoagulants are often used as initial treatment, but efficacy has not been clearly demonstrated. In case reports, eculizumab and treprostinil have shown effectiveness in treating CNS involvement, but there are no uniform dosage recommendations.3,4
In this case, the patient had mild GI symptoms. A colonoscopy showed evidence of microscopic colitis, but there was no evidence of atrophic papulosis in the GI tract.
Additional laboratory work-up was ordered to evaluate for signs of organ involvement and to rule out any associated connective tissue disease or hypercoagulable state. Her results showed a mildly elevated erythrocyte sedimentation rate (29 mm/h) and a positive antinuclear antibodies assay (1:640, speckled pattern). She was referred to a rheumatologist, who found no evidence of a connective tissue disorder. A complete blood count, comprehensive metabolic panel, urinalysis, and hypercoagulability work-up were all within normal limits. A complete eye exam was also normal.
The patient was started on aspirin 81 mg/d. Because she continued to develop new lesions, her dermatologist added pentoxifylline extended release and gradually increased the dose to 400 mg in the morning and 800 mg in the evening. About 4 years after onset of the rash, the patient showed no signs of systemic involvement, but her skin lesions were still present.
1. Theodoridis A, Makrantonaki E, Zouboulis CC, et al. Malignant atrophic papulosis (Köhlmeier-Degos disease)—a review. Orphanet J Rare Dis. 2013;8:10.
2. Theodoridis A, Konstantinidou A, Makrantonaki E, et al. Malignant and benign forms of atrophic papulosis (Köhlmeier-Degos disease): systemic involvement determines the prognosis. Br J Dermatol. 2014;170:110-115.
3. Huang YC, Wang JD, Lee FY, et al. Pediatric malignant atrophic papulosis. Pediatrics. 2018;141(suppl 5):S481-S484.
4. Shapiro LS, Toledo-Garcia AE, Farrell JF. Effective treatment of malignant atrophic papulosis (Köhlmeier-Degos disease) with treprostinil—early experience. Orphanet J Rare Dis. 2013;8:52.
A 50-year-old woman presented to her family physician for a urinary tract infection (UTI) and an itchy rash. She said the rash had developed 2 years earlier and had gotten worse, with additional lesions emerging on her skin as time went on. She noted that other physicians had evaluated the rash but provided no clear diagnosis and had done no testing.
A physical exam revealed scattered erythematous papules with white centers on the patient’s trunk, arms, and legs (FIGURE 1). The patient’s medical history was significant for asthma, obstructive sleep apnea, obesity, gastroesophageal reflux disease, urinary incontinence, and depression. Her medications included montelukast, inhaled fluticasone, albuterol, tolterodine, omeprazole, and fluoxetine.
The patient was prescribed nitrofurantoin, 100 mg twice daily for 5 days, to treat her UTI, and a punch biopsy was performed on one of the patient’s lesions to determine the cause of the rash.
WHAT IS YOUR DIAGNOSIS?
HOW WOULD YOU TREAT THIS PATIENT?
Diagnosis: Atrophic papulosis
Pathology suggested a diagnosis of atrophic papulosis. A consultation with a dermatologist and additional biopsies confirmed the diagnosis. The biopsies showed wedge-shaped areas of superficial dermal sclerosis with thinning of the overlying epidermis. The superficial dermal vessels contained scattered, small thrombi at the periphery of the areas of sclerosis.
Atrophic papulosis (also known as Degos disease or Kölmeier-Degos disease) is a vasculopathy characterized by thrombotic occlusion of small arteries.1 Although rare—with fewer than 200 published case reports in the literature—it is likely underdiagnosed.1 Atrophic papulosis can be distinguished by hallmark skin findings, including 0.5- to 1-cm papular skin lesions with central porcelain-white atrophy and an erythematous, telangiectatic rim.1 It usually manifests between ages 20 to 50 but can occur in infants and children.1 The etiology is unknown, but case evidence suggests the condition is sometimes familial.1,2
Easy to confuse with common conditions
Clinical presentation of atrophic papulosis can vary, but evaluation should rule out systemic lupus erythematosus and other connective tissue diseases.1 In addition, the lesions can easily be confused with other common conditions such as molluscum contagiosum or insect bites.
The hallmark finding of molluscum contagiosum is raised papules with central umbilication, whereas atrophic papulosis lesions are characterized by white centers. While insect bites typically disappear within weeks, atrophic papulosis lesions persist for years or are even lifelong.1
Is it benign or malignant?
Benign atrophic papulosis is limited to the skin.1 The probability of a patient having benign atrophic papulosis is about 70% at the onset of skin lesions and 97% after 7 years without other symptoms.2
Malignant atrophic papulosis—although less common—is systemic and life-threatening. About 30% of patients with atrophic papulosis develop lesions manifesting both on the skin and in internal organs.1,2 Systemic involvement can develop at any time, sometimes years after the appearance of skin lesions, but the risk declines over time.2 In a case series, systemic signs were shown to develop, on average, 1 year after skin lesions.2 Some evidence suggests a mortality rate of 50% within 2 to 3 years of the onset of systemic involvement, making regular follow-up necessary.1
Continue to: Patients with malignant atrophic papulosis...
Patients with malignant atrophic papulosis may have systemic involvement in multiple organ systems. Gastrointestinal (GI) involvement can cause bowel perforation. Central nervous system (CNS) involvement may put the patient at risk for stroke, intracranial bleeding, meningitis, and encephalitis.1,3 There can also be cardiopulmonary involvement that causes pleuritis and pericarditis.1 Ocular involvement can affect the eyelids, conjunctiva, retina, sclera, and choroid plexus.1 Renal involvement has been noted in a few cases.2
In a prospective, single-center cohort study of 39 patients with atrophic papulosis, systemic involvement (malignant atrophic papulosis) was reported in 29% (n = 11) of the patients.2 In these patients, involved organ systems included the GI tract (73%; n = 8), CNS (64%; n = 7), eye (18%; n = 2), heart (18%; n = 2), and lungs (9%; n = 1); 64% (n = 7) had multiorgan involvement. Mortality was reported in 73% of the patients with systemic disease.
Ongoing testing is required
For a patient presenting with atrophic papulosis, initial and follow-up visits should include evaluation for systemic manifestations through a full skin examination, fecal occult blood test, and ocular fundus examination.1,2 If the patient shows any symptoms that suggest systemic involvement, further testing is advised, including evaluation of renal function, colonoscopy, endoscopy, magnetic resonance imaging of the brain, an echocardiogram, and chest computed tomography.
Because internal organ involvement in malignant atrophic papulosis can develop within years of (benign) cutaneous manifestations, regular follow-up is recommended.1 Research suggests evaluation of patients with benign atrophic papulosis every 6 months for the first 7 years after disease onset and then yearly between 7 and 10 years after onset.2
Treatment options are limited
Antiplatelet agents (aspirin, pentoxifylline, dipyridamole, and ticlodipine) and anticoagulants (heparin) have led to partial regression of skin lesions in case reports.1 Some lesions seem to disappear after treatment, but due to limited evidence, it is difficult to determine whether treatment leads to a reduction of future lesions.
When it comes to malignant atrophic papulosis, there is no uniformly effective treatment. Antiplatelet agents and anticoagulants are often used as initial treatment, but efficacy has not been clearly demonstrated. In case reports, eculizumab and treprostinil have shown effectiveness in treating CNS involvement, but there are no uniform dosage recommendations.3,4
In this case, the patient had mild GI symptoms. A colonoscopy showed evidence of microscopic colitis, but there was no evidence of atrophic papulosis in the GI tract.
Additional laboratory work-up was ordered to evaluate for signs of organ involvement and to rule out any associated connective tissue disease or hypercoagulable state. Her results showed a mildly elevated erythrocyte sedimentation rate (29 mm/h) and a positive antinuclear antibodies assay (1:640, speckled pattern). She was referred to a rheumatologist, who found no evidence of a connective tissue disorder. A complete blood count, comprehensive metabolic panel, urinalysis, and hypercoagulability work-up were all within normal limits. A complete eye exam was also normal.
The patient was started on aspirin 81 mg/d. Because she continued to develop new lesions, her dermatologist added pentoxifylline extended release and gradually increased the dose to 400 mg in the morning and 800 mg in the evening. About 4 years after onset of the rash, the patient showed no signs of systemic involvement, but her skin lesions were still present.
A 50-year-old woman presented to her family physician for a urinary tract infection (UTI) and an itchy rash. She said the rash had developed 2 years earlier and had gotten worse, with additional lesions emerging on her skin as time went on. She noted that other physicians had evaluated the rash but provided no clear diagnosis and had done no testing.
A physical exam revealed scattered erythematous papules with white centers on the patient’s trunk, arms, and legs (FIGURE 1). The patient’s medical history was significant for asthma, obstructive sleep apnea, obesity, gastroesophageal reflux disease, urinary incontinence, and depression. Her medications included montelukast, inhaled fluticasone, albuterol, tolterodine, omeprazole, and fluoxetine.
The patient was prescribed nitrofurantoin, 100 mg twice daily for 5 days, to treat her UTI, and a punch biopsy was performed on one of the patient’s lesions to determine the cause of the rash.
WHAT IS YOUR DIAGNOSIS?
HOW WOULD YOU TREAT THIS PATIENT?
Diagnosis: Atrophic papulosis
Pathology suggested a diagnosis of atrophic papulosis. A consultation with a dermatologist and additional biopsies confirmed the diagnosis. The biopsies showed wedge-shaped areas of superficial dermal sclerosis with thinning of the overlying epidermis. The superficial dermal vessels contained scattered, small thrombi at the periphery of the areas of sclerosis.
Atrophic papulosis (also known as Degos disease or Kölmeier-Degos disease) is a vasculopathy characterized by thrombotic occlusion of small arteries.1 Although rare—with fewer than 200 published case reports in the literature—it is likely underdiagnosed.1 Atrophic papulosis can be distinguished by hallmark skin findings, including 0.5- to 1-cm papular skin lesions with central porcelain-white atrophy and an erythematous, telangiectatic rim.1 It usually manifests between ages 20 to 50 but can occur in infants and children.1 The etiology is unknown, but case evidence suggests the condition is sometimes familial.1,2
Easy to confuse with common conditions
Clinical presentation of atrophic papulosis can vary, but evaluation should rule out systemic lupus erythematosus and other connective tissue diseases.1 In addition, the lesions can easily be confused with other common conditions such as molluscum contagiosum or insect bites.
The hallmark finding of molluscum contagiosum is raised papules with central umbilication, whereas atrophic papulosis lesions are characterized by white centers. While insect bites typically disappear within weeks, atrophic papulosis lesions persist for years or are even lifelong.1
Is it benign or malignant?
Benign atrophic papulosis is limited to the skin.1 The probability of a patient having benign atrophic papulosis is about 70% at the onset of skin lesions and 97% after 7 years without other symptoms.2
Malignant atrophic papulosis—although less common—is systemic and life-threatening. About 30% of patients with atrophic papulosis develop lesions manifesting both on the skin and in internal organs.1,2 Systemic involvement can develop at any time, sometimes years after the appearance of skin lesions, but the risk declines over time.2 In a case series, systemic signs were shown to develop, on average, 1 year after skin lesions.2 Some evidence suggests a mortality rate of 50% within 2 to 3 years of the onset of systemic involvement, making regular follow-up necessary.1
Continue to: Patients with malignant atrophic papulosis...
Patients with malignant atrophic papulosis may have systemic involvement in multiple organ systems. Gastrointestinal (GI) involvement can cause bowel perforation. Central nervous system (CNS) involvement may put the patient at risk for stroke, intracranial bleeding, meningitis, and encephalitis.1,3 There can also be cardiopulmonary involvement that causes pleuritis and pericarditis.1 Ocular involvement can affect the eyelids, conjunctiva, retina, sclera, and choroid plexus.1 Renal involvement has been noted in a few cases.2
In a prospective, single-center cohort study of 39 patients with atrophic papulosis, systemic involvement (malignant atrophic papulosis) was reported in 29% (n = 11) of the patients.2 In these patients, involved organ systems included the GI tract (73%; n = 8), CNS (64%; n = 7), eye (18%; n = 2), heart (18%; n = 2), and lungs (9%; n = 1); 64% (n = 7) had multiorgan involvement. Mortality was reported in 73% of the patients with systemic disease.
Ongoing testing is required
For a patient presenting with atrophic papulosis, initial and follow-up visits should include evaluation for systemic manifestations through a full skin examination, fecal occult blood test, and ocular fundus examination.1,2 If the patient shows any symptoms that suggest systemic involvement, further testing is advised, including evaluation of renal function, colonoscopy, endoscopy, magnetic resonance imaging of the brain, an echocardiogram, and chest computed tomography.
Because internal organ involvement in malignant atrophic papulosis can develop within years of (benign) cutaneous manifestations, regular follow-up is recommended.1 Research suggests evaluation of patients with benign atrophic papulosis every 6 months for the first 7 years after disease onset and then yearly between 7 and 10 years after onset.2
Treatment options are limited
Antiplatelet agents (aspirin, pentoxifylline, dipyridamole, and ticlodipine) and anticoagulants (heparin) have led to partial regression of skin lesions in case reports.1 Some lesions seem to disappear after treatment, but due to limited evidence, it is difficult to determine whether treatment leads to a reduction of future lesions.
When it comes to malignant atrophic papulosis, there is no uniformly effective treatment. Antiplatelet agents and anticoagulants are often used as initial treatment, but efficacy has not been clearly demonstrated. In case reports, eculizumab and treprostinil have shown effectiveness in treating CNS involvement, but there are no uniform dosage recommendations.3,4
In this case, the patient had mild GI symptoms. A colonoscopy showed evidence of microscopic colitis, but there was no evidence of atrophic papulosis in the GI tract.
Additional laboratory work-up was ordered to evaluate for signs of organ involvement and to rule out any associated connective tissue disease or hypercoagulable state. Her results showed a mildly elevated erythrocyte sedimentation rate (29 mm/h) and a positive antinuclear antibodies assay (1:640, speckled pattern). She was referred to a rheumatologist, who found no evidence of a connective tissue disorder. A complete blood count, comprehensive metabolic panel, urinalysis, and hypercoagulability work-up were all within normal limits. A complete eye exam was also normal.
The patient was started on aspirin 81 mg/d. Because she continued to develop new lesions, her dermatologist added pentoxifylline extended release and gradually increased the dose to 400 mg in the morning and 800 mg in the evening. About 4 years after onset of the rash, the patient showed no signs of systemic involvement, but her skin lesions were still present.
1. Theodoridis A, Makrantonaki E, Zouboulis CC, et al. Malignant atrophic papulosis (Köhlmeier-Degos disease)—a review. Orphanet J Rare Dis. 2013;8:10.
2. Theodoridis A, Konstantinidou A, Makrantonaki E, et al. Malignant and benign forms of atrophic papulosis (Köhlmeier-Degos disease): systemic involvement determines the prognosis. Br J Dermatol. 2014;170:110-115.
3. Huang YC, Wang JD, Lee FY, et al. Pediatric malignant atrophic papulosis. Pediatrics. 2018;141(suppl 5):S481-S484.
4. Shapiro LS, Toledo-Garcia AE, Farrell JF. Effective treatment of malignant atrophic papulosis (Köhlmeier-Degos disease) with treprostinil—early experience. Orphanet J Rare Dis. 2013;8:52.
1. Theodoridis A, Makrantonaki E, Zouboulis CC, et al. Malignant atrophic papulosis (Köhlmeier-Degos disease)—a review. Orphanet J Rare Dis. 2013;8:10.
2. Theodoridis A, Konstantinidou A, Makrantonaki E, et al. Malignant and benign forms of atrophic papulosis (Köhlmeier-Degos disease): systemic involvement determines the prognosis. Br J Dermatol. 2014;170:110-115.
3. Huang YC, Wang JD, Lee FY, et al. Pediatric malignant atrophic papulosis. Pediatrics. 2018;141(suppl 5):S481-S484.
4. Shapiro LS, Toledo-Garcia AE, Farrell JF. Effective treatment of malignant atrophic papulosis (Köhlmeier-Degos disease) with treprostinil—early experience. Orphanet J Rare Dis. 2013;8:52.
Itchy scalp with scale
An 11-year-old boy sought care at a small village’s health center in Panama for scalp itching and subtle hair loss. He was seen by a family physician (RU) and a team of medical students who were there as part of a humanitarian trip. The patient denied any hair pulling. He had a history of treatment for head lice.
Our physical examination revealed mild alopecia and scaling on the scalp (FIGURE 1), but what we saw through the dermatoscope (FIGURE 2) made the diagnosis clear.
WHAT IS YOUR DIAGNOSIS?
HOW WOULD YOU TREAT THIS PATIENT?
Diagnosis: Tinea capitis
On dermatoscopic examination (10× magnification), there were numerous “black dots” or broken hair shafts within patches of hair loss (FIGURE 3), which is indicative of tinea capitis.1,2 This condition causes hair shafts to break, creating “comma hairs” and black dots. The hairs are uniform in thickness and color and bend distally, like a comma.3
Tinea capitis (commonly called ringworm of the scalp) is a fungal infection caused by Trichophyton and Microsporum dermatophytes. It is the most common pediatric dermatophyte infection in the world; the usual age of onset is 5 to 10 years.2 The incidence of tinea capitis in the United States is not known because cases are no longer registered by public health agencies. That said, a Northern California study that tracked occurrences in children younger than 15 years from 1998 to 2007 found that the incidence was on the decline and lower in girls compared to boys (111.9 vs 146.4, respectively, in 1998; 27.9 vs 39.9, respectively, in 2007).4 Incidence rates were calculated per 10,000 eligible children.4
Tinea capitis can spread by contact with infected individuals and contaminated objects, including combs, towels, toys, and bedding.1 Fungal spores can remain viable on these surfaces for months.
In a study of 69 patients with tinea capitis (23 females, 46 males; mean age, 12 years), the risk factors for spreading infection included participation in sports, contact with an animal, a recent haircut, and use of a swimming pool.5
4 conditions you’ll want to rule out
The following conditions should be considered as part of the differential when a patient presents with an itchy scalp and/or hair loss.
Continue to: Psoriasis of the scalp...
Psoriasis of the scalp is characterized by scaling of the scalp along with crusted plaques. It is often accompanied by similar psoriatic plaques on the elbows, knees, and other areas of the body. Examination of our patient showed no psoriatic plaques.
Seborrhea of the scalp (also known as dandruff) is a very common diagnosis. However, it is unlikely to cause hair loss. It has widespread involvement of the scalp compared to tinea capitis, which is local and patchy. Our patient’s patches of hair loss indicated that seborrhea was unlikely.
Alopecia areata. Individuals develop this condition due to an autoimmune process affecting hair follicles. However, the resulting hair loss does not cause significant scaling, inflammation, scarring, or pain in the affected area. Further, this condition can cause the loss of the entire hair shaft.
Trichotillomania is an impulse control disorder that causes patients to pull out their own hair. There is no scaling of the scalp in this condition.
A dermatoscope can beuseful in making the Dx
Although clinical appearance and patient presentation are adequate to establish the diagnosis of tinea capitis, this case demonstrates the utility of a dermatoscope in making the diagnosis of tinea capitis. Previous studies have shown that dermoscopy allows for rapid identification of the broken hair shafts, which are a key distinction from alopecia areata.3,6
Microscopic inspection. Samples from the scaling of the scalp can be examined with potassium hydroxide (KOH) on a microscope slide. Hyphae, spores, and endo/ectothrix invasion can be seen through the microsope.
Continue to: Laboratory testing is helpful, but not needed.
Laboratory testing is helpful, but not needed. Testing for tinea capitis would require that you obtain a sample from the affected area using a swab, edge of a scalpel blade, or scalp brush.7 Because treatment can require weeks of medication, diagnosis should be confirmed with a KOH or culture when possible.
Newer antifungalsprovide a Tx advantage
Oral antifungal medications are the treatment of choice for tinea capitis. Newer antifungals, such as terbinafine and fluconazole, require a 3- to 6-week course compared to the standard 6- to 8-week course of griseofulvin.1 Also, antifungal shampoos—such as those that contain selenium sulfide—may be used for topical treatment but only as adjuvant therapy.1,2
For our patient, we dispensed a 3-week course of oral fluconazole, 3 to 6 mg/kg, to be given daily by his parents. We also recommended the use of an antidandruff shampoo, if possible. The treatment outcome was not known because our team’s humanitarian global health trip had ended.
1. Usatine R, Smith MA, Mayeaux Jr EJ, Chumley HS. The Color Atlas and Synopsis of Family Medicine. 3rd ed. New York, NY: McGraw-Hill; 2019.
2. Handler MZ. Tinea capitis. Medscape. https://emedicine.medscape.com/article/1091351-overview. Updated February 21, 2020. Accessed November 30, 2020.
3. Hernández-Bel P, Malvehy J, Crocker A, et al. Comma hairs: a new dermoscopic marker for tinea capitis [in Spanish]. Actas Dermosifiliogr. 2012;103:836-837.
4. Mirmirani P, Lue-Yen T. Epidemiologic trends in pediatric tinea capitis: a population-based study from Kaiser Permanente Northern California. J Am Acad Dermatol. 2013;69:916-921.
5. Mikaeili A, Kavaoussi H, Hashemian AH, et al. Clinico-mycological profile of tinea capitis and its comparative response to griseofulvin versus terbinafine. Curr Med Mycol. 2019;5:15-20.
6. Slowinska M, Rudnicka L, Schwartz RA, et al. Comma hairs: a dermatoscopic marker for tinea capitis: a rapid diagnostic method. Journal of the American Academy of Dermatology. 2008;59(suppl 5):S77-S79.
An 11-year-old boy sought care at a small village’s health center in Panama for scalp itching and subtle hair loss. He was seen by a family physician (RU) and a team of medical students who were there as part of a humanitarian trip. The patient denied any hair pulling. He had a history of treatment for head lice.
Our physical examination revealed mild alopecia and scaling on the scalp (FIGURE 1), but what we saw through the dermatoscope (FIGURE 2) made the diagnosis clear.
WHAT IS YOUR DIAGNOSIS?
HOW WOULD YOU TREAT THIS PATIENT?
Diagnosis: Tinea capitis
On dermatoscopic examination (10× magnification), there were numerous “black dots” or broken hair shafts within patches of hair loss (FIGURE 3), which is indicative of tinea capitis.1,2 This condition causes hair shafts to break, creating “comma hairs” and black dots. The hairs are uniform in thickness and color and bend distally, like a comma.3
Tinea capitis (commonly called ringworm of the scalp) is a fungal infection caused by Trichophyton and Microsporum dermatophytes. It is the most common pediatric dermatophyte infection in the world; the usual age of onset is 5 to 10 years.2 The incidence of tinea capitis in the United States is not known because cases are no longer registered by public health agencies. That said, a Northern California study that tracked occurrences in children younger than 15 years from 1998 to 2007 found that the incidence was on the decline and lower in girls compared to boys (111.9 vs 146.4, respectively, in 1998; 27.9 vs 39.9, respectively, in 2007).4 Incidence rates were calculated per 10,000 eligible children.4
Tinea capitis can spread by contact with infected individuals and contaminated objects, including combs, towels, toys, and bedding.1 Fungal spores can remain viable on these surfaces for months.
In a study of 69 patients with tinea capitis (23 females, 46 males; mean age, 12 years), the risk factors for spreading infection included participation in sports, contact with an animal, a recent haircut, and use of a swimming pool.5
4 conditions you’ll want to rule out
The following conditions should be considered as part of the differential when a patient presents with an itchy scalp and/or hair loss.
Continue to: Psoriasis of the scalp...
Psoriasis of the scalp is characterized by scaling of the scalp along with crusted plaques. It is often accompanied by similar psoriatic plaques on the elbows, knees, and other areas of the body. Examination of our patient showed no psoriatic plaques.
Seborrhea of the scalp (also known as dandruff) is a very common diagnosis. However, it is unlikely to cause hair loss. It has widespread involvement of the scalp compared to tinea capitis, which is local and patchy. Our patient’s patches of hair loss indicated that seborrhea was unlikely.
Alopecia areata. Individuals develop this condition due to an autoimmune process affecting hair follicles. However, the resulting hair loss does not cause significant scaling, inflammation, scarring, or pain in the affected area. Further, this condition can cause the loss of the entire hair shaft.
Trichotillomania is an impulse control disorder that causes patients to pull out their own hair. There is no scaling of the scalp in this condition.
A dermatoscope can beuseful in making the Dx
Although clinical appearance and patient presentation are adequate to establish the diagnosis of tinea capitis, this case demonstrates the utility of a dermatoscope in making the diagnosis of tinea capitis. Previous studies have shown that dermoscopy allows for rapid identification of the broken hair shafts, which are a key distinction from alopecia areata.3,6
Microscopic inspection. Samples from the scaling of the scalp can be examined with potassium hydroxide (KOH) on a microscope slide. Hyphae, spores, and endo/ectothrix invasion can be seen through the microsope.
Continue to: Laboratory testing is helpful, but not needed.
Laboratory testing is helpful, but not needed. Testing for tinea capitis would require that you obtain a sample from the affected area using a swab, edge of a scalpel blade, or scalp brush.7 Because treatment can require weeks of medication, diagnosis should be confirmed with a KOH or culture when possible.
Newer antifungalsprovide a Tx advantage
Oral antifungal medications are the treatment of choice for tinea capitis. Newer antifungals, such as terbinafine and fluconazole, require a 3- to 6-week course compared to the standard 6- to 8-week course of griseofulvin.1 Also, antifungal shampoos—such as those that contain selenium sulfide—may be used for topical treatment but only as adjuvant therapy.1,2
For our patient, we dispensed a 3-week course of oral fluconazole, 3 to 6 mg/kg, to be given daily by his parents. We also recommended the use of an antidandruff shampoo, if possible. The treatment outcome was not known because our team’s humanitarian global health trip had ended.
An 11-year-old boy sought care at a small village’s health center in Panama for scalp itching and subtle hair loss. He was seen by a family physician (RU) and a team of medical students who were there as part of a humanitarian trip. The patient denied any hair pulling. He had a history of treatment for head lice.
Our physical examination revealed mild alopecia and scaling on the scalp (FIGURE 1), but what we saw through the dermatoscope (FIGURE 2) made the diagnosis clear.
WHAT IS YOUR DIAGNOSIS?
HOW WOULD YOU TREAT THIS PATIENT?
Diagnosis: Tinea capitis
On dermatoscopic examination (10× magnification), there were numerous “black dots” or broken hair shafts within patches of hair loss (FIGURE 3), which is indicative of tinea capitis.1,2 This condition causes hair shafts to break, creating “comma hairs” and black dots. The hairs are uniform in thickness and color and bend distally, like a comma.3
Tinea capitis (commonly called ringworm of the scalp) is a fungal infection caused by Trichophyton and Microsporum dermatophytes. It is the most common pediatric dermatophyte infection in the world; the usual age of onset is 5 to 10 years.2 The incidence of tinea capitis in the United States is not known because cases are no longer registered by public health agencies. That said, a Northern California study that tracked occurrences in children younger than 15 years from 1998 to 2007 found that the incidence was on the decline and lower in girls compared to boys (111.9 vs 146.4, respectively, in 1998; 27.9 vs 39.9, respectively, in 2007).4 Incidence rates were calculated per 10,000 eligible children.4
Tinea capitis can spread by contact with infected individuals and contaminated objects, including combs, towels, toys, and bedding.1 Fungal spores can remain viable on these surfaces for months.
In a study of 69 patients with tinea capitis (23 females, 46 males; mean age, 12 years), the risk factors for spreading infection included participation in sports, contact with an animal, a recent haircut, and use of a swimming pool.5
4 conditions you’ll want to rule out
The following conditions should be considered as part of the differential when a patient presents with an itchy scalp and/or hair loss.
Continue to: Psoriasis of the scalp...
Psoriasis of the scalp is characterized by scaling of the scalp along with crusted plaques. It is often accompanied by similar psoriatic plaques on the elbows, knees, and other areas of the body. Examination of our patient showed no psoriatic plaques.
Seborrhea of the scalp (also known as dandruff) is a very common diagnosis. However, it is unlikely to cause hair loss. It has widespread involvement of the scalp compared to tinea capitis, which is local and patchy. Our patient’s patches of hair loss indicated that seborrhea was unlikely.
Alopecia areata. Individuals develop this condition due to an autoimmune process affecting hair follicles. However, the resulting hair loss does not cause significant scaling, inflammation, scarring, or pain in the affected area. Further, this condition can cause the loss of the entire hair shaft.
Trichotillomania is an impulse control disorder that causes patients to pull out their own hair. There is no scaling of the scalp in this condition.
A dermatoscope can beuseful in making the Dx
Although clinical appearance and patient presentation are adequate to establish the diagnosis of tinea capitis, this case demonstrates the utility of a dermatoscope in making the diagnosis of tinea capitis. Previous studies have shown that dermoscopy allows for rapid identification of the broken hair shafts, which are a key distinction from alopecia areata.3,6
Microscopic inspection. Samples from the scaling of the scalp can be examined with potassium hydroxide (KOH) on a microscope slide. Hyphae, spores, and endo/ectothrix invasion can be seen through the microsope.
Continue to: Laboratory testing is helpful, but not needed.
Laboratory testing is helpful, but not needed. Testing for tinea capitis would require that you obtain a sample from the affected area using a swab, edge of a scalpel blade, or scalp brush.7 Because treatment can require weeks of medication, diagnosis should be confirmed with a KOH or culture when possible.
Newer antifungalsprovide a Tx advantage
Oral antifungal medications are the treatment of choice for tinea capitis. Newer antifungals, such as terbinafine and fluconazole, require a 3- to 6-week course compared to the standard 6- to 8-week course of griseofulvin.1 Also, antifungal shampoos—such as those that contain selenium sulfide—may be used for topical treatment but only as adjuvant therapy.1,2
For our patient, we dispensed a 3-week course of oral fluconazole, 3 to 6 mg/kg, to be given daily by his parents. We also recommended the use of an antidandruff shampoo, if possible. The treatment outcome was not known because our team’s humanitarian global health trip had ended.
1. Usatine R, Smith MA, Mayeaux Jr EJ, Chumley HS. The Color Atlas and Synopsis of Family Medicine. 3rd ed. New York, NY: McGraw-Hill; 2019.
2. Handler MZ. Tinea capitis. Medscape. https://emedicine.medscape.com/article/1091351-overview. Updated February 21, 2020. Accessed November 30, 2020.
3. Hernández-Bel P, Malvehy J, Crocker A, et al. Comma hairs: a new dermoscopic marker for tinea capitis [in Spanish]. Actas Dermosifiliogr. 2012;103:836-837.
4. Mirmirani P, Lue-Yen T. Epidemiologic trends in pediatric tinea capitis: a population-based study from Kaiser Permanente Northern California. J Am Acad Dermatol. 2013;69:916-921.
5. Mikaeili A, Kavaoussi H, Hashemian AH, et al. Clinico-mycological profile of tinea capitis and its comparative response to griseofulvin versus terbinafine. Curr Med Mycol. 2019;5:15-20.
6. Slowinska M, Rudnicka L, Schwartz RA, et al. Comma hairs: a dermatoscopic marker for tinea capitis: a rapid diagnostic method. Journal of the American Academy of Dermatology. 2008;59(suppl 5):S77-S79.
1. Usatine R, Smith MA, Mayeaux Jr EJ, Chumley HS. The Color Atlas and Synopsis of Family Medicine. 3rd ed. New York, NY: McGraw-Hill; 2019.
2. Handler MZ. Tinea capitis. Medscape. https://emedicine.medscape.com/article/1091351-overview. Updated February 21, 2020. Accessed November 30, 2020.
3. Hernández-Bel P, Malvehy J, Crocker A, et al. Comma hairs: a new dermoscopic marker for tinea capitis [in Spanish]. Actas Dermosifiliogr. 2012;103:836-837.
4. Mirmirani P, Lue-Yen T. Epidemiologic trends in pediatric tinea capitis: a population-based study from Kaiser Permanente Northern California. J Am Acad Dermatol. 2013;69:916-921.
5. Mikaeili A, Kavaoussi H, Hashemian AH, et al. Clinico-mycological profile of tinea capitis and its comparative response to griseofulvin versus terbinafine. Curr Med Mycol. 2019;5:15-20.
6. Slowinska M, Rudnicka L, Schwartz RA, et al. Comma hairs: a dermatoscopic marker for tinea capitis: a rapid diagnostic method. Journal of the American Academy of Dermatology. 2008;59(suppl 5):S77-S79.
A new model of care to return holism to family medicine
Here is our problem: Family medicine has allowed itself, and its patients, to be picked apart by the forces of reductionism and a system that profits from the sick and suffering. We have lost sight of our purpose and our vision to care for the whole person. We have lost our way as healers.
The result is not only a decline in the specialty of family medicine as a leader in primary care but declining value and worsening outcomes in health care overall. We need to get our mojo back. We can do this by focusing less on trying to be all things to all people at all times, and more on creating better models for preventing, managing, and reversing chronic disease. This means providing health care that is person centered, relationship based, recovery focused, and paid for comprehensively.
I call this model Advanced Primary Care, or APC (FIGURE). In this article, I describe exemplars of APC from across the United States. I also provide tools to help you recover its central feature, holism—care of the whole person in mind, body, community, and spirit—in your practice, thus returning us to the core purpose of family medicine.
Holism is central to family medicine
More than 40 years ago, psychiatrist George Engel, MD, published a seminal article in Science that inspired a radical vision of how health care should be practiced.1 Called the biopsychosocial model, it stated what, in some ways, is obvious: Human beings are complex organisms embedded in complex environments made up of distinct, yet interacting, dimensions. These dimensions included physical, psychological, and social components. Engel’s radical proposition was that these dimensions are definable and measurable and that good medicine cannot afford to ignore any of them.
Engel’s assertion that good medicine requires holism was a clarion call during a time of rapidly expanding knowledge and subspecialization. That call was the inspiration for a new medical specialty called family medicine, which dared to proclaim that the best way to heal was to care for the whole person within the context of that person’s emotional and social environment. Family medicine reinvigorated primary care and grew rapidly, becoming a preeminent primary care specialty in the United States.
Continue to : Reductionism is relentless
Reductionism is relentless
But the forces of medicine were—and still are—driving relentlessly the other way. The science of the small and particular (reductionism), with dazzling technology and exploding subspecialty knowledge, and backed by powerful economic drivers, rewards health care for pulling the patient and the medical profession apart. We pay more to those who treat small parts of a person over a short period than to those who attend to the whole person over the lifetime.
Today, family medicine—for all of its common sense, scientific soundness, connectedness to patients, and demonstrated value—struggles to survive.2-6 The holistic vision of Engel is declining. The struggle in primary care is that its holistic vision gets co-opted by specialized medical science—and then it desperately attempts to apply those small and specialized tools to the care of patients in their wholeness. Holism is largely dead in health care, and everyone pays the consequences.7
Health care is losing its value
The damage from this decline in holism is not just to primary care but to the value of health care in general. Most medical care being delivered today—comprising diagnosis, treatment, and payment (the innermost circle of the FIGURE)—is not producing good health.8 Only 15% to 20% of the healing of an individual or a population comes from health care.9 The rest—nearly 80%—comes from other factors rarely addressed in the health care system: behavioral and lifestyle choices that people make in their daily life, including those related to food, movement, sleep, stress, and substance use.10 Increasingly, it is the economic and social determinants of health that influence this behavior and have a greater impact on health and lifespan than physiology or genes.11 The same social determinants of health also influence patients’ ability to obtain medical care and pursue a meaningful life.12
The result of this decline in holism and in the value of health care in general has been a relentless rise in the cost of medical care13-15 and the need for social services; declining life expectancy16,17 and quality of life18; growing patient dissatisfaction; and burnout in providers.19,20 Health care has become, as investor and business leader Warren Buffet remarked, the “tapeworm” of the economy and a major contributor to growing disparities in health and well-being between the haves and have-nots.21 Engel’s prediction that good medicine cannot afford to ignore holism has come to pass.
3-step solution:Return to whole-person care
Family medicine needs to return to whole-person care, but it can do so only if it attends to, and effectively delivers on, the prevention, treatment, and reversal of chronic disease and the enhancement of health and well-being. This can happen only if family medicine stops trying to be all things to all people at all times and, instead, focuses on what matters to the patient as a person.
Continue to: This means that the core...
This means that the core interaction in family medicine must be to assess the whole person—mind, body, social, spirit—and help that person make changes that improve his/her/their health and well-being based on his/her/their individualized needs and social context. In other words, family medicine needs to deliver a holistic model of APC that is person centered, relationship based, recovery focused, and paid for comprehensively.
How does one get from “standard” primary care of today (the innermost circle of the FIGURE) to a framework that truly delivers on the promise of healing? I propose 3 steps to return holism to family medicine.
STEP 1: Start with comprehensive, coordinated primary care. We know that this works. Starfield and others demonstrated this 2 decades ago, defining and devising what we know as quality primary care—characterized by first-contact care, comprehensive primary care (CPC), continuous care, and coordinated care.22 This type of primary care improves outcomes, lowers costs, and is satisfying to patients and providers.23 The physician cares for the patient throughout that person’s entire life cycle and provides all evidence-based services needed to prevent and treat common conditions. Comprehensive primary care is positioned in the first circle outward from the innermost circle of the FIGURE.
As medicine has become increasingly complex and subspecialized, however, the ability to coordinate care is often frayed, adding cost and reducing quality.24-26 Today, comprehensive primary care needs enhanced coordination. At a minimum, this means coordinating services for:
- chronic disease management (outpatient and inpatient transitions and emergency department use)
- referral (specialists and tests)
- pharmacy services (including delivery and patient education support).
An example of a primary care system that meets these requirements is the Catalyst Health Network in central Texas, which supplies coordination services to more than 1000 comprehensive primary care practices and 1.5 million patients.27 The Catalyst Network makes money for those practices, saves money in the system, enhances patient and provider satisfaction, and improves population health in the community.27 I call this enhanced primary care (EPC), shown in the second circle out from the innermost circle of the FIGURE.
STEP 2: Add integrative medicine and mental health. EPC improves fragmented care but does not necessarily address a patient’s underlying determinants of healing. We know that health behaviors such as smoking cessation, avoidance of alcohol and drug abuse, improved diet, physical activity, sleep, and stress management contribute 40% to 60% of a person’s and a population’s health.10 In addition, evidence shows that behavioral health services, along with lifestyle change support, can even reverse many chronic diseases seen in primary care, such as obesity, diabetes, hypertension, cardiovascular disease, depression, and substance abuse.28,29
Continue to: Therefore, we need to add...
Therefore, we need to add routine mental health services and nonpharmacotherapeutic approaches (eg, complementary and alternative medicine) to primary care.30 Doing so requires that behavioral change and self-care become a central feature of the doctor–patient dialogue and team skills31 and be added to primary care.30,31 I call this integrative primary care (IPC), shown on the left side in the third circle out from the innermost circle of the FIGURE.
An example of IPC is Whole Health, an initiative of the US Veteran’s Health Administration. Whole Health empowers and informs a person-centered approach and integrates it into the delivery of routine care.32 Evaluation of Whole Health implementation, which involved more than 130,000 veterans followed for 2 years, found a net overall reduction in the total cost of care of 20%—saving nearly $650 million or, on average, more than $4500 per veteran.33
STEP 3: Address social determinants of health. Primary care will not fully be part of the solution for producing health and well-being unless it becomes instrumental in addressing the social determinants of health (SDH), defined as “… conditions in the environments in which people are born, live, learn, work, play, worship, and age that affect a wide range of health, functioning, and quality-of-life outcomes and risks.”34 These determinants include not only basic needs, such as housing, food, safety, and transportation (ie, social needs), but also what are known as structural determinants, such as income, education, language, and racial and ethnic bias. Health care cannot solve all of these social ills,but it is increasingly being called on to be the nexus of coordination for services that address these needs when they affect health outcomes.35,36
Examples of health systems that provide for social needs include the free “food prescription” program of Pennsylvania’s Geisinger Health System, for patients with diabetes who do not have the resources to pay for food.37 This approach improves blood glucose control by patients and saves money on medications and other interventions. Similarly, Kaiser Permanente has experimented with housing vouchers for homeless patients,and most Federally Qualified Health Centers provide bus or other transportation tickets to patients for their appointments and free or discounted tests and specialty care.38
Implementing whole-person care for all
I propose that we make APC the central focus of family medicine. This model would comprise CPC, plus EPC, IPC, and community coordination to address SDH. This is expressed as:
CPC + EPC + IPC + SDH = APC
Continue to: APC would mean...
APC would mean health for the whole person and for all people. Again, the FIGURE shows how this model, encompassing the entire third circle out from the center circle, could be created from current models of care.
How do we pay for this? We already do—and way too much. The problem is not lack of money in the health care system but how it is organized and distributed. The Centers for Medicare and Medicaid Services and other payers are developing value-based payment models to help cover this type of care,39 but payers cannot pay for something if it is unavailable.
Can family physicians deliver APC? I believe they can, and have given a few examples here to show how this is already happening. To help primary care providers start to deliver APC in their system, my team and I have built the HOPE (Healing Oriented Practices & Environments) Note Toolkit to use in daily practice.40 These and other tools are being used by a number of large hospital systems and health care networks around the country. (You can download the HOPE Note Toolkit, at no cost, at https://drwaynejonas.com/resources/hope-note/.)
Whatever we call this new type of primary care, it needs to care for the whole person and to be available to all. It finds expression in these assertions:
- We cannot ignore an essential part of what a human being is and expect them to heal or become whole.
- We cannot ignore essential people in our communities and expect our costs to go down or our compassion to go up.
- We need to stop allowing family medicine to be co-opted by reductionism and its profits.
In sum, we need a new vision of primary care—like Engel’s holistic vision in the 1970s—to motivate us, and we need to return to fundamental concepts of how healing works in medicine.41
CORRESPONDENCE
Wayne B. Jonas, MD, Samueli Integrative Health Programs, 1800 Diagonal Road, Suite 617, Alexandria, VA 22314; [email protected].
1. Engel GL. The need for a new medical model: a challenge for biomedicine. Science. 1977;196:129-136.
2. Schwartz MD, Durning S, Linzer M, et al. Changes in medical students’ views of internal medicine careers from 1990 to 2007. Arch Intern Med. 2011;171:744-749.
3. Bronchetti ET, Christensen GS, Hoynes HW. Local food prices, SNAP purchasing power, and child health. Cambridge, MA: National Bureau of Economic Research. June 2018. www.nber.org/papers/w24762?mc_cid=8c7211d34b&mc_eid=fbbc7df813. Accessed November 24, 2020.
4. Federal Student Aid, US Department of Education. Public Service Loan Forgiveness (PSLF). 2018. https://studentaid.ed.gov/sa/repay-loans/forgiveness-cancellation/public-service. Accessed November 24, 2020.
5. Aten B, Figueroa E, Martin T. Notes on estimating the multi-year regional price parities by 16 expenditure categories: 2005-2009. WP2011-03. Washington, DC: Bureau of Economic Analysis, US Department of Commerce; April 2011. www.bea.gov/system/files/papers/WP2011-3.pdf. Accessed November 24, 2020.
6. Aten BH, Figueroa EB, Martin TM. Regional price parities for states and metropolitan areas, 2006-2010. Washington, DC: Bureau of Economic Analysis, US Department of Commerce; August 2012. https://apps.bea.gov/scb/pdf/2012/08%20August/0812_regional_price_parities.pdf. Accessed November 24, 2020.
7. Stange KC, Ferrer RL. The paradox of primary care. Ann Fam Med. 2009;7:293-299.
8. Panel on Understanding Cross-national Health Differences Among High-income Countries, Committee on Population, Division of Behavioral and Social Sciences and Education, and Board on Population Health and Public Health Practice, National Research Council and Institute of Medicine of the National Academies. US Health in International Perspective: Shorter Lives, Poorer Health. Woolf SH, Aron L, eds. The National Academies Press; 2013.
9. Hood CM, Gennuso KP, Swain GR, et al. County health rankings: relationships between determinant factors and health outcomes. Am J Prev Med. 2016;50:129-135.
10. McGinnis JM, Williams-Russo P, Knickman JR. The case for more active policy attention to health promotion. Health Aff (Millwood). 2002;21:78-93.
11. Roeder A. Zip code better predictor of health than genetic code. Harvard T. H. Chan School of Public Health Web site. News release. August 4, 2014. www.hsph.harvard.edu/news/features/zip-code-better-predictor-of-health-than-genetic-code/. Accessed November 24, 2020.
12. US health map. Seattle, WA: University of Washington Institute for Health Metrics and Evaluation; March 13, 2018. www.healthdata.org/data-visualization/us-health-map. Accessed November 24, 2020.
13. Highfill T. Comparing estimates of U.S. health care expenditures by medical condition, 2000-2012. Survey of Current Business. 2016;1-5. https://apps.bea.gov/scb/pdf/2016/3%20March/0316_comparing_u.s._health_care_expenditures_by_medical_condition.pdf. Accessed November 24, 2020.
14. Waters H, Graf M. The Costs of Chronic Disease in the US. Washington, DC: Milken Institute; August 2018. https://milkeninstitute.org/sites/default/files/reports-pdf/ChronicDiseases-HighRes-FINAL.pdf. Accessed November 24, 2020.
15. Meyer H. Health care spending will hit 19.4% of GDP in the next decade, CMS projects. Modern Health care. February 20, 2019. www.modernhealthcare.com/article/20190220/NEWS/190229989/healthcare-spending-will-hit-19-4-of-gdp-in-the-next-decade-cms-projects. Accessed November 24, 2020.
16. Woolf SH, Schoomaker H. Life expectancy and mortality rates in the United States, 1959-2017. JAMA. 2019;322:1996-2016.
17. Basu S, Berkowitz SA, Phillips RL, et al. Association of primary care physician supply with population mortality in the United States, 2005-2015. JAMA Intern Med. 2019;179:506-514.
18. Zack MM, Moriarty DG, Stroup DF, et al. Worsening trends in adult health-related quality of life and self-rated health—United States, 1993–2001. Public Health Rep. 2004;119:493-505.
19. Windover AK, Martinez K, Mercer, MB, et al. Correlates and outcomes of physician burnout within a large academic medical center. Research letter. JAMA Intern Med. 2018;178:856-858.
20. West CP, Dyrbye LN, Shanafelt TD. Physician burnout: contributors, consequences and solutions. J Intern Med. 2018;283:516-529.
21. Buffett: Health care is a tapeworm on the economic system. CNBC Squawk Box. February 26, 2018. www.cnbc.com/video/2018/02/26/buffett-health-care-is-a-tapeworm-on-the-economic-system.html. Accessed November 24, 2020.
22. Starfield B. Primary Care: Concept, Evaluation, and Policy. Oxford University Press; 1992.
23. Starfield B, Shi L, Macinko J. Contribution of primary care to health systems and health. Milbank Q. 2005;83:457-502.
24. Institute of Medicine (US) Committee on Quality of Health Care in America. Crossing the Quality Chasm: A New Health System for the 21st Century. National Academies Press (US); 2001.
25. Burton R. Health policy brief: improving care transitions. Health Affairs. September 13, 2012. www.healthaffairs.org/do/10.1377/hpb20120913.327236/full/healthpolicybrief_76.pdf. Accessed November 24, 2020.
26. Toulany A, Stukel TA, Kurdyak P, et al. Association of primary care continuity with outcomes following transition to adult care for adolescents with severe mental illness. JAMA Netw Open. 2019;2:e198415.
27. Helping communities thrive. Catalyst Health Network Web site. www.catalysthealthnetwork.com/. Accessed November 24, 2020.
28. Diabetes Prevention Program (DPP) Research Group. The Diabetes Prevention Program (DPP): description of lifestyle intervention. Diabetes Care. 2002;25:2165-2171.
29. Scherger JE. Lean and Fit: A Doctor’s Journey to Healthy Nutrition and Greater Wellness. 2nd ed. Scotts Valley, CA: CreateSpace Publishing; 2016.
30. Qaseem A, Wilt TJ, McLean RM, et al; . Noninvasive treatments for acute, subacute, and chronic low back pain: a clinical practice guideline from the American College of Physicians. Ann Intern Med. 2017;166:514-530.
31. Hibbard JH, Greene J. What the evidence shows about patient activation: better health outcomes and care experiences; fewer data on costs. Health Aff (Millwood). 2013;32:207-214.
32. What is whole health? Washington, DC: US Department of Veterans Affairs. October 13, 2020. www.va.gov/patientcenteredcare/explore/about-whole-health.asp. Accessed November 25, 2020.
33. COVER Commission. Creating options for veterans’ expedited recovery. Final report. Washington, DC: US Veterans Administration. January 24, 2020. www.va.gov/COVER/docs/COVER-Commission-Final-Report-2020-01-24.pdf. Accessed November 24, 2020.
34. Social determinants of health. Washington, DC: Office of Disease Prevention and Health Promotion, US Department of Health and Human Services. HealthyPeople.gov Web site. www.healthypeople.gov/2020/topics-objectives/topic/social-determinants-of-health. Accessed November 24, 2020.
35. Breslin E, Lambertino A. Medicaid and social determinants of health: adjusting payment and measuring health outcomes. Princeton University Woodrow Wilson School of Public and International Affairs, State Health and Value Strategies Program Web site. July 2017. www.shvs.org/wp-content/uploads/2017/07/SHVS_SocialDeterminants_HMA_July2017.pdf. Accessed November 24, 2020.
36. James CV. Actively addressing social determinants of health will help us achieve health equity. US Centers for Medicare & Medicaid Services Web site. April 26, 2019. www.cms.gov/blog/actively-addressing-social-determinants-health-will-help-us-achieve-health-equity. Accessed November 24, 2020.
37. Geisinger receives “Innovation in Advancing Health Equity” award. Geisinger Health Web site. April 24, 2018. www.geisinger.org/health-plan/news-releases/2018/04/23/19/28/geisinger-receives-innovation-in-advancing-health-equity-award. Accessed November 24, 2020.
38. Bresnick J. Kaiser Permanente launches full-network social determinants program. HealthITAnalytics Web site. May 6, 2019. https://healthitanalytics.com/news/kaiser-permanente-launches-full-network-social-determinants-program. Accessed November 25, 2020.
39. Medicare Payment Advisory Commission (MEDPAC). Physician and other health Professional services. In: Report to the Congress: Medicare Payment Policy. March 2016: 115-117. http://medpac.gov/docs/default-source/reports/chapter-4-physician-and-other-health-professional-services-march-2016-report-.pdf. Accessed November 24, 2020.
40. Jonas W. Helping patients with chronic diseases and conditions heal with the HOPE Note: integrative primary care case study. https://drwaynejonas.com/wp-content/uploads/2018/09/CS_HOPE-Note_FINAL.pdf. Accessed November 24, 2020.
41. Jonas W. How Healing Works. Berkley, CA: Lorena Jones Books; 2018.
Here is our problem: Family medicine has allowed itself, and its patients, to be picked apart by the forces of reductionism and a system that profits from the sick and suffering. We have lost sight of our purpose and our vision to care for the whole person. We have lost our way as healers.
The result is not only a decline in the specialty of family medicine as a leader in primary care but declining value and worsening outcomes in health care overall. We need to get our mojo back. We can do this by focusing less on trying to be all things to all people at all times, and more on creating better models for preventing, managing, and reversing chronic disease. This means providing health care that is person centered, relationship based, recovery focused, and paid for comprehensively.
I call this model Advanced Primary Care, or APC (FIGURE). In this article, I describe exemplars of APC from across the United States. I also provide tools to help you recover its central feature, holism—care of the whole person in mind, body, community, and spirit—in your practice, thus returning us to the core purpose of family medicine.
Holism is central to family medicine
More than 40 years ago, psychiatrist George Engel, MD, published a seminal article in Science that inspired a radical vision of how health care should be practiced.1 Called the biopsychosocial model, it stated what, in some ways, is obvious: Human beings are complex organisms embedded in complex environments made up of distinct, yet interacting, dimensions. These dimensions included physical, psychological, and social components. Engel’s radical proposition was that these dimensions are definable and measurable and that good medicine cannot afford to ignore any of them.
Engel’s assertion that good medicine requires holism was a clarion call during a time of rapidly expanding knowledge and subspecialization. That call was the inspiration for a new medical specialty called family medicine, which dared to proclaim that the best way to heal was to care for the whole person within the context of that person’s emotional and social environment. Family medicine reinvigorated primary care and grew rapidly, becoming a preeminent primary care specialty in the United States.
Continue to : Reductionism is relentless
Reductionism is relentless
But the forces of medicine were—and still are—driving relentlessly the other way. The science of the small and particular (reductionism), with dazzling technology and exploding subspecialty knowledge, and backed by powerful economic drivers, rewards health care for pulling the patient and the medical profession apart. We pay more to those who treat small parts of a person over a short period than to those who attend to the whole person over the lifetime.
Today, family medicine—for all of its common sense, scientific soundness, connectedness to patients, and demonstrated value—struggles to survive.2-6 The holistic vision of Engel is declining. The struggle in primary care is that its holistic vision gets co-opted by specialized medical science—and then it desperately attempts to apply those small and specialized tools to the care of patients in their wholeness. Holism is largely dead in health care, and everyone pays the consequences.7
Health care is losing its value
The damage from this decline in holism is not just to primary care but to the value of health care in general. Most medical care being delivered today—comprising diagnosis, treatment, and payment (the innermost circle of the FIGURE)—is not producing good health.8 Only 15% to 20% of the healing of an individual or a population comes from health care.9 The rest—nearly 80%—comes from other factors rarely addressed in the health care system: behavioral and lifestyle choices that people make in their daily life, including those related to food, movement, sleep, stress, and substance use.10 Increasingly, it is the economic and social determinants of health that influence this behavior and have a greater impact on health and lifespan than physiology or genes.11 The same social determinants of health also influence patients’ ability to obtain medical care and pursue a meaningful life.12
The result of this decline in holism and in the value of health care in general has been a relentless rise in the cost of medical care13-15 and the need for social services; declining life expectancy16,17 and quality of life18; growing patient dissatisfaction; and burnout in providers.19,20 Health care has become, as investor and business leader Warren Buffet remarked, the “tapeworm” of the economy and a major contributor to growing disparities in health and well-being between the haves and have-nots.21 Engel’s prediction that good medicine cannot afford to ignore holism has come to pass.
3-step solution:Return to whole-person care
Family medicine needs to return to whole-person care, but it can do so only if it attends to, and effectively delivers on, the prevention, treatment, and reversal of chronic disease and the enhancement of health and well-being. This can happen only if family medicine stops trying to be all things to all people at all times and, instead, focuses on what matters to the patient as a person.
Continue to: This means that the core...
This means that the core interaction in family medicine must be to assess the whole person—mind, body, social, spirit—and help that person make changes that improve his/her/their health and well-being based on his/her/their individualized needs and social context. In other words, family medicine needs to deliver a holistic model of APC that is person centered, relationship based, recovery focused, and paid for comprehensively.
How does one get from “standard” primary care of today (the innermost circle of the FIGURE) to a framework that truly delivers on the promise of healing? I propose 3 steps to return holism to family medicine.
STEP 1: Start with comprehensive, coordinated primary care. We know that this works. Starfield and others demonstrated this 2 decades ago, defining and devising what we know as quality primary care—characterized by first-contact care, comprehensive primary care (CPC), continuous care, and coordinated care.22 This type of primary care improves outcomes, lowers costs, and is satisfying to patients and providers.23 The physician cares for the patient throughout that person’s entire life cycle and provides all evidence-based services needed to prevent and treat common conditions. Comprehensive primary care is positioned in the first circle outward from the innermost circle of the FIGURE.
As medicine has become increasingly complex and subspecialized, however, the ability to coordinate care is often frayed, adding cost and reducing quality.24-26 Today, comprehensive primary care needs enhanced coordination. At a minimum, this means coordinating services for:
- chronic disease management (outpatient and inpatient transitions and emergency department use)
- referral (specialists and tests)
- pharmacy services (including delivery and patient education support).
An example of a primary care system that meets these requirements is the Catalyst Health Network in central Texas, which supplies coordination services to more than 1000 comprehensive primary care practices and 1.5 million patients.27 The Catalyst Network makes money for those practices, saves money in the system, enhances patient and provider satisfaction, and improves population health in the community.27 I call this enhanced primary care (EPC), shown in the second circle out from the innermost circle of the FIGURE.
STEP 2: Add integrative medicine and mental health. EPC improves fragmented care but does not necessarily address a patient’s underlying determinants of healing. We know that health behaviors such as smoking cessation, avoidance of alcohol and drug abuse, improved diet, physical activity, sleep, and stress management contribute 40% to 60% of a person’s and a population’s health.10 In addition, evidence shows that behavioral health services, along with lifestyle change support, can even reverse many chronic diseases seen in primary care, such as obesity, diabetes, hypertension, cardiovascular disease, depression, and substance abuse.28,29
Continue to: Therefore, we need to add...
Therefore, we need to add routine mental health services and nonpharmacotherapeutic approaches (eg, complementary and alternative medicine) to primary care.30 Doing so requires that behavioral change and self-care become a central feature of the doctor–patient dialogue and team skills31 and be added to primary care.30,31 I call this integrative primary care (IPC), shown on the left side in the third circle out from the innermost circle of the FIGURE.
An example of IPC is Whole Health, an initiative of the US Veteran’s Health Administration. Whole Health empowers and informs a person-centered approach and integrates it into the delivery of routine care.32 Evaluation of Whole Health implementation, which involved more than 130,000 veterans followed for 2 years, found a net overall reduction in the total cost of care of 20%—saving nearly $650 million or, on average, more than $4500 per veteran.33
STEP 3: Address social determinants of health. Primary care will not fully be part of the solution for producing health and well-being unless it becomes instrumental in addressing the social determinants of health (SDH), defined as “… conditions in the environments in which people are born, live, learn, work, play, worship, and age that affect a wide range of health, functioning, and quality-of-life outcomes and risks.”34 These determinants include not only basic needs, such as housing, food, safety, and transportation (ie, social needs), but also what are known as structural determinants, such as income, education, language, and racial and ethnic bias. Health care cannot solve all of these social ills,but it is increasingly being called on to be the nexus of coordination for services that address these needs when they affect health outcomes.35,36
Examples of health systems that provide for social needs include the free “food prescription” program of Pennsylvania’s Geisinger Health System, for patients with diabetes who do not have the resources to pay for food.37 This approach improves blood glucose control by patients and saves money on medications and other interventions. Similarly, Kaiser Permanente has experimented with housing vouchers for homeless patients,and most Federally Qualified Health Centers provide bus or other transportation tickets to patients for their appointments and free or discounted tests and specialty care.38
Implementing whole-person care for all
I propose that we make APC the central focus of family medicine. This model would comprise CPC, plus EPC, IPC, and community coordination to address SDH. This is expressed as:
CPC + EPC + IPC + SDH = APC
Continue to: APC would mean...
APC would mean health for the whole person and for all people. Again, the FIGURE shows how this model, encompassing the entire third circle out from the center circle, could be created from current models of care.
How do we pay for this? We already do—and way too much. The problem is not lack of money in the health care system but how it is organized and distributed. The Centers for Medicare and Medicaid Services and other payers are developing value-based payment models to help cover this type of care,39 but payers cannot pay for something if it is unavailable.
Can family physicians deliver APC? I believe they can, and have given a few examples here to show how this is already happening. To help primary care providers start to deliver APC in their system, my team and I have built the HOPE (Healing Oriented Practices & Environments) Note Toolkit to use in daily practice.40 These and other tools are being used by a number of large hospital systems and health care networks around the country. (You can download the HOPE Note Toolkit, at no cost, at https://drwaynejonas.com/resources/hope-note/.)
Whatever we call this new type of primary care, it needs to care for the whole person and to be available to all. It finds expression in these assertions:
- We cannot ignore an essential part of what a human being is and expect them to heal or become whole.
- We cannot ignore essential people in our communities and expect our costs to go down or our compassion to go up.
- We need to stop allowing family medicine to be co-opted by reductionism and its profits.
In sum, we need a new vision of primary care—like Engel’s holistic vision in the 1970s—to motivate us, and we need to return to fundamental concepts of how healing works in medicine.41
CORRESPONDENCE
Wayne B. Jonas, MD, Samueli Integrative Health Programs, 1800 Diagonal Road, Suite 617, Alexandria, VA 22314; [email protected].
Here is our problem: Family medicine has allowed itself, and its patients, to be picked apart by the forces of reductionism and a system that profits from the sick and suffering. We have lost sight of our purpose and our vision to care for the whole person. We have lost our way as healers.
The result is not only a decline in the specialty of family medicine as a leader in primary care but declining value and worsening outcomes in health care overall. We need to get our mojo back. We can do this by focusing less on trying to be all things to all people at all times, and more on creating better models for preventing, managing, and reversing chronic disease. This means providing health care that is person centered, relationship based, recovery focused, and paid for comprehensively.
I call this model Advanced Primary Care, or APC (FIGURE). In this article, I describe exemplars of APC from across the United States. I also provide tools to help you recover its central feature, holism—care of the whole person in mind, body, community, and spirit—in your practice, thus returning us to the core purpose of family medicine.
Holism is central to family medicine
More than 40 years ago, psychiatrist George Engel, MD, published a seminal article in Science that inspired a radical vision of how health care should be practiced.1 Called the biopsychosocial model, it stated what, in some ways, is obvious: Human beings are complex organisms embedded in complex environments made up of distinct, yet interacting, dimensions. These dimensions included physical, psychological, and social components. Engel’s radical proposition was that these dimensions are definable and measurable and that good medicine cannot afford to ignore any of them.
Engel’s assertion that good medicine requires holism was a clarion call during a time of rapidly expanding knowledge and subspecialization. That call was the inspiration for a new medical specialty called family medicine, which dared to proclaim that the best way to heal was to care for the whole person within the context of that person’s emotional and social environment. Family medicine reinvigorated primary care and grew rapidly, becoming a preeminent primary care specialty in the United States.
Continue to : Reductionism is relentless
Reductionism is relentless
But the forces of medicine were—and still are—driving relentlessly the other way. The science of the small and particular (reductionism), with dazzling technology and exploding subspecialty knowledge, and backed by powerful economic drivers, rewards health care for pulling the patient and the medical profession apart. We pay more to those who treat small parts of a person over a short period than to those who attend to the whole person over the lifetime.
Today, family medicine—for all of its common sense, scientific soundness, connectedness to patients, and demonstrated value—struggles to survive.2-6 The holistic vision of Engel is declining. The struggle in primary care is that its holistic vision gets co-opted by specialized medical science—and then it desperately attempts to apply those small and specialized tools to the care of patients in their wholeness. Holism is largely dead in health care, and everyone pays the consequences.7
Health care is losing its value
The damage from this decline in holism is not just to primary care but to the value of health care in general. Most medical care being delivered today—comprising diagnosis, treatment, and payment (the innermost circle of the FIGURE)—is not producing good health.8 Only 15% to 20% of the healing of an individual or a population comes from health care.9 The rest—nearly 80%—comes from other factors rarely addressed in the health care system: behavioral and lifestyle choices that people make in their daily life, including those related to food, movement, sleep, stress, and substance use.10 Increasingly, it is the economic and social determinants of health that influence this behavior and have a greater impact on health and lifespan than physiology or genes.11 The same social determinants of health also influence patients’ ability to obtain medical care and pursue a meaningful life.12
The result of this decline in holism and in the value of health care in general has been a relentless rise in the cost of medical care13-15 and the need for social services; declining life expectancy16,17 and quality of life18; growing patient dissatisfaction; and burnout in providers.19,20 Health care has become, as investor and business leader Warren Buffet remarked, the “tapeworm” of the economy and a major contributor to growing disparities in health and well-being between the haves and have-nots.21 Engel’s prediction that good medicine cannot afford to ignore holism has come to pass.
3-step solution:Return to whole-person care
Family medicine needs to return to whole-person care, but it can do so only if it attends to, and effectively delivers on, the prevention, treatment, and reversal of chronic disease and the enhancement of health and well-being. This can happen only if family medicine stops trying to be all things to all people at all times and, instead, focuses on what matters to the patient as a person.
Continue to: This means that the core...
This means that the core interaction in family medicine must be to assess the whole person—mind, body, social, spirit—and help that person make changes that improve his/her/their health and well-being based on his/her/their individualized needs and social context. In other words, family medicine needs to deliver a holistic model of APC that is person centered, relationship based, recovery focused, and paid for comprehensively.
How does one get from “standard” primary care of today (the innermost circle of the FIGURE) to a framework that truly delivers on the promise of healing? I propose 3 steps to return holism to family medicine.
STEP 1: Start with comprehensive, coordinated primary care. We know that this works. Starfield and others demonstrated this 2 decades ago, defining and devising what we know as quality primary care—characterized by first-contact care, comprehensive primary care (CPC), continuous care, and coordinated care.22 This type of primary care improves outcomes, lowers costs, and is satisfying to patients and providers.23 The physician cares for the patient throughout that person’s entire life cycle and provides all evidence-based services needed to prevent and treat common conditions. Comprehensive primary care is positioned in the first circle outward from the innermost circle of the FIGURE.
As medicine has become increasingly complex and subspecialized, however, the ability to coordinate care is often frayed, adding cost and reducing quality.24-26 Today, comprehensive primary care needs enhanced coordination. At a minimum, this means coordinating services for:
- chronic disease management (outpatient and inpatient transitions and emergency department use)
- referral (specialists and tests)
- pharmacy services (including delivery and patient education support).
An example of a primary care system that meets these requirements is the Catalyst Health Network in central Texas, which supplies coordination services to more than 1000 comprehensive primary care practices and 1.5 million patients.27 The Catalyst Network makes money for those practices, saves money in the system, enhances patient and provider satisfaction, and improves population health in the community.27 I call this enhanced primary care (EPC), shown in the second circle out from the innermost circle of the FIGURE.
STEP 2: Add integrative medicine and mental health. EPC improves fragmented care but does not necessarily address a patient’s underlying determinants of healing. We know that health behaviors such as smoking cessation, avoidance of alcohol and drug abuse, improved diet, physical activity, sleep, and stress management contribute 40% to 60% of a person’s and a population’s health.10 In addition, evidence shows that behavioral health services, along with lifestyle change support, can even reverse many chronic diseases seen in primary care, such as obesity, diabetes, hypertension, cardiovascular disease, depression, and substance abuse.28,29
Continue to: Therefore, we need to add...
Therefore, we need to add routine mental health services and nonpharmacotherapeutic approaches (eg, complementary and alternative medicine) to primary care.30 Doing so requires that behavioral change and self-care become a central feature of the doctor–patient dialogue and team skills31 and be added to primary care.30,31 I call this integrative primary care (IPC), shown on the left side in the third circle out from the innermost circle of the FIGURE.
An example of IPC is Whole Health, an initiative of the US Veteran’s Health Administration. Whole Health empowers and informs a person-centered approach and integrates it into the delivery of routine care.32 Evaluation of Whole Health implementation, which involved more than 130,000 veterans followed for 2 years, found a net overall reduction in the total cost of care of 20%—saving nearly $650 million or, on average, more than $4500 per veteran.33
STEP 3: Address social determinants of health. Primary care will not fully be part of the solution for producing health and well-being unless it becomes instrumental in addressing the social determinants of health (SDH), defined as “… conditions in the environments in which people are born, live, learn, work, play, worship, and age that affect a wide range of health, functioning, and quality-of-life outcomes and risks.”34 These determinants include not only basic needs, such as housing, food, safety, and transportation (ie, social needs), but also what are known as structural determinants, such as income, education, language, and racial and ethnic bias. Health care cannot solve all of these social ills,but it is increasingly being called on to be the nexus of coordination for services that address these needs when they affect health outcomes.35,36
Examples of health systems that provide for social needs include the free “food prescription” program of Pennsylvania’s Geisinger Health System, for patients with diabetes who do not have the resources to pay for food.37 This approach improves blood glucose control by patients and saves money on medications and other interventions. Similarly, Kaiser Permanente has experimented with housing vouchers for homeless patients,and most Federally Qualified Health Centers provide bus or other transportation tickets to patients for their appointments and free or discounted tests and specialty care.38
Implementing whole-person care for all
I propose that we make APC the central focus of family medicine. This model would comprise CPC, plus EPC, IPC, and community coordination to address SDH. This is expressed as:
CPC + EPC + IPC + SDH = APC
Continue to: APC would mean...
APC would mean health for the whole person and for all people. Again, the FIGURE shows how this model, encompassing the entire third circle out from the center circle, could be created from current models of care.
How do we pay for this? We already do—and way too much. The problem is not lack of money in the health care system but how it is organized and distributed. The Centers for Medicare and Medicaid Services and other payers are developing value-based payment models to help cover this type of care,39 but payers cannot pay for something if it is unavailable.
Can family physicians deliver APC? I believe they can, and have given a few examples here to show how this is already happening. To help primary care providers start to deliver APC in their system, my team and I have built the HOPE (Healing Oriented Practices & Environments) Note Toolkit to use in daily practice.40 These and other tools are being used by a number of large hospital systems and health care networks around the country. (You can download the HOPE Note Toolkit, at no cost, at https://drwaynejonas.com/resources/hope-note/.)
Whatever we call this new type of primary care, it needs to care for the whole person and to be available to all. It finds expression in these assertions:
- We cannot ignore an essential part of what a human being is and expect them to heal or become whole.
- We cannot ignore essential people in our communities and expect our costs to go down or our compassion to go up.
- We need to stop allowing family medicine to be co-opted by reductionism and its profits.
In sum, we need a new vision of primary care—like Engel’s holistic vision in the 1970s—to motivate us, and we need to return to fundamental concepts of how healing works in medicine.41
CORRESPONDENCE
Wayne B. Jonas, MD, Samueli Integrative Health Programs, 1800 Diagonal Road, Suite 617, Alexandria, VA 22314; [email protected].
1. Engel GL. The need for a new medical model: a challenge for biomedicine. Science. 1977;196:129-136.
2. Schwartz MD, Durning S, Linzer M, et al. Changes in medical students’ views of internal medicine careers from 1990 to 2007. Arch Intern Med. 2011;171:744-749.
3. Bronchetti ET, Christensen GS, Hoynes HW. Local food prices, SNAP purchasing power, and child health. Cambridge, MA: National Bureau of Economic Research. June 2018. www.nber.org/papers/w24762?mc_cid=8c7211d34b&mc_eid=fbbc7df813. Accessed November 24, 2020.
4. Federal Student Aid, US Department of Education. Public Service Loan Forgiveness (PSLF). 2018. https://studentaid.ed.gov/sa/repay-loans/forgiveness-cancellation/public-service. Accessed November 24, 2020.
5. Aten B, Figueroa E, Martin T. Notes on estimating the multi-year regional price parities by 16 expenditure categories: 2005-2009. WP2011-03. Washington, DC: Bureau of Economic Analysis, US Department of Commerce; April 2011. www.bea.gov/system/files/papers/WP2011-3.pdf. Accessed November 24, 2020.
6. Aten BH, Figueroa EB, Martin TM. Regional price parities for states and metropolitan areas, 2006-2010. Washington, DC: Bureau of Economic Analysis, US Department of Commerce; August 2012. https://apps.bea.gov/scb/pdf/2012/08%20August/0812_regional_price_parities.pdf. Accessed November 24, 2020.
7. Stange KC, Ferrer RL. The paradox of primary care. Ann Fam Med. 2009;7:293-299.
8. Panel on Understanding Cross-national Health Differences Among High-income Countries, Committee on Population, Division of Behavioral and Social Sciences and Education, and Board on Population Health and Public Health Practice, National Research Council and Institute of Medicine of the National Academies. US Health in International Perspective: Shorter Lives, Poorer Health. Woolf SH, Aron L, eds. The National Academies Press; 2013.
9. Hood CM, Gennuso KP, Swain GR, et al. County health rankings: relationships between determinant factors and health outcomes. Am J Prev Med. 2016;50:129-135.
10. McGinnis JM, Williams-Russo P, Knickman JR. The case for more active policy attention to health promotion. Health Aff (Millwood). 2002;21:78-93.
11. Roeder A. Zip code better predictor of health than genetic code. Harvard T. H. Chan School of Public Health Web site. News release. August 4, 2014. www.hsph.harvard.edu/news/features/zip-code-better-predictor-of-health-than-genetic-code/. Accessed November 24, 2020.
12. US health map. Seattle, WA: University of Washington Institute for Health Metrics and Evaluation; March 13, 2018. www.healthdata.org/data-visualization/us-health-map. Accessed November 24, 2020.
13. Highfill T. Comparing estimates of U.S. health care expenditures by medical condition, 2000-2012. Survey of Current Business. 2016;1-5. https://apps.bea.gov/scb/pdf/2016/3%20March/0316_comparing_u.s._health_care_expenditures_by_medical_condition.pdf. Accessed November 24, 2020.
14. Waters H, Graf M. The Costs of Chronic Disease in the US. Washington, DC: Milken Institute; August 2018. https://milkeninstitute.org/sites/default/files/reports-pdf/ChronicDiseases-HighRes-FINAL.pdf. Accessed November 24, 2020.
15. Meyer H. Health care spending will hit 19.4% of GDP in the next decade, CMS projects. Modern Health care. February 20, 2019. www.modernhealthcare.com/article/20190220/NEWS/190229989/healthcare-spending-will-hit-19-4-of-gdp-in-the-next-decade-cms-projects. Accessed November 24, 2020.
16. Woolf SH, Schoomaker H. Life expectancy and mortality rates in the United States, 1959-2017. JAMA. 2019;322:1996-2016.
17. Basu S, Berkowitz SA, Phillips RL, et al. Association of primary care physician supply with population mortality in the United States, 2005-2015. JAMA Intern Med. 2019;179:506-514.
18. Zack MM, Moriarty DG, Stroup DF, et al. Worsening trends in adult health-related quality of life and self-rated health—United States, 1993–2001. Public Health Rep. 2004;119:493-505.
19. Windover AK, Martinez K, Mercer, MB, et al. Correlates and outcomes of physician burnout within a large academic medical center. Research letter. JAMA Intern Med. 2018;178:856-858.
20. West CP, Dyrbye LN, Shanafelt TD. Physician burnout: contributors, consequences and solutions. J Intern Med. 2018;283:516-529.
21. Buffett: Health care is a tapeworm on the economic system. CNBC Squawk Box. February 26, 2018. www.cnbc.com/video/2018/02/26/buffett-health-care-is-a-tapeworm-on-the-economic-system.html. Accessed November 24, 2020.
22. Starfield B. Primary Care: Concept, Evaluation, and Policy. Oxford University Press; 1992.
23. Starfield B, Shi L, Macinko J. Contribution of primary care to health systems and health. Milbank Q. 2005;83:457-502.
24. Institute of Medicine (US) Committee on Quality of Health Care in America. Crossing the Quality Chasm: A New Health System for the 21st Century. National Academies Press (US); 2001.
25. Burton R. Health policy brief: improving care transitions. Health Affairs. September 13, 2012. www.healthaffairs.org/do/10.1377/hpb20120913.327236/full/healthpolicybrief_76.pdf. Accessed November 24, 2020.
26. Toulany A, Stukel TA, Kurdyak P, et al. Association of primary care continuity with outcomes following transition to adult care for adolescents with severe mental illness. JAMA Netw Open. 2019;2:e198415.
27. Helping communities thrive. Catalyst Health Network Web site. www.catalysthealthnetwork.com/. Accessed November 24, 2020.
28. Diabetes Prevention Program (DPP) Research Group. The Diabetes Prevention Program (DPP): description of lifestyle intervention. Diabetes Care. 2002;25:2165-2171.
29. Scherger JE. Lean and Fit: A Doctor’s Journey to Healthy Nutrition and Greater Wellness. 2nd ed. Scotts Valley, CA: CreateSpace Publishing; 2016.
30. Qaseem A, Wilt TJ, McLean RM, et al; . Noninvasive treatments for acute, subacute, and chronic low back pain: a clinical practice guideline from the American College of Physicians. Ann Intern Med. 2017;166:514-530.
31. Hibbard JH, Greene J. What the evidence shows about patient activation: better health outcomes and care experiences; fewer data on costs. Health Aff (Millwood). 2013;32:207-214.
32. What is whole health? Washington, DC: US Department of Veterans Affairs. October 13, 2020. www.va.gov/patientcenteredcare/explore/about-whole-health.asp. Accessed November 25, 2020.
33. COVER Commission. Creating options for veterans’ expedited recovery. Final report. Washington, DC: US Veterans Administration. January 24, 2020. www.va.gov/COVER/docs/COVER-Commission-Final-Report-2020-01-24.pdf. Accessed November 24, 2020.
34. Social determinants of health. Washington, DC: Office of Disease Prevention and Health Promotion, US Department of Health and Human Services. HealthyPeople.gov Web site. www.healthypeople.gov/2020/topics-objectives/topic/social-determinants-of-health. Accessed November 24, 2020.
35. Breslin E, Lambertino A. Medicaid and social determinants of health: adjusting payment and measuring health outcomes. Princeton University Woodrow Wilson School of Public and International Affairs, State Health and Value Strategies Program Web site. July 2017. www.shvs.org/wp-content/uploads/2017/07/SHVS_SocialDeterminants_HMA_July2017.pdf. Accessed November 24, 2020.
36. James CV. Actively addressing social determinants of health will help us achieve health equity. US Centers for Medicare & Medicaid Services Web site. April 26, 2019. www.cms.gov/blog/actively-addressing-social-determinants-health-will-help-us-achieve-health-equity. Accessed November 24, 2020.
37. Geisinger receives “Innovation in Advancing Health Equity” award. Geisinger Health Web site. April 24, 2018. www.geisinger.org/health-plan/news-releases/2018/04/23/19/28/geisinger-receives-innovation-in-advancing-health-equity-award. Accessed November 24, 2020.
38. Bresnick J. Kaiser Permanente launches full-network social determinants program. HealthITAnalytics Web site. May 6, 2019. https://healthitanalytics.com/news/kaiser-permanente-launches-full-network-social-determinants-program. Accessed November 25, 2020.
39. Medicare Payment Advisory Commission (MEDPAC). Physician and other health Professional services. In: Report to the Congress: Medicare Payment Policy. March 2016: 115-117. http://medpac.gov/docs/default-source/reports/chapter-4-physician-and-other-health-professional-services-march-2016-report-.pdf. Accessed November 24, 2020.
40. Jonas W. Helping patients with chronic diseases and conditions heal with the HOPE Note: integrative primary care case study. https://drwaynejonas.com/wp-content/uploads/2018/09/CS_HOPE-Note_FINAL.pdf. Accessed November 24, 2020.
41. Jonas W. How Healing Works. Berkley, CA: Lorena Jones Books; 2018.
1. Engel GL. The need for a new medical model: a challenge for biomedicine. Science. 1977;196:129-136.
2. Schwartz MD, Durning S, Linzer M, et al. Changes in medical students’ views of internal medicine careers from 1990 to 2007. Arch Intern Med. 2011;171:744-749.
3. Bronchetti ET, Christensen GS, Hoynes HW. Local food prices, SNAP purchasing power, and child health. Cambridge, MA: National Bureau of Economic Research. June 2018. www.nber.org/papers/w24762?mc_cid=8c7211d34b&mc_eid=fbbc7df813. Accessed November 24, 2020.
4. Federal Student Aid, US Department of Education. Public Service Loan Forgiveness (PSLF). 2018. https://studentaid.ed.gov/sa/repay-loans/forgiveness-cancellation/public-service. Accessed November 24, 2020.
5. Aten B, Figueroa E, Martin T. Notes on estimating the multi-year regional price parities by 16 expenditure categories: 2005-2009. WP2011-03. Washington, DC: Bureau of Economic Analysis, US Department of Commerce; April 2011. www.bea.gov/system/files/papers/WP2011-3.pdf. Accessed November 24, 2020.
6. Aten BH, Figueroa EB, Martin TM. Regional price parities for states and metropolitan areas, 2006-2010. Washington, DC: Bureau of Economic Analysis, US Department of Commerce; August 2012. https://apps.bea.gov/scb/pdf/2012/08%20August/0812_regional_price_parities.pdf. Accessed November 24, 2020.
7. Stange KC, Ferrer RL. The paradox of primary care. Ann Fam Med. 2009;7:293-299.
8. Panel on Understanding Cross-national Health Differences Among High-income Countries, Committee on Population, Division of Behavioral and Social Sciences and Education, and Board on Population Health and Public Health Practice, National Research Council and Institute of Medicine of the National Academies. US Health in International Perspective: Shorter Lives, Poorer Health. Woolf SH, Aron L, eds. The National Academies Press; 2013.
9. Hood CM, Gennuso KP, Swain GR, et al. County health rankings: relationships between determinant factors and health outcomes. Am J Prev Med. 2016;50:129-135.
10. McGinnis JM, Williams-Russo P, Knickman JR. The case for more active policy attention to health promotion. Health Aff (Millwood). 2002;21:78-93.
11. Roeder A. Zip code better predictor of health than genetic code. Harvard T. H. Chan School of Public Health Web site. News release. August 4, 2014. www.hsph.harvard.edu/news/features/zip-code-better-predictor-of-health-than-genetic-code/. Accessed November 24, 2020.
12. US health map. Seattle, WA: University of Washington Institute for Health Metrics and Evaluation; March 13, 2018. www.healthdata.org/data-visualization/us-health-map. Accessed November 24, 2020.
13. Highfill T. Comparing estimates of U.S. health care expenditures by medical condition, 2000-2012. Survey of Current Business. 2016;1-5. https://apps.bea.gov/scb/pdf/2016/3%20March/0316_comparing_u.s._health_care_expenditures_by_medical_condition.pdf. Accessed November 24, 2020.
14. Waters H, Graf M. The Costs of Chronic Disease in the US. Washington, DC: Milken Institute; August 2018. https://milkeninstitute.org/sites/default/files/reports-pdf/ChronicDiseases-HighRes-FINAL.pdf. Accessed November 24, 2020.
15. Meyer H. Health care spending will hit 19.4% of GDP in the next decade, CMS projects. Modern Health care. February 20, 2019. www.modernhealthcare.com/article/20190220/NEWS/190229989/healthcare-spending-will-hit-19-4-of-gdp-in-the-next-decade-cms-projects. Accessed November 24, 2020.
16. Woolf SH, Schoomaker H. Life expectancy and mortality rates in the United States, 1959-2017. JAMA. 2019;322:1996-2016.
17. Basu S, Berkowitz SA, Phillips RL, et al. Association of primary care physician supply with population mortality in the United States, 2005-2015. JAMA Intern Med. 2019;179:506-514.
18. Zack MM, Moriarty DG, Stroup DF, et al. Worsening trends in adult health-related quality of life and self-rated health—United States, 1993–2001. Public Health Rep. 2004;119:493-505.
19. Windover AK, Martinez K, Mercer, MB, et al. Correlates and outcomes of physician burnout within a large academic medical center. Research letter. JAMA Intern Med. 2018;178:856-858.
20. West CP, Dyrbye LN, Shanafelt TD. Physician burnout: contributors, consequences and solutions. J Intern Med. 2018;283:516-529.
21. Buffett: Health care is a tapeworm on the economic system. CNBC Squawk Box. February 26, 2018. www.cnbc.com/video/2018/02/26/buffett-health-care-is-a-tapeworm-on-the-economic-system.html. Accessed November 24, 2020.
22. Starfield B. Primary Care: Concept, Evaluation, and Policy. Oxford University Press; 1992.
23. Starfield B, Shi L, Macinko J. Contribution of primary care to health systems and health. Milbank Q. 2005;83:457-502.
24. Institute of Medicine (US) Committee on Quality of Health Care in America. Crossing the Quality Chasm: A New Health System for the 21st Century. National Academies Press (US); 2001.
25. Burton R. Health policy brief: improving care transitions. Health Affairs. September 13, 2012. www.healthaffairs.org/do/10.1377/hpb20120913.327236/full/healthpolicybrief_76.pdf. Accessed November 24, 2020.
26. Toulany A, Stukel TA, Kurdyak P, et al. Association of primary care continuity with outcomes following transition to adult care for adolescents with severe mental illness. JAMA Netw Open. 2019;2:e198415.
27. Helping communities thrive. Catalyst Health Network Web site. www.catalysthealthnetwork.com/. Accessed November 24, 2020.
28. Diabetes Prevention Program (DPP) Research Group. The Diabetes Prevention Program (DPP): description of lifestyle intervention. Diabetes Care. 2002;25:2165-2171.
29. Scherger JE. Lean and Fit: A Doctor’s Journey to Healthy Nutrition and Greater Wellness. 2nd ed. Scotts Valley, CA: CreateSpace Publishing; 2016.
30. Qaseem A, Wilt TJ, McLean RM, et al; . Noninvasive treatments for acute, subacute, and chronic low back pain: a clinical practice guideline from the American College of Physicians. Ann Intern Med. 2017;166:514-530.
31. Hibbard JH, Greene J. What the evidence shows about patient activation: better health outcomes and care experiences; fewer data on costs. Health Aff (Millwood). 2013;32:207-214.
32. What is whole health? Washington, DC: US Department of Veterans Affairs. October 13, 2020. www.va.gov/patientcenteredcare/explore/about-whole-health.asp. Accessed November 25, 2020.
33. COVER Commission. Creating options for veterans’ expedited recovery. Final report. Washington, DC: US Veterans Administration. January 24, 2020. www.va.gov/COVER/docs/COVER-Commission-Final-Report-2020-01-24.pdf. Accessed November 24, 2020.
34. Social determinants of health. Washington, DC: Office of Disease Prevention and Health Promotion, US Department of Health and Human Services. HealthyPeople.gov Web site. www.healthypeople.gov/2020/topics-objectives/topic/social-determinants-of-health. Accessed November 24, 2020.
35. Breslin E, Lambertino A. Medicaid and social determinants of health: adjusting payment and measuring health outcomes. Princeton University Woodrow Wilson School of Public and International Affairs, State Health and Value Strategies Program Web site. July 2017. www.shvs.org/wp-content/uploads/2017/07/SHVS_SocialDeterminants_HMA_July2017.pdf. Accessed November 24, 2020.
36. James CV. Actively addressing social determinants of health will help us achieve health equity. US Centers for Medicare & Medicaid Services Web site. April 26, 2019. www.cms.gov/blog/actively-addressing-social-determinants-health-will-help-us-achieve-health-equity. Accessed November 24, 2020.
37. Geisinger receives “Innovation in Advancing Health Equity” award. Geisinger Health Web site. April 24, 2018. www.geisinger.org/health-plan/news-releases/2018/04/23/19/28/geisinger-receives-innovation-in-advancing-health-equity-award. Accessed November 24, 2020.
38. Bresnick J. Kaiser Permanente launches full-network social determinants program. HealthITAnalytics Web site. May 6, 2019. https://healthitanalytics.com/news/kaiser-permanente-launches-full-network-social-determinants-program. Accessed November 25, 2020.
39. Medicare Payment Advisory Commission (MEDPAC). Physician and other health Professional services. In: Report to the Congress: Medicare Payment Policy. March 2016: 115-117. http://medpac.gov/docs/default-source/reports/chapter-4-physician-and-other-health-professional-services-march-2016-report-.pdf. Accessed November 24, 2020.
40. Jonas W. Helping patients with chronic diseases and conditions heal with the HOPE Note: integrative primary care case study. https://drwaynejonas.com/wp-content/uploads/2018/09/CS_HOPE-Note_FINAL.pdf. Accessed November 24, 2020.
41. Jonas W. How Healing Works. Berkley, CA: Lorena Jones Books; 2018.
PRACTICE RECOMMENDATIONS
❯ Build care teams into your practice so that you integrate “what matters” into the center of the clinical encounter. C
❯ Add practice approaches that help patients engage in healthy lifestyles and that remove social and economic barriers for improving health and well-being. B
Strength of recommendation (SOR)
A Good-quality patient-oriented evidence
B Inconsistent or limited-quality patient-oriented evidence
C Consensus, usual practice, opinion, disease-oriented evidence, case series
How to identify and treat common bites and stings
Insect, arachnid, and other arthropod bites and stings are common patient complaints in a primary care office. A thorough history and physical exam can often isolate the specific offender and guide management. In this article, we outline how to identify, diagnose, and treat common bites and stings from bees and wasps; centipedes and spiders; fleas; flies and biting midges; mosquitoes; and ticks, and discuss how high-risk patients should be triaged and referred for additional testing and treatment, such as venom immunotherapy (VIT).
Insects and arachnids:Background and epidemiology
Insects are arthropods with 3-part exoskeletons: head, thorax, and abdomen. They have 6 jointed legs, compound eyes, and antennae. There are approximately 91,000 insect species in the United States, the most abundant orders being Coleoptera (beetles), Diptera (flies), and Hymenoptera (includes ants, bees, wasps, and sawflies).1
The reported incidence of insect bites and stings varies widely because most people experience mild symptoms and therefore do not seek medical care. Best statistics are for Hymenoptera stings, which are more likely to cause a severe reaction. In Europe, 56% to 94% of the general population has reported being bitten or stung by one of the Hymenoptera species.2 In many areas of Australia, the incidence of jack jumper ant stings is only 2% to 3%3; in the United States, 55% of people report being stung by nonnative fire ants within 3 weeks of moving into an endemic area.4
Arachnids are some of the earliest terrestrial organisms, of the class Arachnida, which includes scorpions, ticks, spiders, mites, and daddy longlegs (harvestmen).5 Arachnids are wingless and characterized by segmented bodies, jointed appendages, and exoskeletons.6,7 In most, the body is separated into 2 segments (the cephalothorax and abdomen), except for mites, ticks, and daddy longlegs, in which the entire body comprises a single segment.5
Arthropod bites are common in the United States; almost one-half are caused by spiders.7 Brown recluse (Loxosceles spp) and black widow (Latrodectus spp) spider bites are the most concerning: Although usually mild, these bites can be life-threatening but are rarely fatal. In 2013, almost 3500 bites by black widow and brown recluse spiders were reported.8
Risk factors
Risk factors for insect, arachnid, and other arthropod bites and stings are primarily environmental. People who live or work in proximity of biting or stinging insects (eg, gardeners and beekeepers) are more likely to be affected; so are those who work with animals or live next to standing water or grassy or wooded locales.
Continue to: There are also risk factors...
There are also risk factors for a systemic sting reaction:
- A sting reaction < 2 months earlier increases the risk of a subsequent systemic sting reaction by ≥ 50%.9
- Among beekeepers, paradoxically, the risk of a systemic reaction is higher in those stung < 15 times a year than in those stung > 200 times.10
- Patients with an elevated baseline serum level of tryptase (reference range, < 11.4 ng/mL), which is part of the allergenic response, or with biopsy-proven systemic mastocytosis are at increased risk of a systemic sting reaction.11
Presentation: Signs and symptomsvary with severity
Insect bites and stings usually cause transient local inflammation and, occasionally, a toxic reaction. Allergic hypersensitivity can result in a large local reaction or a generalized systemic reaction12:
- A small local reaction is transient and mild, develops directly at the site of the sting, and can last several days.13
- A large (or significant) local reaction, defined as swelling > 10 cm in diameter (FIGURE 1) and lasting > 24 hours, occurs in 2% to 26% of people who have been bitten or stung.14 This is an immunoglobulin (Ig) E–mediated late-phase reaction that can be accompanied by fatigue and nausea.12,13,15 For a patient with a large local reaction, the risk of a concomitant systemic reaction is 4% to 10%, typically beginning within 30 minutes after envenomation or, possibly, delayed for several hours or marked by a biphasic interval.16
- Characteristics of a systemic reaction are urticaria, angioedema, bronchospasm, large-airway edema, hypotension, and other clinical manifestations of anaphylaxis.17 In the United States, a systemic sting reaction is reported to occur in approximately 3% of bite and sting victims. Mortality among the general population from a systemic bite or sting reaction is 0.16 for every 100,000 people,2 and at least 40 to 100 die every year in the United States from anaphylaxis resulting from an insect bite or sting.18
- The most severe anaphylactic reactions involve the cardiovascular and respiratory systems, commonly including hypotension and symptoms of upper- or lower-airway obstruction. Laryngeal edema and circulatory failure are the most common mechanisms of anaphylactic death.19
Bees and wasps
Hymenoptera stinging insects include the family Apidae (honey bee, bumblebee, and sweat bee) and Vespidae (yellow jacket, yellow- and white-faced hornets, and paper wasp). A worker honey bee can sting only once, leaving its barbed stinger in the skin; a wasp, hornet, and yellow jacket can sting multiple times (FIGURE 2).2
Continue to: Bee and wasp sting...
Bee and wasp sting allergies are the most common insect venom allergic reactions. A bee sting is more likely to lead to a severe allergic reaction than a wasp sting. Allergic reactions to hornet and bumblebee stings are less common but can occur in patients already sensitized to wasp and honey bee stings.20,21
Management. Remove honey bee stingers by scraping the skin with a fingernail or credit card. Ideally, the stinger should be removed in the first 30 seconds, before the venom sac empties. Otherwise, intense local inflammation, with possible lymphangitic streaking, can result.22
For guidance on localized symptomatic care of bee and wasp stings and bites and stings from other sources discussed in this article, see “Providing relief and advanced care” on page E6.
Centipedes and spiders
Centipedes are arthropods of the class Chilopoda, subphylum Myriapoda, that are characterized by repeating linear (metameric) segments, each containing 1 pair of legs.23 Centipedes have a pair of poison claws behind the head that are used to paralyze prey—usually, small insects.23,24 The bite of a larger centipede can cause a painful reaction that generally subsides after a few hours but can last several days. Centipede bites are usually nonfatal to humans.23
Spiders belong to the class Arachnida, order Araneae. They have 8 legs with chelicerae (mouthpiece, or “jaws”) that inject venom into prey.25 Most spiders found in the United States cannot bite through human skin.26,27 Common exceptions are black widow and brown recluse spiders, which each produce a distinct toxic venom that can cause significant morbidity in humans through a bite, although bites are rarely fatal.26,27
The brown recluse spider is described as having a violin-shaped marking on the abdomen; the body is yellowish, tan, or dark brown. A bite can produce tiny fang marks and cause dull pain at the site of the bite that spreads quickly; myalgia; and pain in the stomach, back, chest, and legs.28,29 The bite takes approximately 7 days to resolve. In a minority of cases, a tender erythematous halo develops, followed by a severe necrotic ulcer, or loxoscelism (FIGURE 3; 40% of cases) or scarring (13%), or both.29,30
Continue to: In contrast...
In contrast, the body of a black widow spider is black; females exhibit a distinctive red or yellow hourglass marking on their ventral aspect.28,31 The pinprick sensation of a bite leads to symptoms that can include erythema, swelling, pain, stiffness, chills, fever, nausea, and stomach pain.30,32
Management. Again, see “Providing relief and advanced care” on page E6. Consider providing antivenin treatment for moderate or severe bites of brown recluse and black widow spiders.
Fleas
Fleas are members of the order Siphonaptera. They are small (1.5-3.2 mm long), reddish brown, wingless, blood-sucking insects with long legs that allow them to jump far (12 or 13 inches) and high (6 or 7 inches).33 Domesticated cats and dogs are the source of most flea infestations, resulting in an increased risk of exposure for humans.34,35 Flea bites, which generally occur on lower extremities, develop into a small, erythematous papule with a halo (FIGURE 4) and associated mild edema, and cause intense pruritus 30 minutes after the bite.35-37
Fleas are a vector for severe microbial infections, including bartonellosis, bubonic plague, cat-flea typhus, murine typhus, cat-scratch disease, rickettsial disease, and tularemia. Tungiasis is an inflammatory burrowing flea infestation—not a secondary infection for which the flea is a vector.34,35
Preventive management. Repellents, including products that contain DEET (N,N-diethyl-meta-toluamide), picaridin (2-[2-hydroxyethyl]-1-piperidinecarboxylic acid 1-methylpropyl ester), and PMD (p-menthane-3,8-diol, a chemical constituent of Eucalyptus citriodora oil) can be used to prevent flea bites in humans.33,38 Studies show that the scent of other botanic oils, including lavender, cedarwood, and peppermint, can also help prevent infestation by fleas; however, these compounds are not as effective as traditional insect repellents.33,38
Flea control is difficult, requiring a multimodal approach to treating the infested animal and its environment.39 Treatment of the infested domestic animal is the primary method of preventing human bites. Nonpesticidal control involves frequent cleaning of carpeting, furniture, animal bedding, and kennels. Insecticides can be applied throughout the house to combat severe infestation.33,38
Continue to: The Centers for Disease Control and Prevention...
The Centers for Disease Control and Prevention provide a general introduction to getting rid of fleas for pet owners.40 For specific guidance on flea-eradication strategies and specific flea-control products, advise patients to seek the advice of their veterinarian.
Flies and biting midges
Flies are 2-winged insects belonging to the order Diptera. Several fly species can bite, causing a local inflammatory reaction; these include black flies, deer flies, horse flies, and sand flies. Signs and symptoms of a fly bite include pain, pruritus, erythema, and mild swelling (FIGURE 5).41,42 Flies can transmit several infections, including bartonellosis, enteric bacterial disease (eg, caused by Campylobacter spp), leishmaniasis, loiasis, onchocerciasis, and trypanosomiasis.43
Biting midges, also called “no-see-ums,” biting gnats, moose flies, and “punkies,”44 are tiny (1-3 mm long) blood-sucking flies.45 Bitten patients often report not having seen the midge because it is so small. The bite typically starts as a small, erythematous papule that develops into a dome-shaped blister and can be extraordinarily pruritic and painful.44 The majority of people who have been bitten develop a hypersensitivity reaction, which usually resolves in a few weeks.
Management. Suppressing adult biting midges with an environmental insecticide is typically insufficient because the insecticide must be sprayed daily to eradicate active midges and generally does not affect larval habitat. Insect repellents and biopesticides, such as oil of lemon eucalyptus, can be effective in reducing the risk of bites.44,45
Mosquitoes
Mosquitoes are flying, blood-sucking insects of the order Diptera and family Culicidae. Anopheles, Culex, and Aedes genera are responsible for most bites of humans.
The bite of a mosquito produces an indurated, limited local reaction characterized by a pruritic wheal (3-29 mm in diameter) with surrounding erythema (FIGURE 6) that peaks in approximately 30 minutes, although patients might have a delayed reaction hours later.46 Immunocompromised patients might experience a more significant local inflammatory reaction that is accompanied by low-grade fever, hives, or swollen lymph nodes.46,47
Mosquitoes are a vector for serious infections, including dengue, Japanese encephalitis, malaria, and yellow fever, and disease caused by Chikungunya, West Nile, and Zika viruses.
Continue to: Management
Management. Advise patients to reduce their risk by using insect repellent, sleeping under mosquito netting, and wearing a long-sleeve shirt and long pants when traveling to endemic areas or when a local outbreak occurs.48
Ticks
Ticks belong to the order Parasitiformes and families Ixodidae and Argasidae. Hard ticks are found in brushy fields and tall grasses and can bite and feed on humans for days. Soft ticks are generally found around animal nests.29 Tick bites can cause a local reaction that includes painful, erythematous, inflammatory papular lesions (FIGURE 7).49
Ticks can transmit several infectious diseases. Depending on the microbial pathogen and the genus and species of tick, it takes 2 to 96 hours for the tick to attach to skin and transmit the pathogen to the human host. The TABLE29,49,50 provides an overview of tick species in the United States, diseases that they can transmit, and the geographic distribution of those diseases.
Management. Ticks should be removed with fine-tipped tweezers. Grasp the body of the tick close to the skin and pull upward while applying steady, even pressure. After removing the tick, clean the bite and the surrounding area with alcohol or with soap and water. Dispose of a live tick by flushing it down the toilet; or, kill it in alcohol and either seal it in a bag with tape or place it in a container.50
Diagnosis and the utilityof special testing
The diagnosis of insect, arachnid, and other arthropod bites and stings depends on the history, including obtaining a record of possible exposure and a travel history; the timing of the bite or sting; and associated signs and symptoms.18,51
Venom skin testing. For Hymenoptera stings, intradermal tests using a venom concentration of 0.001 to 1 μg/mL are positive in 65% to 80% of patients with a history of a systemic insect-sting allergic reaction. A negative venom skin test can occur during the 3-to-6-week refractory period after a sting reaction or many years later, which represents a loss of sensitivity. Positive venom skin tests are used to confirm allergy and identify specific insects to which the patient is allergic.11,12
Continue to: Allergen-specific IgE antibody testing.
Allergen-specific IgE antibody testing. These serum assays—typically, radioallergosorbent testing (RAST)—are less sensitive than venom skin tests. RAST is useful when venom skin testing cannot be performed or when skin testing is negative in a patient who has had a severe allergic reaction to an insect bite or sting. Serum IgE-specific antibody testing is preferred over venom skin testing in patients who are at high risk of anaphylaxis.52,53
Providing reliefand advanced care
Symptomatic treatment of mild bites and stings includes washing the affected area with soap and water and applying a cold compress to reduce swelling.54 For painful lesions, an oral analgesic can be prescribed.
For mild or moderate pruritus, a low- to midpotency topical corticosteroid (eg, hydrocortisone valerate cream 0.2% bid), topical calamine, or pramoxine can be applied,or a nonsedating oral antihistamine, such as loratadine (10 mg/d) or cetirizine (10 mg/d), can be used.14,55 For severe itching, a sedating antihistamine, such as hydroxyzine (10-25 mg every 4 to 6 hours prn), might help relieve symptoms; H1- and H2-receptor antagonists can be used concomitantly.54,55
Significant local symptoms. Large local reactions are treated with a midpotency topical corticosteroid (eg, triamcinolone acetonide cream 0.1% bid) plus an oral antihistamine to relieve pruritus and reduce allergic inflammation. For a more severe reaction, an oral corticosteroid (prednisone 1 mg/kg; maximum dosage, 50 mg/d) can be given for 5 to 7 days.54-56
Management of a necrotic ulcer secondary to a brown recluse spider bite is symptomatic and supportive. The size of these wounds can increase for as long as 10 days after the bite; resolution can require months of wound care, possibly with debridement. Rarely, skin grafting is required.27,28,31
VIT. Some studies show that VIT can improve quality of life in patients with prolonged, frequent, and worsening reactions to insect bites or stings and repeated, unavoidable exposures.55,56 VIT is recommended for patients with systemic hypersensitivity and a positive venom skin test result. It is approximately 95% effective in preventing or reducing severe systemic reactions and reduces the risk of anaphylaxis (see next section) and death.57 The maintenance dosage of VIT is usually 100 μg every 4 to 6 weeks; optimal duration of treatment is 3 to 5 years.58
Continue to: After VIT is complete...
After VIT is complete, counsel patients that a mild systemic reaction is still possible after an insect bite or sting. More prolonged, even lifetime, treatment should be considered for patients who have58,59
- a history of severe, life-threatening allergic reactions to bites and stings
- honey bee sting allergy
- mast-cell disease
- a history of anaphylaxis while receiving VIT.
Absolute contraindications to VIT include a history of serious immune disease, chronic infection, or cancer.58,59
Managing anaphylaxis
This severe allergic reaction can lead to death if untreated. First-line therapy is intramuscular epinephrine, 0.01 mg/kg (maximum single dose, 0.5 mg) given every 5 to 15 minutes.14,60 Epinephrine auto-injectors deliver a fixed dose and are labeled according to weight. Administration of O2 and intravenous fluids is recommended for hemodynamically unstable patients.60,61 Antihistamines and corticosteroids can be used as secondary treatment but should not replace epinephrine.56
After preliminary improvement, patients might decompensate when the epinephrine dose wears off. Furthermore, a biphasic reaction, variously reported in < 5% to as many as 20% of patients,61,62 occurs hours after the initial anaphylactic reaction. Patients should be monitored, therefore, for at least 6 to 8 hours after an anaphylactic reaction, preferably in a facility equipped to treat anaphylaxis.17,56
Before discharge, patients who have had an anaphylactic reaction should be given a prescription for epinephrine and training in the use of an epinephrine auto-injector. Allergen avoidance, along with an emergency plan in the event of a bite or sting, is recommended. Follow-up evaluation with an allergist or immunologist is essential for proper diagnosis and to determine whether the patient is a candidate for VIT.14,17
CORRESPONDENCE
Ecler Ercole Jaqua, MD, DipABLM, FAAFP, 1200 California Street, Suite 240, Redlands, CA 92374; [email protected].
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2. Antonicelli L, Bilò MB, Bonifazi F. Epidemiology of Hymenoptera allergy. Curr Opin Allergy Clin Immunol. 2002;2:341-346.
3. Jack jumper ant allergy. Australasian Society of Clinical Immunology and Allergy (ASCIA) Web site. Updated October 19, 2019. www.allergy.org.au/patients/insect-allergy-bites-and-stings/jack-jumper-ant-allergy. Accessed November 25, 2020.
4. Kemp SF, deShazo RD, Moffit JE, et al. Expanding habitat of the imported fire ant (Solenopsis invicta): a public health concern. J Allergy Clin Immunol. 2000;105:683-691.
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7. Diaz JH, Leblanc KE. Common spider bites. Am Fam Physician. 2007;75:869-873.
8. Mowry JB, Spyker DA, Cantilena LR Jr, McMillan N, Ford M. 2013 Annual report of the American Association of Poison Control Centers’ National Poison Data System (NPDS): 31st Annual Report. Clin Toxicol (Phila). 2014;52:1032-1283.
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11. Müller UR. Cardiovascular disease and anaphylaxis. Curr Opin Allergy Clin Immunol. 2007;7:337-341.
12. Golden DBK. Stinging insect allergy. Am Fam Physician. 2003;67:2541-2546.
13. Golden DBK, Demain T, Freeman T, et al. Stinging insect hypersensitivity: a practice parameter update 2016. Ann Allergy Asthma Immunol. 2017;118:28-54.
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23. Shelley RM. Centipedes and millipedes with emphasis on North American fauna. Kansas School Naturalist. 1999;45:1-16. https://sites.google.com/g.emporia.edu/ksn/ksn-home/vol-45-no-3-centipedes-and-millipedes-with-emphasis-on-n-america-fauna#h.p_JEf3uDlTg0jw. Accessed November 25, 2020.
24. Ogg B. Centipedes and millipedes. Nebraska Extension in Lancaster County Web site. https://lancaster.unl.edu/pest/resources/CentipedeMillipede012.shtml. Accessed November 25, 2020.
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27. The National Institute for Occupational Safety and Health (NIOSH), Centers for Disease Control and Prevention. Venomous spiders. www.cdc.gov/niosh/topics/spiders/. Accessed November 25, 2020.
28. Starr S. What you need to know to prevent a poisonous spider bite. AAP News. 2013;34:42. www.aappublications.org/content/aapnews/34/9/42.5.full.pdf. Accessed November 25, 2020.
29. Spider bites. Mayo Clinic Web site. www.mayoclinic.org/diseases-conditions/spider-bites/symptoms-causes/syc-20352371. Accessed November 25, 2020.
30. Barish RA, Arnold T. Spider bites. In: Merck Manual (Professional Version). Merck Sharp & Dohme Corp.; 2016. www.merckmanuals.com/professional/injuries-poisoning/bites-and-stings/spider-bites. Accessed November 25, 2020.
31. Juckett G. Arthropod bites. Am Fam Physician. 2013;88:841-847.
32. Clark RF, Wethern-Kestner S, Vance MV, et al. Clinical presentation and treatment of black widow spider envenomation: a review of 163 cases. Ann Emerg Med. 1992;21:782-787.
33. Koehler PG, Pereira RM, Diclaro JW II. Fleas. Publication ENY-025. University of Florida IFAS Extension. Revised January 2012. https://edis.ifas.ufl.edu/ig087. Accessed November 25, 2020.
34. Bitam I, Dittmar K, Parola P, et al. Fleas and flea-borne diseases. Int J Infect Dis. 2010;14:e667-e676.
35. Leulmi H, Socolovschi C, Laudisoit A, et al. Detection of Rickettsia felis, Rickettsia typhi, Bartonella species and Yersinia pestis in fleas (Siphonaptera) from Africa. PLoS Negl Trop Dis. 2014;8:e3152.
36. Naimer SA, Cohen AD, Mumcuoglu KY, et al. Household papular urticaria. Isr Med Assoc J. 2002;4(11 suppl):911-913.
37. Golomb MR, Golomb HS. What’s eating you? Cat flea (Ctenocephalides felis). Cutis. 2010;85:10-11.
38. Dryden MW. Flea and tick control in the 21st century: challenges and opportunities. Vet Dermatol. 2009;20:435-440.
39. Dryden MW. Fleas in dogs and cats. Merck Sharp & Dohme Corporation: Merck Manual Veterinary Manual. Updated December 2014. www.merckvetmanual.com/integumentary-system/fleas-and-flea-allergy-dermatitis/fleas-in-dogs-and-cats. Accessed November 25, 2020.
40. Centers for Disease Control and Prevention. Getting rid of fleas. www.cdc.gov/fleas/getting_rid.html. Accessed November 25, 2020.
41. Chattopadhyay P, Goyary D, Dhiman S, et al. Immunomodulating effects and hypersensitivity reactions caused by Northeast Indian black fly salivary gland extract. J Immunotoxicol. 2014;11:126-132.
42. Hrabak TM, Dice JP. Use of immunotherapy in the management of presumed anaphylaxis to the deer fly. Ann Allergy Asthma Immunol. 2003;90:351-354.
43. Royden A, Wedley A, Merga JY, et al. A role for flies (Diptera) in the transmission of Campylobacter to broilers? Epidemiol Infect. 2016;144:3326-3334.
44. Fradin MS, Day JF. Comparative efficacy of insect repellents against mosquito bites. N Engl J Med. 2002;347:13-18.
45. Carpenter S, Groschup MH, Garros C, et al. Culicoides biting midges, arboviruses and public health in Europe. Antiviral Res. 2013;100:102-113.
46. Peng Z, Yang M, Simons FE. Immunologic mechanisms in mosquito allergy: correlation of skin reactions with specific IgE and IgG anti-bodies and lymphocyte proliferation response to mosquito antigens. Ann Allergy Asthma Immunol. 1996;77:238-244.
47. Simons FE, Peng Z. Skeeter syndrome. J Allergy Clin Immunol. 1999;104:705-707.
48. Centers for Disease Control and Prevention. Travelers’ health. Clinician resources. wwwnc.cdc.gov/travel/page/clinician-information-center. Accessed November 25, 2020.
49. Gauci M, Loh RK, Stone BF, et al. Allergic reactions to the Australian paralysis tick, Ixodes holocyclus: diagnostic evaluation by skin test and radioimmunoassay. Clin Exp Allergy. 1989;19:279-283.
50. Centers for Disease Control and Prevention. Ticks. Removing a tick. www.cdc.gov/ticks/removing_a_tick.html. Accessed November 25, 2020.
51. Golden DB, Kagey-Sobotka A, Norman PS, et al. Insect sting allergy with negative venom skin test responses. J Allergy Clin Immunol. 2001;107:897-901.
52. Arzt L, Bokanovic D, Schrautzer C, et al. Immunological differences between insect venom-allergic patients with and without immunotherapy and asymptomatically sensitized subjects. Allergy. 2018;73:1223-1231.
53. Heddle R, Golden DBK. Allergy to insect stings and bites. World Allergy Organization Web site. Updated August 2015. www.worldallergy.org/education-and-programs/education/allergic-disease-resource-center/professionals/allergy-to-insect-stings-and-bites. Accessed November 25, 2020.
54. RuëffF, Przybilla B, Müller U, et al. The sting challenge test in Hymenoptera venom allergy. Position paper of the Subcommittee on Insect Venom Allergy of the European Academy of Allergology and Clinical Immunology. Allergy. 1996;51:216-225.
55. Management of simple insect bites: where’s the evidence? Drug Ther Bull. 2012;50:45-48.
56. Tracy JM. Insect allergy. Mt Sinai J Med. 2011;78:773-783.
57. Golden DBK. Insect sting allergy and venom immunotherapy: a model and a mystery. J Allergy Clin Immunol. 2005;115:439-447.
58. Winther L, Arnved J, Malling H-J, et al. Side-effects of allergen-specific immunotherapy: a prospective multi-centre study. Clin Exp Allergy. 2006;36:254-260.
59. Mellerup MT, Hahn GW, Poulsen LK, et al. Safety of allergen-specific immunotherapy. Relation between dosage regimen, allergen extract, disease and systemic side-effects during induction treatment. Clin Exp Allergy. 2000;30:1423-1429.
60. Anaphylaxis and insect stings and bites. Med Lett Drugs Ther. 2017;59:e79-e82.
61. Sampson HA, Muñoz-Furlong A, Campbell RL, et al. Second symposium on the definition and management of anaphylaxis: summary report—second National Institute of Allergy and Infectious Disease/Food Allergy and Anaphylaxis Network symposium. Ann Emerg Med. 2006;47:373-380.
62. Pflipsen MC, Vega Colon KM. Anaphylaxis: recognition and management. Am Fam Physician. 2020;102:355-362. Accessed November 25, 2020.
Insect, arachnid, and other arthropod bites and stings are common patient complaints in a primary care office. A thorough history and physical exam can often isolate the specific offender and guide management. In this article, we outline how to identify, diagnose, and treat common bites and stings from bees and wasps; centipedes and spiders; fleas; flies and biting midges; mosquitoes; and ticks, and discuss how high-risk patients should be triaged and referred for additional testing and treatment, such as venom immunotherapy (VIT).
Insects and arachnids:Background and epidemiology
Insects are arthropods with 3-part exoskeletons: head, thorax, and abdomen. They have 6 jointed legs, compound eyes, and antennae. There are approximately 91,000 insect species in the United States, the most abundant orders being Coleoptera (beetles), Diptera (flies), and Hymenoptera (includes ants, bees, wasps, and sawflies).1
The reported incidence of insect bites and stings varies widely because most people experience mild symptoms and therefore do not seek medical care. Best statistics are for Hymenoptera stings, which are more likely to cause a severe reaction. In Europe, 56% to 94% of the general population has reported being bitten or stung by one of the Hymenoptera species.2 In many areas of Australia, the incidence of jack jumper ant stings is only 2% to 3%3; in the United States, 55% of people report being stung by nonnative fire ants within 3 weeks of moving into an endemic area.4
Arachnids are some of the earliest terrestrial organisms, of the class Arachnida, which includes scorpions, ticks, spiders, mites, and daddy longlegs (harvestmen).5 Arachnids are wingless and characterized by segmented bodies, jointed appendages, and exoskeletons.6,7 In most, the body is separated into 2 segments (the cephalothorax and abdomen), except for mites, ticks, and daddy longlegs, in which the entire body comprises a single segment.5
Arthropod bites are common in the United States; almost one-half are caused by spiders.7 Brown recluse (Loxosceles spp) and black widow (Latrodectus spp) spider bites are the most concerning: Although usually mild, these bites can be life-threatening but are rarely fatal. In 2013, almost 3500 bites by black widow and brown recluse spiders were reported.8
Risk factors
Risk factors for insect, arachnid, and other arthropod bites and stings are primarily environmental. People who live or work in proximity of biting or stinging insects (eg, gardeners and beekeepers) are more likely to be affected; so are those who work with animals or live next to standing water or grassy or wooded locales.
Continue to: There are also risk factors...
There are also risk factors for a systemic sting reaction:
- A sting reaction < 2 months earlier increases the risk of a subsequent systemic sting reaction by ≥ 50%.9
- Among beekeepers, paradoxically, the risk of a systemic reaction is higher in those stung < 15 times a year than in those stung > 200 times.10
- Patients with an elevated baseline serum level of tryptase (reference range, < 11.4 ng/mL), which is part of the allergenic response, or with biopsy-proven systemic mastocytosis are at increased risk of a systemic sting reaction.11
Presentation: Signs and symptomsvary with severity
Insect bites and stings usually cause transient local inflammation and, occasionally, a toxic reaction. Allergic hypersensitivity can result in a large local reaction or a generalized systemic reaction12:
- A small local reaction is transient and mild, develops directly at the site of the sting, and can last several days.13
- A large (or significant) local reaction, defined as swelling > 10 cm in diameter (FIGURE 1) and lasting > 24 hours, occurs in 2% to 26% of people who have been bitten or stung.14 This is an immunoglobulin (Ig) E–mediated late-phase reaction that can be accompanied by fatigue and nausea.12,13,15 For a patient with a large local reaction, the risk of a concomitant systemic reaction is 4% to 10%, typically beginning within 30 minutes after envenomation or, possibly, delayed for several hours or marked by a biphasic interval.16
- Characteristics of a systemic reaction are urticaria, angioedema, bronchospasm, large-airway edema, hypotension, and other clinical manifestations of anaphylaxis.17 In the United States, a systemic sting reaction is reported to occur in approximately 3% of bite and sting victims. Mortality among the general population from a systemic bite or sting reaction is 0.16 for every 100,000 people,2 and at least 40 to 100 die every year in the United States from anaphylaxis resulting from an insect bite or sting.18
- The most severe anaphylactic reactions involve the cardiovascular and respiratory systems, commonly including hypotension and symptoms of upper- or lower-airway obstruction. Laryngeal edema and circulatory failure are the most common mechanisms of anaphylactic death.19
Bees and wasps
Hymenoptera stinging insects include the family Apidae (honey bee, bumblebee, and sweat bee) and Vespidae (yellow jacket, yellow- and white-faced hornets, and paper wasp). A worker honey bee can sting only once, leaving its barbed stinger in the skin; a wasp, hornet, and yellow jacket can sting multiple times (FIGURE 2).2
Continue to: Bee and wasp sting...
Bee and wasp sting allergies are the most common insect venom allergic reactions. A bee sting is more likely to lead to a severe allergic reaction than a wasp sting. Allergic reactions to hornet and bumblebee stings are less common but can occur in patients already sensitized to wasp and honey bee stings.20,21
Management. Remove honey bee stingers by scraping the skin with a fingernail or credit card. Ideally, the stinger should be removed in the first 30 seconds, before the venom sac empties. Otherwise, intense local inflammation, with possible lymphangitic streaking, can result.22
For guidance on localized symptomatic care of bee and wasp stings and bites and stings from other sources discussed in this article, see “Providing relief and advanced care” on page E6.
Centipedes and spiders
Centipedes are arthropods of the class Chilopoda, subphylum Myriapoda, that are characterized by repeating linear (metameric) segments, each containing 1 pair of legs.23 Centipedes have a pair of poison claws behind the head that are used to paralyze prey—usually, small insects.23,24 The bite of a larger centipede can cause a painful reaction that generally subsides after a few hours but can last several days. Centipede bites are usually nonfatal to humans.23
Spiders belong to the class Arachnida, order Araneae. They have 8 legs with chelicerae (mouthpiece, or “jaws”) that inject venom into prey.25 Most spiders found in the United States cannot bite through human skin.26,27 Common exceptions are black widow and brown recluse spiders, which each produce a distinct toxic venom that can cause significant morbidity in humans through a bite, although bites are rarely fatal.26,27
The brown recluse spider is described as having a violin-shaped marking on the abdomen; the body is yellowish, tan, or dark brown. A bite can produce tiny fang marks and cause dull pain at the site of the bite that spreads quickly; myalgia; and pain in the stomach, back, chest, and legs.28,29 The bite takes approximately 7 days to resolve. In a minority of cases, a tender erythematous halo develops, followed by a severe necrotic ulcer, or loxoscelism (FIGURE 3; 40% of cases) or scarring (13%), or both.29,30
Continue to: In contrast...
In contrast, the body of a black widow spider is black; females exhibit a distinctive red or yellow hourglass marking on their ventral aspect.28,31 The pinprick sensation of a bite leads to symptoms that can include erythema, swelling, pain, stiffness, chills, fever, nausea, and stomach pain.30,32
Management. Again, see “Providing relief and advanced care” on page E6. Consider providing antivenin treatment for moderate or severe bites of brown recluse and black widow spiders.
Fleas
Fleas are members of the order Siphonaptera. They are small (1.5-3.2 mm long), reddish brown, wingless, blood-sucking insects with long legs that allow them to jump far (12 or 13 inches) and high (6 or 7 inches).33 Domesticated cats and dogs are the source of most flea infestations, resulting in an increased risk of exposure for humans.34,35 Flea bites, which generally occur on lower extremities, develop into a small, erythematous papule with a halo (FIGURE 4) and associated mild edema, and cause intense pruritus 30 minutes after the bite.35-37
Fleas are a vector for severe microbial infections, including bartonellosis, bubonic plague, cat-flea typhus, murine typhus, cat-scratch disease, rickettsial disease, and tularemia. Tungiasis is an inflammatory burrowing flea infestation—not a secondary infection for which the flea is a vector.34,35
Preventive management. Repellents, including products that contain DEET (N,N-diethyl-meta-toluamide), picaridin (2-[2-hydroxyethyl]-1-piperidinecarboxylic acid 1-methylpropyl ester), and PMD (p-menthane-3,8-diol, a chemical constituent of Eucalyptus citriodora oil) can be used to prevent flea bites in humans.33,38 Studies show that the scent of other botanic oils, including lavender, cedarwood, and peppermint, can also help prevent infestation by fleas; however, these compounds are not as effective as traditional insect repellents.33,38
Flea control is difficult, requiring a multimodal approach to treating the infested animal and its environment.39 Treatment of the infested domestic animal is the primary method of preventing human bites. Nonpesticidal control involves frequent cleaning of carpeting, furniture, animal bedding, and kennels. Insecticides can be applied throughout the house to combat severe infestation.33,38
Continue to: The Centers for Disease Control and Prevention...
The Centers for Disease Control and Prevention provide a general introduction to getting rid of fleas for pet owners.40 For specific guidance on flea-eradication strategies and specific flea-control products, advise patients to seek the advice of their veterinarian.
Flies and biting midges
Flies are 2-winged insects belonging to the order Diptera. Several fly species can bite, causing a local inflammatory reaction; these include black flies, deer flies, horse flies, and sand flies. Signs and symptoms of a fly bite include pain, pruritus, erythema, and mild swelling (FIGURE 5).41,42 Flies can transmit several infections, including bartonellosis, enteric bacterial disease (eg, caused by Campylobacter spp), leishmaniasis, loiasis, onchocerciasis, and trypanosomiasis.43
Biting midges, also called “no-see-ums,” biting gnats, moose flies, and “punkies,”44 are tiny (1-3 mm long) blood-sucking flies.45 Bitten patients often report not having seen the midge because it is so small. The bite typically starts as a small, erythematous papule that develops into a dome-shaped blister and can be extraordinarily pruritic and painful.44 The majority of people who have been bitten develop a hypersensitivity reaction, which usually resolves in a few weeks.
Management. Suppressing adult biting midges with an environmental insecticide is typically insufficient because the insecticide must be sprayed daily to eradicate active midges and generally does not affect larval habitat. Insect repellents and biopesticides, such as oil of lemon eucalyptus, can be effective in reducing the risk of bites.44,45
Mosquitoes
Mosquitoes are flying, blood-sucking insects of the order Diptera and family Culicidae. Anopheles, Culex, and Aedes genera are responsible for most bites of humans.
The bite of a mosquito produces an indurated, limited local reaction characterized by a pruritic wheal (3-29 mm in diameter) with surrounding erythema (FIGURE 6) that peaks in approximately 30 minutes, although patients might have a delayed reaction hours later.46 Immunocompromised patients might experience a more significant local inflammatory reaction that is accompanied by low-grade fever, hives, or swollen lymph nodes.46,47
Mosquitoes are a vector for serious infections, including dengue, Japanese encephalitis, malaria, and yellow fever, and disease caused by Chikungunya, West Nile, and Zika viruses.
Continue to: Management
Management. Advise patients to reduce their risk by using insect repellent, sleeping under mosquito netting, and wearing a long-sleeve shirt and long pants when traveling to endemic areas or when a local outbreak occurs.48
Ticks
Ticks belong to the order Parasitiformes and families Ixodidae and Argasidae. Hard ticks are found in brushy fields and tall grasses and can bite and feed on humans for days. Soft ticks are generally found around animal nests.29 Tick bites can cause a local reaction that includes painful, erythematous, inflammatory papular lesions (FIGURE 7).49
Ticks can transmit several infectious diseases. Depending on the microbial pathogen and the genus and species of tick, it takes 2 to 96 hours for the tick to attach to skin and transmit the pathogen to the human host. The TABLE29,49,50 provides an overview of tick species in the United States, diseases that they can transmit, and the geographic distribution of those diseases.
Management. Ticks should be removed with fine-tipped tweezers. Grasp the body of the tick close to the skin and pull upward while applying steady, even pressure. After removing the tick, clean the bite and the surrounding area with alcohol or with soap and water. Dispose of a live tick by flushing it down the toilet; or, kill it in alcohol and either seal it in a bag with tape or place it in a container.50
Diagnosis and the utilityof special testing
The diagnosis of insect, arachnid, and other arthropod bites and stings depends on the history, including obtaining a record of possible exposure and a travel history; the timing of the bite or sting; and associated signs and symptoms.18,51
Venom skin testing. For Hymenoptera stings, intradermal tests using a venom concentration of 0.001 to 1 μg/mL are positive in 65% to 80% of patients with a history of a systemic insect-sting allergic reaction. A negative venom skin test can occur during the 3-to-6-week refractory period after a sting reaction or many years later, which represents a loss of sensitivity. Positive venom skin tests are used to confirm allergy and identify specific insects to which the patient is allergic.11,12
Continue to: Allergen-specific IgE antibody testing.
Allergen-specific IgE antibody testing. These serum assays—typically, radioallergosorbent testing (RAST)—are less sensitive than venom skin tests. RAST is useful when venom skin testing cannot be performed or when skin testing is negative in a patient who has had a severe allergic reaction to an insect bite or sting. Serum IgE-specific antibody testing is preferred over venom skin testing in patients who are at high risk of anaphylaxis.52,53
Providing reliefand advanced care
Symptomatic treatment of mild bites and stings includes washing the affected area with soap and water and applying a cold compress to reduce swelling.54 For painful lesions, an oral analgesic can be prescribed.
For mild or moderate pruritus, a low- to midpotency topical corticosteroid (eg, hydrocortisone valerate cream 0.2% bid), topical calamine, or pramoxine can be applied,or a nonsedating oral antihistamine, such as loratadine (10 mg/d) or cetirizine (10 mg/d), can be used.14,55 For severe itching, a sedating antihistamine, such as hydroxyzine (10-25 mg every 4 to 6 hours prn), might help relieve symptoms; H1- and H2-receptor antagonists can be used concomitantly.54,55
Significant local symptoms. Large local reactions are treated with a midpotency topical corticosteroid (eg, triamcinolone acetonide cream 0.1% bid) plus an oral antihistamine to relieve pruritus and reduce allergic inflammation. For a more severe reaction, an oral corticosteroid (prednisone 1 mg/kg; maximum dosage, 50 mg/d) can be given for 5 to 7 days.54-56
Management of a necrotic ulcer secondary to a brown recluse spider bite is symptomatic and supportive. The size of these wounds can increase for as long as 10 days after the bite; resolution can require months of wound care, possibly with debridement. Rarely, skin grafting is required.27,28,31
VIT. Some studies show that VIT can improve quality of life in patients with prolonged, frequent, and worsening reactions to insect bites or stings and repeated, unavoidable exposures.55,56 VIT is recommended for patients with systemic hypersensitivity and a positive venom skin test result. It is approximately 95% effective in preventing or reducing severe systemic reactions and reduces the risk of anaphylaxis (see next section) and death.57 The maintenance dosage of VIT is usually 100 μg every 4 to 6 weeks; optimal duration of treatment is 3 to 5 years.58
Continue to: After VIT is complete...
After VIT is complete, counsel patients that a mild systemic reaction is still possible after an insect bite or sting. More prolonged, even lifetime, treatment should be considered for patients who have58,59
- a history of severe, life-threatening allergic reactions to bites and stings
- honey bee sting allergy
- mast-cell disease
- a history of anaphylaxis while receiving VIT.
Absolute contraindications to VIT include a history of serious immune disease, chronic infection, or cancer.58,59
Managing anaphylaxis
This severe allergic reaction can lead to death if untreated. First-line therapy is intramuscular epinephrine, 0.01 mg/kg (maximum single dose, 0.5 mg) given every 5 to 15 minutes.14,60 Epinephrine auto-injectors deliver a fixed dose and are labeled according to weight. Administration of O2 and intravenous fluids is recommended for hemodynamically unstable patients.60,61 Antihistamines and corticosteroids can be used as secondary treatment but should not replace epinephrine.56
After preliminary improvement, patients might decompensate when the epinephrine dose wears off. Furthermore, a biphasic reaction, variously reported in < 5% to as many as 20% of patients,61,62 occurs hours after the initial anaphylactic reaction. Patients should be monitored, therefore, for at least 6 to 8 hours after an anaphylactic reaction, preferably in a facility equipped to treat anaphylaxis.17,56
Before discharge, patients who have had an anaphylactic reaction should be given a prescription for epinephrine and training in the use of an epinephrine auto-injector. Allergen avoidance, along with an emergency plan in the event of a bite or sting, is recommended. Follow-up evaluation with an allergist or immunologist is essential for proper diagnosis and to determine whether the patient is a candidate for VIT.14,17
CORRESPONDENCE
Ecler Ercole Jaqua, MD, DipABLM, FAAFP, 1200 California Street, Suite 240, Redlands, CA 92374; [email protected].
Insect, arachnid, and other arthropod bites and stings are common patient complaints in a primary care office. A thorough history and physical exam can often isolate the specific offender and guide management. In this article, we outline how to identify, diagnose, and treat common bites and stings from bees and wasps; centipedes and spiders; fleas; flies and biting midges; mosquitoes; and ticks, and discuss how high-risk patients should be triaged and referred for additional testing and treatment, such as venom immunotherapy (VIT).
Insects and arachnids:Background and epidemiology
Insects are arthropods with 3-part exoskeletons: head, thorax, and abdomen. They have 6 jointed legs, compound eyes, and antennae. There are approximately 91,000 insect species in the United States, the most abundant orders being Coleoptera (beetles), Diptera (flies), and Hymenoptera (includes ants, bees, wasps, and sawflies).1
The reported incidence of insect bites and stings varies widely because most people experience mild symptoms and therefore do not seek medical care. Best statistics are for Hymenoptera stings, which are more likely to cause a severe reaction. In Europe, 56% to 94% of the general population has reported being bitten or stung by one of the Hymenoptera species.2 In many areas of Australia, the incidence of jack jumper ant stings is only 2% to 3%3; in the United States, 55% of people report being stung by nonnative fire ants within 3 weeks of moving into an endemic area.4
Arachnids are some of the earliest terrestrial organisms, of the class Arachnida, which includes scorpions, ticks, spiders, mites, and daddy longlegs (harvestmen).5 Arachnids are wingless and characterized by segmented bodies, jointed appendages, and exoskeletons.6,7 In most, the body is separated into 2 segments (the cephalothorax and abdomen), except for mites, ticks, and daddy longlegs, in which the entire body comprises a single segment.5
Arthropod bites are common in the United States; almost one-half are caused by spiders.7 Brown recluse (Loxosceles spp) and black widow (Latrodectus spp) spider bites are the most concerning: Although usually mild, these bites can be life-threatening but are rarely fatal. In 2013, almost 3500 bites by black widow and brown recluse spiders were reported.8
Risk factors
Risk factors for insect, arachnid, and other arthropod bites and stings are primarily environmental. People who live or work in proximity of biting or stinging insects (eg, gardeners and beekeepers) are more likely to be affected; so are those who work with animals or live next to standing water or grassy or wooded locales.
Continue to: There are also risk factors...
There are also risk factors for a systemic sting reaction:
- A sting reaction < 2 months earlier increases the risk of a subsequent systemic sting reaction by ≥ 50%.9
- Among beekeepers, paradoxically, the risk of a systemic reaction is higher in those stung < 15 times a year than in those stung > 200 times.10
- Patients with an elevated baseline serum level of tryptase (reference range, < 11.4 ng/mL), which is part of the allergenic response, or with biopsy-proven systemic mastocytosis are at increased risk of a systemic sting reaction.11
Presentation: Signs and symptomsvary with severity
Insect bites and stings usually cause transient local inflammation and, occasionally, a toxic reaction. Allergic hypersensitivity can result in a large local reaction or a generalized systemic reaction12:
- A small local reaction is transient and mild, develops directly at the site of the sting, and can last several days.13
- A large (or significant) local reaction, defined as swelling > 10 cm in diameter (FIGURE 1) and lasting > 24 hours, occurs in 2% to 26% of people who have been bitten or stung.14 This is an immunoglobulin (Ig) E–mediated late-phase reaction that can be accompanied by fatigue and nausea.12,13,15 For a patient with a large local reaction, the risk of a concomitant systemic reaction is 4% to 10%, typically beginning within 30 minutes after envenomation or, possibly, delayed for several hours or marked by a biphasic interval.16
- Characteristics of a systemic reaction are urticaria, angioedema, bronchospasm, large-airway edema, hypotension, and other clinical manifestations of anaphylaxis.17 In the United States, a systemic sting reaction is reported to occur in approximately 3% of bite and sting victims. Mortality among the general population from a systemic bite or sting reaction is 0.16 for every 100,000 people,2 and at least 40 to 100 die every year in the United States from anaphylaxis resulting from an insect bite or sting.18
- The most severe anaphylactic reactions involve the cardiovascular and respiratory systems, commonly including hypotension and symptoms of upper- or lower-airway obstruction. Laryngeal edema and circulatory failure are the most common mechanisms of anaphylactic death.19
Bees and wasps
Hymenoptera stinging insects include the family Apidae (honey bee, bumblebee, and sweat bee) and Vespidae (yellow jacket, yellow- and white-faced hornets, and paper wasp). A worker honey bee can sting only once, leaving its barbed stinger in the skin; a wasp, hornet, and yellow jacket can sting multiple times (FIGURE 2).2
Continue to: Bee and wasp sting...
Bee and wasp sting allergies are the most common insect venom allergic reactions. A bee sting is more likely to lead to a severe allergic reaction than a wasp sting. Allergic reactions to hornet and bumblebee stings are less common but can occur in patients already sensitized to wasp and honey bee stings.20,21
Management. Remove honey bee stingers by scraping the skin with a fingernail or credit card. Ideally, the stinger should be removed in the first 30 seconds, before the venom sac empties. Otherwise, intense local inflammation, with possible lymphangitic streaking, can result.22
For guidance on localized symptomatic care of bee and wasp stings and bites and stings from other sources discussed in this article, see “Providing relief and advanced care” on page E6.
Centipedes and spiders
Centipedes are arthropods of the class Chilopoda, subphylum Myriapoda, that are characterized by repeating linear (metameric) segments, each containing 1 pair of legs.23 Centipedes have a pair of poison claws behind the head that are used to paralyze prey—usually, small insects.23,24 The bite of a larger centipede can cause a painful reaction that generally subsides after a few hours but can last several days. Centipede bites are usually nonfatal to humans.23
Spiders belong to the class Arachnida, order Araneae. They have 8 legs with chelicerae (mouthpiece, or “jaws”) that inject venom into prey.25 Most spiders found in the United States cannot bite through human skin.26,27 Common exceptions are black widow and brown recluse spiders, which each produce a distinct toxic venom that can cause significant morbidity in humans through a bite, although bites are rarely fatal.26,27
The brown recluse spider is described as having a violin-shaped marking on the abdomen; the body is yellowish, tan, or dark brown. A bite can produce tiny fang marks and cause dull pain at the site of the bite that spreads quickly; myalgia; and pain in the stomach, back, chest, and legs.28,29 The bite takes approximately 7 days to resolve. In a minority of cases, a tender erythematous halo develops, followed by a severe necrotic ulcer, or loxoscelism (FIGURE 3; 40% of cases) or scarring (13%), or both.29,30
Continue to: In contrast...
In contrast, the body of a black widow spider is black; females exhibit a distinctive red or yellow hourglass marking on their ventral aspect.28,31 The pinprick sensation of a bite leads to symptoms that can include erythema, swelling, pain, stiffness, chills, fever, nausea, and stomach pain.30,32
Management. Again, see “Providing relief and advanced care” on page E6. Consider providing antivenin treatment for moderate or severe bites of brown recluse and black widow spiders.
Fleas
Fleas are members of the order Siphonaptera. They are small (1.5-3.2 mm long), reddish brown, wingless, blood-sucking insects with long legs that allow them to jump far (12 or 13 inches) and high (6 or 7 inches).33 Domesticated cats and dogs are the source of most flea infestations, resulting in an increased risk of exposure for humans.34,35 Flea bites, which generally occur on lower extremities, develop into a small, erythematous papule with a halo (FIGURE 4) and associated mild edema, and cause intense pruritus 30 minutes after the bite.35-37
Fleas are a vector for severe microbial infections, including bartonellosis, bubonic plague, cat-flea typhus, murine typhus, cat-scratch disease, rickettsial disease, and tularemia. Tungiasis is an inflammatory burrowing flea infestation—not a secondary infection for which the flea is a vector.34,35
Preventive management. Repellents, including products that contain DEET (N,N-diethyl-meta-toluamide), picaridin (2-[2-hydroxyethyl]-1-piperidinecarboxylic acid 1-methylpropyl ester), and PMD (p-menthane-3,8-diol, a chemical constituent of Eucalyptus citriodora oil) can be used to prevent flea bites in humans.33,38 Studies show that the scent of other botanic oils, including lavender, cedarwood, and peppermint, can also help prevent infestation by fleas; however, these compounds are not as effective as traditional insect repellents.33,38
Flea control is difficult, requiring a multimodal approach to treating the infested animal and its environment.39 Treatment of the infested domestic animal is the primary method of preventing human bites. Nonpesticidal control involves frequent cleaning of carpeting, furniture, animal bedding, and kennels. Insecticides can be applied throughout the house to combat severe infestation.33,38
Continue to: The Centers for Disease Control and Prevention...
The Centers for Disease Control and Prevention provide a general introduction to getting rid of fleas for pet owners.40 For specific guidance on flea-eradication strategies and specific flea-control products, advise patients to seek the advice of their veterinarian.
Flies and biting midges
Flies are 2-winged insects belonging to the order Diptera. Several fly species can bite, causing a local inflammatory reaction; these include black flies, deer flies, horse flies, and sand flies. Signs and symptoms of a fly bite include pain, pruritus, erythema, and mild swelling (FIGURE 5).41,42 Flies can transmit several infections, including bartonellosis, enteric bacterial disease (eg, caused by Campylobacter spp), leishmaniasis, loiasis, onchocerciasis, and trypanosomiasis.43
Biting midges, also called “no-see-ums,” biting gnats, moose flies, and “punkies,”44 are tiny (1-3 mm long) blood-sucking flies.45 Bitten patients often report not having seen the midge because it is so small. The bite typically starts as a small, erythematous papule that develops into a dome-shaped blister and can be extraordinarily pruritic and painful.44 The majority of people who have been bitten develop a hypersensitivity reaction, which usually resolves in a few weeks.
Management. Suppressing adult biting midges with an environmental insecticide is typically insufficient because the insecticide must be sprayed daily to eradicate active midges and generally does not affect larval habitat. Insect repellents and biopesticides, such as oil of lemon eucalyptus, can be effective in reducing the risk of bites.44,45
Mosquitoes
Mosquitoes are flying, blood-sucking insects of the order Diptera and family Culicidae. Anopheles, Culex, and Aedes genera are responsible for most bites of humans.
The bite of a mosquito produces an indurated, limited local reaction characterized by a pruritic wheal (3-29 mm in diameter) with surrounding erythema (FIGURE 6) that peaks in approximately 30 minutes, although patients might have a delayed reaction hours later.46 Immunocompromised patients might experience a more significant local inflammatory reaction that is accompanied by low-grade fever, hives, or swollen lymph nodes.46,47
Mosquitoes are a vector for serious infections, including dengue, Japanese encephalitis, malaria, and yellow fever, and disease caused by Chikungunya, West Nile, and Zika viruses.
Continue to: Management
Management. Advise patients to reduce their risk by using insect repellent, sleeping under mosquito netting, and wearing a long-sleeve shirt and long pants when traveling to endemic areas or when a local outbreak occurs.48
Ticks
Ticks belong to the order Parasitiformes and families Ixodidae and Argasidae. Hard ticks are found in brushy fields and tall grasses and can bite and feed on humans for days. Soft ticks are generally found around animal nests.29 Tick bites can cause a local reaction that includes painful, erythematous, inflammatory papular lesions (FIGURE 7).49
Ticks can transmit several infectious diseases. Depending on the microbial pathogen and the genus and species of tick, it takes 2 to 96 hours for the tick to attach to skin and transmit the pathogen to the human host. The TABLE29,49,50 provides an overview of tick species in the United States, diseases that they can transmit, and the geographic distribution of those diseases.
Management. Ticks should be removed with fine-tipped tweezers. Grasp the body of the tick close to the skin and pull upward while applying steady, even pressure. After removing the tick, clean the bite and the surrounding area with alcohol or with soap and water. Dispose of a live tick by flushing it down the toilet; or, kill it in alcohol and either seal it in a bag with tape or place it in a container.50
Diagnosis and the utilityof special testing
The diagnosis of insect, arachnid, and other arthropod bites and stings depends on the history, including obtaining a record of possible exposure and a travel history; the timing of the bite or sting; and associated signs and symptoms.18,51
Venom skin testing. For Hymenoptera stings, intradermal tests using a venom concentration of 0.001 to 1 μg/mL are positive in 65% to 80% of patients with a history of a systemic insect-sting allergic reaction. A negative venom skin test can occur during the 3-to-6-week refractory period after a sting reaction or many years later, which represents a loss of sensitivity. Positive venom skin tests are used to confirm allergy and identify specific insects to which the patient is allergic.11,12
Continue to: Allergen-specific IgE antibody testing.
Allergen-specific IgE antibody testing. These serum assays—typically, radioallergosorbent testing (RAST)—are less sensitive than venom skin tests. RAST is useful when venom skin testing cannot be performed or when skin testing is negative in a patient who has had a severe allergic reaction to an insect bite or sting. Serum IgE-specific antibody testing is preferred over venom skin testing in patients who are at high risk of anaphylaxis.52,53
Providing reliefand advanced care
Symptomatic treatment of mild bites and stings includes washing the affected area with soap and water and applying a cold compress to reduce swelling.54 For painful lesions, an oral analgesic can be prescribed.
For mild or moderate pruritus, a low- to midpotency topical corticosteroid (eg, hydrocortisone valerate cream 0.2% bid), topical calamine, or pramoxine can be applied,or a nonsedating oral antihistamine, such as loratadine (10 mg/d) or cetirizine (10 mg/d), can be used.14,55 For severe itching, a sedating antihistamine, such as hydroxyzine (10-25 mg every 4 to 6 hours prn), might help relieve symptoms; H1- and H2-receptor antagonists can be used concomitantly.54,55
Significant local symptoms. Large local reactions are treated with a midpotency topical corticosteroid (eg, triamcinolone acetonide cream 0.1% bid) plus an oral antihistamine to relieve pruritus and reduce allergic inflammation. For a more severe reaction, an oral corticosteroid (prednisone 1 mg/kg; maximum dosage, 50 mg/d) can be given for 5 to 7 days.54-56
Management of a necrotic ulcer secondary to a brown recluse spider bite is symptomatic and supportive. The size of these wounds can increase for as long as 10 days after the bite; resolution can require months of wound care, possibly with debridement. Rarely, skin grafting is required.27,28,31
VIT. Some studies show that VIT can improve quality of life in patients with prolonged, frequent, and worsening reactions to insect bites or stings and repeated, unavoidable exposures.55,56 VIT is recommended for patients with systemic hypersensitivity and a positive venom skin test result. It is approximately 95% effective in preventing or reducing severe systemic reactions and reduces the risk of anaphylaxis (see next section) and death.57 The maintenance dosage of VIT is usually 100 μg every 4 to 6 weeks; optimal duration of treatment is 3 to 5 years.58
Continue to: After VIT is complete...
After VIT is complete, counsel patients that a mild systemic reaction is still possible after an insect bite or sting. More prolonged, even lifetime, treatment should be considered for patients who have58,59
- a history of severe, life-threatening allergic reactions to bites and stings
- honey bee sting allergy
- mast-cell disease
- a history of anaphylaxis while receiving VIT.
Absolute contraindications to VIT include a history of serious immune disease, chronic infection, or cancer.58,59
Managing anaphylaxis
This severe allergic reaction can lead to death if untreated. First-line therapy is intramuscular epinephrine, 0.01 mg/kg (maximum single dose, 0.5 mg) given every 5 to 15 minutes.14,60 Epinephrine auto-injectors deliver a fixed dose and are labeled according to weight. Administration of O2 and intravenous fluids is recommended for hemodynamically unstable patients.60,61 Antihistamines and corticosteroids can be used as secondary treatment but should not replace epinephrine.56
After preliminary improvement, patients might decompensate when the epinephrine dose wears off. Furthermore, a biphasic reaction, variously reported in < 5% to as many as 20% of patients,61,62 occurs hours after the initial anaphylactic reaction. Patients should be monitored, therefore, for at least 6 to 8 hours after an anaphylactic reaction, preferably in a facility equipped to treat anaphylaxis.17,56
Before discharge, patients who have had an anaphylactic reaction should be given a prescription for epinephrine and training in the use of an epinephrine auto-injector. Allergen avoidance, along with an emergency plan in the event of a bite or sting, is recommended. Follow-up evaluation with an allergist or immunologist is essential for proper diagnosis and to determine whether the patient is a candidate for VIT.14,17
CORRESPONDENCE
Ecler Ercole Jaqua, MD, DipABLM, FAAFP, 1200 California Street, Suite 240, Redlands, CA 92374; [email protected].
1. Numbers of insects (species and individuals). Smithsonian BugInfo Web site. www.si.edu/spotlight/buginfo/bugnos. Accessed November 25, 2020.
2. Antonicelli L, Bilò MB, Bonifazi F. Epidemiology of Hymenoptera allergy. Curr Opin Allergy Clin Immunol. 2002;2:341-346.
3. Jack jumper ant allergy. Australasian Society of Clinical Immunology and Allergy (ASCIA) Web site. Updated October 19, 2019. www.allergy.org.au/patients/insect-allergy-bites-and-stings/jack-jumper-ant-allergy. Accessed November 25, 2020.
4. Kemp SF, deShazo RD, Moffit JE, et al. Expanding habitat of the imported fire ant (Solenopsis invicta): a public health concern. J Allergy Clin Immunol. 2000;105:683-691.
5. Goodnight ML. Arachnid. In: Encyclopædia Britannica. 2012. www.britannica.com/animal/arachnid. Accessed November 25, 2020.
6. Despommier DD, Gwadz RW, Hotez PJ. Arachnids. In: Despommier DD, Gwadz RW, Hotez PJ. Parasitic Diseases. 3rd ed. Springer-Verlag; 1995:268-283.
7. Diaz JH, Leblanc KE. Common spider bites. Am Fam Physician. 2007;75:869-873.
8. Mowry JB, Spyker DA, Cantilena LR Jr, McMillan N, Ford M. 2013 Annual report of the American Association of Poison Control Centers’ National Poison Data System (NPDS): 31st Annual Report. Clin Toxicol (Phila). 2014;52:1032-1283.
9. Pucci S, Antonicelli L, Bilò MB, et al. Shortness of interval between two stings as risk factor for developing Hymenoptera venom allergy. Allergy.1994;49:894-896.
10. Müller UR. Bee venom allergy in beekeepers and their family members. Curr Opin Allergy Clin Immunol. 2005;5:343-347.
11. Müller UR. Cardiovascular disease and anaphylaxis. Curr Opin Allergy Clin Immunol. 2007;7:337-341.
12. Golden DBK. Stinging insect allergy. Am Fam Physician. 2003;67:2541-2546.
13. Golden DBK, Demain T, Freeman T, et al. Stinging insect hypersensitivity: a practice parameter update 2016. Ann Allergy Asthma Immunol. 2017;118:28-54.
14. Bilò BM, Rueff F, Mosbech H, et al; EAACI Interest Group on Insect Venom Hypersensitivity. Diagnosis of Hymenoptera venom allergy. Allergy. 2005;60:1339-1349.
15. Reisman RE. Insect stings. N Engl J Med. 1994;331:523-527.
16. Pucci S, D’Alò S, De Pasquale T, et al. Risk of anaphylaxis in patients with large local reactions to hymenoptera stings: a retrospective and prospective study. Clin Mol Allergy. 2015;13:21.
17. Golden DBK. Large local reactions to insect stings. J Allergy Clin Immunol Pract. 2015;3:331-334.
18. Clark S, Camargo CA Jr. Emergency treatment and prevention of insect-sting anaphylaxis. Curr Opin Allergy Clin Immunol. 2006;6:279-283.
19. Stinging insect allergy. In: Volcheck GW. Clinical Allergy: Diagnosis and Management. Humana Press; 2009:465-479.
20. Järvinen KM, Celestin J. Anaphylaxis avoidance and management: educating patients and their caregivers. J Asthma Allergy. 2014;7:95-104.
21. Institute for Quality and Efficiency in Health Care (IQWiG). Insect venom allergies: overview. InformedHealth.org. Updated May 7, 2020. www.ncbi.nlm.nih.gov/pubmedhealth/PMH0096282/. Accessed November 25, 2020.
22. Casale TB, Burks AW. Clinical practice. Hymenoptera-sting hypersensitivity. N Engl J Med. 2014;370:1432-1439.
23. Shelley RM. Centipedes and millipedes with emphasis on North American fauna. Kansas School Naturalist. 1999;45:1-16. https://sites.google.com/g.emporia.edu/ksn/ksn-home/vol-45-no-3-centipedes-and-millipedes-with-emphasis-on-n-america-fauna#h.p_JEf3uDlTg0jw. Accessed November 25, 2020.
24. Ogg B. Centipedes and millipedes. Nebraska Extension in Lancaster County Web site. https://lancaster.unl.edu/pest/resources/CentipedeMillipede012.shtml. Accessed November 25, 2020.
25. Cushing PE. Spiders (Arachnida: Araneae). In: Capinera JL, ed. Encyclopedia of Entomology. Springer, Dordrecht; 2008:226.
26. Diaz JH, Leblanc KE. Common spider bites. Am Fam Physician. 2007;75:869-873.
27. The National Institute for Occupational Safety and Health (NIOSH), Centers for Disease Control and Prevention. Venomous spiders. www.cdc.gov/niosh/topics/spiders/. Accessed November 25, 2020.
28. Starr S. What you need to know to prevent a poisonous spider bite. AAP News. 2013;34:42. www.aappublications.org/content/aapnews/34/9/42.5.full.pdf. Accessed November 25, 2020.
29. Spider bites. Mayo Clinic Web site. www.mayoclinic.org/diseases-conditions/spider-bites/symptoms-causes/syc-20352371. Accessed November 25, 2020.
30. Barish RA, Arnold T. Spider bites. In: Merck Manual (Professional Version). Merck Sharp & Dohme Corp.; 2016. www.merckmanuals.com/professional/injuries-poisoning/bites-and-stings/spider-bites. Accessed November 25, 2020.
31. Juckett G. Arthropod bites. Am Fam Physician. 2013;88:841-847.
32. Clark RF, Wethern-Kestner S, Vance MV, et al. Clinical presentation and treatment of black widow spider envenomation: a review of 163 cases. Ann Emerg Med. 1992;21:782-787.
33. Koehler PG, Pereira RM, Diclaro JW II. Fleas. Publication ENY-025. University of Florida IFAS Extension. Revised January 2012. https://edis.ifas.ufl.edu/ig087. Accessed November 25, 2020.
34. Bitam I, Dittmar K, Parola P, et al. Fleas and flea-borne diseases. Int J Infect Dis. 2010;14:e667-e676.
35. Leulmi H, Socolovschi C, Laudisoit A, et al. Detection of Rickettsia felis, Rickettsia typhi, Bartonella species and Yersinia pestis in fleas (Siphonaptera) from Africa. PLoS Negl Trop Dis. 2014;8:e3152.
36. Naimer SA, Cohen AD, Mumcuoglu KY, et al. Household papular urticaria. Isr Med Assoc J. 2002;4(11 suppl):911-913.
37. Golomb MR, Golomb HS. What’s eating you? Cat flea (Ctenocephalides felis). Cutis. 2010;85:10-11.
38. Dryden MW. Flea and tick control in the 21st century: challenges and opportunities. Vet Dermatol. 2009;20:435-440.
39. Dryden MW. Fleas in dogs and cats. Merck Sharp & Dohme Corporation: Merck Manual Veterinary Manual. Updated December 2014. www.merckvetmanual.com/integumentary-system/fleas-and-flea-allergy-dermatitis/fleas-in-dogs-and-cats. Accessed November 25, 2020.
40. Centers for Disease Control and Prevention. Getting rid of fleas. www.cdc.gov/fleas/getting_rid.html. Accessed November 25, 2020.
41. Chattopadhyay P, Goyary D, Dhiman S, et al. Immunomodulating effects and hypersensitivity reactions caused by Northeast Indian black fly salivary gland extract. J Immunotoxicol. 2014;11:126-132.
42. Hrabak TM, Dice JP. Use of immunotherapy in the management of presumed anaphylaxis to the deer fly. Ann Allergy Asthma Immunol. 2003;90:351-354.
43. Royden A, Wedley A, Merga JY, et al. A role for flies (Diptera) in the transmission of Campylobacter to broilers? Epidemiol Infect. 2016;144:3326-3334.
44. Fradin MS, Day JF. Comparative efficacy of insect repellents against mosquito bites. N Engl J Med. 2002;347:13-18.
45. Carpenter S, Groschup MH, Garros C, et al. Culicoides biting midges, arboviruses and public health in Europe. Antiviral Res. 2013;100:102-113.
46. Peng Z, Yang M, Simons FE. Immunologic mechanisms in mosquito allergy: correlation of skin reactions with specific IgE and IgG anti-bodies and lymphocyte proliferation response to mosquito antigens. Ann Allergy Asthma Immunol. 1996;77:238-244.
47. Simons FE, Peng Z. Skeeter syndrome. J Allergy Clin Immunol. 1999;104:705-707.
48. Centers for Disease Control and Prevention. Travelers’ health. Clinician resources. wwwnc.cdc.gov/travel/page/clinician-information-center. Accessed November 25, 2020.
49. Gauci M, Loh RK, Stone BF, et al. Allergic reactions to the Australian paralysis tick, Ixodes holocyclus: diagnostic evaluation by skin test and radioimmunoassay. Clin Exp Allergy. 1989;19:279-283.
50. Centers for Disease Control and Prevention. Ticks. Removing a tick. www.cdc.gov/ticks/removing_a_tick.html. Accessed November 25, 2020.
51. Golden DB, Kagey-Sobotka A, Norman PS, et al. Insect sting allergy with negative venom skin test responses. J Allergy Clin Immunol. 2001;107:897-901.
52. Arzt L, Bokanovic D, Schrautzer C, et al. Immunological differences between insect venom-allergic patients with and without immunotherapy and asymptomatically sensitized subjects. Allergy. 2018;73:1223-1231.
53. Heddle R, Golden DBK. Allergy to insect stings and bites. World Allergy Organization Web site. Updated August 2015. www.worldallergy.org/education-and-programs/education/allergic-disease-resource-center/professionals/allergy-to-insect-stings-and-bites. Accessed November 25, 2020.
54. RuëffF, Przybilla B, Müller U, et al. The sting challenge test in Hymenoptera venom allergy. Position paper of the Subcommittee on Insect Venom Allergy of the European Academy of Allergology and Clinical Immunology. Allergy. 1996;51:216-225.
55. Management of simple insect bites: where’s the evidence? Drug Ther Bull. 2012;50:45-48.
56. Tracy JM. Insect allergy. Mt Sinai J Med. 2011;78:773-783.
57. Golden DBK. Insect sting allergy and venom immunotherapy: a model and a mystery. J Allergy Clin Immunol. 2005;115:439-447.
58. Winther L, Arnved J, Malling H-J, et al. Side-effects of allergen-specific immunotherapy: a prospective multi-centre study. Clin Exp Allergy. 2006;36:254-260.
59. Mellerup MT, Hahn GW, Poulsen LK, et al. Safety of allergen-specific immunotherapy. Relation between dosage regimen, allergen extract, disease and systemic side-effects during induction treatment. Clin Exp Allergy. 2000;30:1423-1429.
60. Anaphylaxis and insect stings and bites. Med Lett Drugs Ther. 2017;59:e79-e82.
61. Sampson HA, Muñoz-Furlong A, Campbell RL, et al. Second symposium on the definition and management of anaphylaxis: summary report—second National Institute of Allergy and Infectious Disease/Food Allergy and Anaphylaxis Network symposium. Ann Emerg Med. 2006;47:373-380.
62. Pflipsen MC, Vega Colon KM. Anaphylaxis: recognition and management. Am Fam Physician. 2020;102:355-362. Accessed November 25, 2020.
1. Numbers of insects (species and individuals). Smithsonian BugInfo Web site. www.si.edu/spotlight/buginfo/bugnos. Accessed November 25, 2020.
2. Antonicelli L, Bilò MB, Bonifazi F. Epidemiology of Hymenoptera allergy. Curr Opin Allergy Clin Immunol. 2002;2:341-346.
3. Jack jumper ant allergy. Australasian Society of Clinical Immunology and Allergy (ASCIA) Web site. Updated October 19, 2019. www.allergy.org.au/patients/insect-allergy-bites-and-stings/jack-jumper-ant-allergy. Accessed November 25, 2020.
4. Kemp SF, deShazo RD, Moffit JE, et al. Expanding habitat of the imported fire ant (Solenopsis invicta): a public health concern. J Allergy Clin Immunol. 2000;105:683-691.
5. Goodnight ML. Arachnid. In: Encyclopædia Britannica. 2012. www.britannica.com/animal/arachnid. Accessed November 25, 2020.
6. Despommier DD, Gwadz RW, Hotez PJ. Arachnids. In: Despommier DD, Gwadz RW, Hotez PJ. Parasitic Diseases. 3rd ed. Springer-Verlag; 1995:268-283.
7. Diaz JH, Leblanc KE. Common spider bites. Am Fam Physician. 2007;75:869-873.
8. Mowry JB, Spyker DA, Cantilena LR Jr, McMillan N, Ford M. 2013 Annual report of the American Association of Poison Control Centers’ National Poison Data System (NPDS): 31st Annual Report. Clin Toxicol (Phila). 2014;52:1032-1283.
9. Pucci S, Antonicelli L, Bilò MB, et al. Shortness of interval between two stings as risk factor for developing Hymenoptera venom allergy. Allergy.1994;49:894-896.
10. Müller UR. Bee venom allergy in beekeepers and their family members. Curr Opin Allergy Clin Immunol. 2005;5:343-347.
11. Müller UR. Cardiovascular disease and anaphylaxis. Curr Opin Allergy Clin Immunol. 2007;7:337-341.
12. Golden DBK. Stinging insect allergy. Am Fam Physician. 2003;67:2541-2546.
13. Golden DBK, Demain T, Freeman T, et al. Stinging insect hypersensitivity: a practice parameter update 2016. Ann Allergy Asthma Immunol. 2017;118:28-54.
14. Bilò BM, Rueff F, Mosbech H, et al; EAACI Interest Group on Insect Venom Hypersensitivity. Diagnosis of Hymenoptera venom allergy. Allergy. 2005;60:1339-1349.
15. Reisman RE. Insect stings. N Engl J Med. 1994;331:523-527.
16. Pucci S, D’Alò S, De Pasquale T, et al. Risk of anaphylaxis in patients with large local reactions to hymenoptera stings: a retrospective and prospective study. Clin Mol Allergy. 2015;13:21.
17. Golden DBK. Large local reactions to insect stings. J Allergy Clin Immunol Pract. 2015;3:331-334.
18. Clark S, Camargo CA Jr. Emergency treatment and prevention of insect-sting anaphylaxis. Curr Opin Allergy Clin Immunol. 2006;6:279-283.
19. Stinging insect allergy. In: Volcheck GW. Clinical Allergy: Diagnosis and Management. Humana Press; 2009:465-479.
20. Järvinen KM, Celestin J. Anaphylaxis avoidance and management: educating patients and their caregivers. J Asthma Allergy. 2014;7:95-104.
21. Institute for Quality and Efficiency in Health Care (IQWiG). Insect venom allergies: overview. InformedHealth.org. Updated May 7, 2020. www.ncbi.nlm.nih.gov/pubmedhealth/PMH0096282/. Accessed November 25, 2020.
22. Casale TB, Burks AW. Clinical practice. Hymenoptera-sting hypersensitivity. N Engl J Med. 2014;370:1432-1439.
23. Shelley RM. Centipedes and millipedes with emphasis on North American fauna. Kansas School Naturalist. 1999;45:1-16. https://sites.google.com/g.emporia.edu/ksn/ksn-home/vol-45-no-3-centipedes-and-millipedes-with-emphasis-on-n-america-fauna#h.p_JEf3uDlTg0jw. Accessed November 25, 2020.
24. Ogg B. Centipedes and millipedes. Nebraska Extension in Lancaster County Web site. https://lancaster.unl.edu/pest/resources/CentipedeMillipede012.shtml. Accessed November 25, 2020.
25. Cushing PE. Spiders (Arachnida: Araneae). In: Capinera JL, ed. Encyclopedia of Entomology. Springer, Dordrecht; 2008:226.
26. Diaz JH, Leblanc KE. Common spider bites. Am Fam Physician. 2007;75:869-873.
27. The National Institute for Occupational Safety and Health (NIOSH), Centers for Disease Control and Prevention. Venomous spiders. www.cdc.gov/niosh/topics/spiders/. Accessed November 25, 2020.
28. Starr S. What you need to know to prevent a poisonous spider bite. AAP News. 2013;34:42. www.aappublications.org/content/aapnews/34/9/42.5.full.pdf. Accessed November 25, 2020.
29. Spider bites. Mayo Clinic Web site. www.mayoclinic.org/diseases-conditions/spider-bites/symptoms-causes/syc-20352371. Accessed November 25, 2020.
30. Barish RA, Arnold T. Spider bites. In: Merck Manual (Professional Version). Merck Sharp & Dohme Corp.; 2016. www.merckmanuals.com/professional/injuries-poisoning/bites-and-stings/spider-bites. Accessed November 25, 2020.
31. Juckett G. Arthropod bites. Am Fam Physician. 2013;88:841-847.
32. Clark RF, Wethern-Kestner S, Vance MV, et al. Clinical presentation and treatment of black widow spider envenomation: a review of 163 cases. Ann Emerg Med. 1992;21:782-787.
33. Koehler PG, Pereira RM, Diclaro JW II. Fleas. Publication ENY-025. University of Florida IFAS Extension. Revised January 2012. https://edis.ifas.ufl.edu/ig087. Accessed November 25, 2020.
34. Bitam I, Dittmar K, Parola P, et al. Fleas and flea-borne diseases. Int J Infect Dis. 2010;14:e667-e676.
35. Leulmi H, Socolovschi C, Laudisoit A, et al. Detection of Rickettsia felis, Rickettsia typhi, Bartonella species and Yersinia pestis in fleas (Siphonaptera) from Africa. PLoS Negl Trop Dis. 2014;8:e3152.
36. Naimer SA, Cohen AD, Mumcuoglu KY, et al. Household papular urticaria. Isr Med Assoc J. 2002;4(11 suppl):911-913.
37. Golomb MR, Golomb HS. What’s eating you? Cat flea (Ctenocephalides felis). Cutis. 2010;85:10-11.
38. Dryden MW. Flea and tick control in the 21st century: challenges and opportunities. Vet Dermatol. 2009;20:435-440.
39. Dryden MW. Fleas in dogs and cats. Merck Sharp & Dohme Corporation: Merck Manual Veterinary Manual. Updated December 2014. www.merckvetmanual.com/integumentary-system/fleas-and-flea-allergy-dermatitis/fleas-in-dogs-and-cats. Accessed November 25, 2020.
40. Centers for Disease Control and Prevention. Getting rid of fleas. www.cdc.gov/fleas/getting_rid.html. Accessed November 25, 2020.
41. Chattopadhyay P, Goyary D, Dhiman S, et al. Immunomodulating effects and hypersensitivity reactions caused by Northeast Indian black fly salivary gland extract. J Immunotoxicol. 2014;11:126-132.
42. Hrabak TM, Dice JP. Use of immunotherapy in the management of presumed anaphylaxis to the deer fly. Ann Allergy Asthma Immunol. 2003;90:351-354.
43. Royden A, Wedley A, Merga JY, et al. A role for flies (Diptera) in the transmission of Campylobacter to broilers? Epidemiol Infect. 2016;144:3326-3334.
44. Fradin MS, Day JF. Comparative efficacy of insect repellents against mosquito bites. N Engl J Med. 2002;347:13-18.
45. Carpenter S, Groschup MH, Garros C, et al. Culicoides biting midges, arboviruses and public health in Europe. Antiviral Res. 2013;100:102-113.
46. Peng Z, Yang M, Simons FE. Immunologic mechanisms in mosquito allergy: correlation of skin reactions with specific IgE and IgG anti-bodies and lymphocyte proliferation response to mosquito antigens. Ann Allergy Asthma Immunol. 1996;77:238-244.
47. Simons FE, Peng Z. Skeeter syndrome. J Allergy Clin Immunol. 1999;104:705-707.
48. Centers for Disease Control and Prevention. Travelers’ health. Clinician resources. wwwnc.cdc.gov/travel/page/clinician-information-center. Accessed November 25, 2020.
49. Gauci M, Loh RK, Stone BF, et al. Allergic reactions to the Australian paralysis tick, Ixodes holocyclus: diagnostic evaluation by skin test and radioimmunoassay. Clin Exp Allergy. 1989;19:279-283.
50. Centers for Disease Control and Prevention. Ticks. Removing a tick. www.cdc.gov/ticks/removing_a_tick.html. Accessed November 25, 2020.
51. Golden DB, Kagey-Sobotka A, Norman PS, et al. Insect sting allergy with negative venom skin test responses. J Allergy Clin Immunol. 2001;107:897-901.
52. Arzt L, Bokanovic D, Schrautzer C, et al. Immunological differences between insect venom-allergic patients with and without immunotherapy and asymptomatically sensitized subjects. Allergy. 2018;73:1223-1231.
53. Heddle R, Golden DBK. Allergy to insect stings and bites. World Allergy Organization Web site. Updated August 2015. www.worldallergy.org/education-and-programs/education/allergic-disease-resource-center/professionals/allergy-to-insect-stings-and-bites. Accessed November 25, 2020.
54. RuëffF, Przybilla B, Müller U, et al. The sting challenge test in Hymenoptera venom allergy. Position paper of the Subcommittee on Insect Venom Allergy of the European Academy of Allergology and Clinical Immunology. Allergy. 1996;51:216-225.
55. Management of simple insect bites: where’s the evidence? Drug Ther Bull. 2012;50:45-48.
56. Tracy JM. Insect allergy. Mt Sinai J Med. 2011;78:773-783.
57. Golden DBK. Insect sting allergy and venom immunotherapy: a model and a mystery. J Allergy Clin Immunol. 2005;115:439-447.
58. Winther L, Arnved J, Malling H-J, et al. Side-effects of allergen-specific immunotherapy: a prospective multi-centre study. Clin Exp Allergy. 2006;36:254-260.
59. Mellerup MT, Hahn GW, Poulsen LK, et al. Safety of allergen-specific immunotherapy. Relation between dosage regimen, allergen extract, disease and systemic side-effects during induction treatment. Clin Exp Allergy. 2000;30:1423-1429.
60. Anaphylaxis and insect stings and bites. Med Lett Drugs Ther. 2017;59:e79-e82.
61. Sampson HA, Muñoz-Furlong A, Campbell RL, et al. Second symposium on the definition and management of anaphylaxis: summary report—second National Institute of Allergy and Infectious Disease/Food Allergy and Anaphylaxis Network symposium. Ann Emerg Med. 2006;47:373-380.
62. Pflipsen MC, Vega Colon KM. Anaphylaxis: recognition and management. Am Fam Physician. 2020;102:355-362. Accessed November 25, 2020.
PRACTICE RECOMMENDATIONS
❯ Recommend that patients use an insect repellent, such as an over-the-counter formulation that contains DEET, picaridin, or PMD (a chemical constituent of Eucalyptus citriodora oil) to prevent flea bites. C
❯ Prescribe nonsedating oral antihistamines as first-line symptomatic treatment of mild-to-moderate pruritus secondary to an insect bite. C
❯ When indicated, refer patients for venom immunotherapy, which is approximately 95% effective in preventing or reducing severe systemic reactions and reduces the risk of anaphylaxis and death. C
Strength of recommendation (SOR)
A Good-quality patient-oriented evidence
B Inconsistent or limited-quality patient-oriented evidence
C Consensus, usual practice, opinion, disease-oriented evidence, case series
Home visits: A practical approach
CASE
Mr. A is a 30-year-old man with neurofibromatosis and myelopathy with associated quadriplegia, complicated by dysphasia and chronic hypercapnic respiratory failure requiring a tracheostomy. He is cared for at home by his very competent mother but requires regular visits with his medical providers for assistance with his complex care needs. Due to logistical challenges, he had been receiving regular home visits even before the COVID-19 pandemic.
After estimating the risk of exposure to the patient, Mr. A’s family and his physician’s office staff scheduled a home visit. Before the appointment, the doctor conducted a virtual visit with the patient and family members to screen for COVID-19 infection, which proved negative. The doctor arranged a visit to coincide with Mr. A’s regular appointment with the home health nurse. He invited the patient’s social worker to attend, as well.
The providers donned masks, face shields, and gloves before entering the home. Mr. A’s temperature was checked and was normal. The team completed a physical exam, assessed the patient’s current needs, and refilled prescriptions. The doctor, nurse, and social worker met afterward in the family’s driveway to coordinate plans for the patient’s future care.
This encounter allowed a vulnerable patient with special needs to have access to care while reducing his risk of undesirable exposure. Also, his health care team’s provision of care in the home setting reduced Mr. A’s anxiety and that of his family members.
Home visits have long been an integral part of what it means to be a family physician. In 1930, roughly 40% of all patient-physician encounters in the United States occurred in patients’ homes. By 1980, this number had dropped to < 1%.1 Still, a 1994 survey of American doctors in 3 primary care specialties revealed that 63% of family physicians, more than the other 2 specialties, still made house calls.2 A 2016 analysis of Medicare claims data showed that between 2006 and 2011, only 5% of American doctors overall made house calls on Medicare recipients, but interestingly, the total number of home visits was increasing.3
This resurgence of interest in home health care is due in part to the increasing number of homebound patients in America, which exceeds the number of those in nursing homes.4 Further, a growing body of evidence indicates that home visits improve patient outcomes. And finally, many family physicians whose work lives have been centered around a busy office or hospital practice have found satisfaction in once again seeing patients in their own homes.
The COVID-19 pandemic has of course presented unique challenges—and opportunities, too—for home visits, which we discuss at the end of the article.
Why aren’t more of us making home visits?
For most of us, the decision not to make home visits is simply a matter of time and money. Although Medicare reimbursement for a home visit is typically about 150% that of a comparable office visit,5 it’s difficult, if not impossible, to make 2 home visits in the time you could see 3 patients in the office. So, economically it’s a net loss. Furthermore, we tend to feel less comfortable in our patients’ homes than in our offices. We have less control outside our own environment, and what happens away from our office is often less predictable—sometimes to the point that we may be concerned for our safety.
Continue to: So why make home visits at all?
So why make home visits at all?
First and foremost, home visits improve patient outcomes. This is most evident in our more vulnerable patients: newborns and the elderly, those who have been recently hospitalized, and those at risk because of their particular home situation. Multiple studies have shown that, for elders, home visits reduce functional decline, nursing home admissions, and mortality by around 25% to 33%.6-8 For those at risk of abuse, a recent systematic review showed that home visits reduce intimate partner violence and child abuse.9 Another systematic review demonstrated that patients with diabetes who received home visits vs usual care were more likely to show improvements in quality of life.10 These patients were also more likely to have lower HbA1c levels and lower systolic blood pressure readings.10 A few caveats apply to these studies:
- all of them targeted “vulnerable” patients
- most studies enlisted interdisciplinary teams and had regular team meetings
- most findings reached significance only after multiple home visits.
A further reason for choosing to become involved in home care is that it builds relationships, understanding, and empathy with our patients. “There is deep symbolism in the home visit.... It says, ‘I care enough about you to leave my power base … to come and see you on your own ground.’”11 And this benefit is 2-way; we also grow to understand and appreciate our patients better, especially if they are different from us culturally or socioeconomically.
Home visits allow the medical team to see challenges the patient has grown accustomed to, and perhaps ones that the patient has deemed too insignificant to mention. For the patient, home visits foster a strong sense of trust with the individual doctor and our health delivery network, and they decrease the need to seek emergency services. Finally, it has been demonstrated that provider satisfaction improves when home visits are incorporated into the work week.12
What is the role of community health workers in home-based care?
Community health workers (CHWs), defined as “frontline public health workers who are trusted members of and/or have an unusually close understanding of the community they serve,”13 can be an integral part of the home-based care team. Although CHWs have variable amounts of formal training, they have a unique perspective on local health beliefs and practices, which can assist the home-care team in providing culturally competent health care services and reduce health care costs.
In a study of children with asthma in Seattle, Washington, patients were randomized to a group that had 4 home visits by CHWs and a group that received usual care. The group that received home visits demonstrated more asthma symptom–free days, improved quality-of-life scores, and fewer urgent care visits.14 Furthermore, the intervention was estimated to save approximately $1300 per patient, resulting in a return on investment of 190%. Similarly, in a study comparing inappropriate emergency department (ED) visits between children who received CHW visits and those who did not, patients in the intervention group were significantly less likely to visit the ED for ambulatory complaints (18.2% vs 35.1%; P = .004).15
Continue to: What is the role of social workersin home-based care?
What is the role of social workersin home-based care?
Social workers can help meet the complex medical and biopsychosocial needs of the homebound population.16 A study by Cohen et al based in Israel concluded that homebound participants had a significantly higher risk for mortality, higher rates of depression, and difficulty completing instrumental activities of daily living when compared with their non-homebound counterparts.17
The Mount Sinai (New York) Visiting Doctors Program (MSVD) is a home-based care team that uses social workers to meet the needs of their complex patients.18 The social workers in the MSVD program provide direct counseling, make referrals to government and community resources, and monitor caregiver burden. Using a combination of measurement tools to assess caregiver burden, Ornstein et al demonstrated that the MSVD program led to a decrease in unmet needs and in caregiver burden.19,20 Caregiver burnout can be assessed using the Caregiver Burden Inventory, a validated 24-item questionnaire.21
What electronic tools are availableto monitor patients at home?
Although expensive in terms of both dollars and personnel time, telemonitoring allows home care providers to receive real-time, updated information regarding their patients.
Chronic obstructive pulmonary disease (COPD). One systematic review showed that although telemonitoring of patients with COPD improved quality of life and decreased COPD exacerbations, it did not reduce the risk of hospitalization and, therefore, did not reduce health care costs.22 Telemonitoring in COPD can include transmission of data about spirometry parameters, weight, temperature, blood pressure, sputum color, and 6-minute walk distance.23,24
Congestive heart failure (CHF). A 2010 Cochrane review found that telemonitoring of patients with CHF reduced all-cause mortality (risk ratio [RR] = 0.66; P < .0001).25 The Telemedical Interventional Management in Heart Failure II (TIM-HF2) trial,conducted from 2013 to 2017, compared usual care for CHF patients with care incorporating daily transmission of body weight, blood pressure, heart rate, electrocardiogram tracings, pulse oximetry, and self-rated health status.26 This study showed that the average number of days lost per year due to hospital admission was less in the telemonitoring group than in the usual care group (17.8 days vs. 24.2 days; P = .046). All-cause mortality was also reduced in the telemonitoring group (hazard ratio = 0.70; P = .028).
Continue to: What role do “home hospitals” play?
What role do “home hospitals” play?
Home hospitals provide acute or subacute treatment in a patient’s home for a condition that would normally require hospitalization.27 In a meta-analysis of 61 studies evaluating the effectiveness of home hospitals, this option was more likely to reduce mortality (odds ratio [OR] = 0.81; P = .008) and to reduce readmission rates (OR = 0.75; P = .02).28 In a study of 455 older adults, Leff et al found that hospital-at-home was associated with a shorter length of stay (3.2 vs. 4.9 days; P = .004) and that the mean cost was lower for hospital-at-home vs traditional hospital care.29
However, a 2016 Cochrane review of 16 randomized controlled trials comparing hospital-at-home with traditional hospital care showed that while care in a hospital-at-home may decrease formal costs, if costs for caregivers are taken into account, any difference in cost may disappear.30
Although the evidence for cost saving is variable, hospital-at-home admission has been shown to reduce the likelihood of living in a residential care facility at 6 months (RR = 0.35; P < .0001).30 Further, the same Cochrane review showed that admission avoidance may increase patient satisfaction with the care provided.30
Finally, a recent randomized trial in a Boston-area hospital system showed that patients cared for in hospital-at-home were significantly less likely to be readmitted within 30 days and that adjusted cost was about two-thirds the cost of traditional hospital care.31
What is the physician’s rolein home health care?
While home health care is a team effort, the physician has several crucial roles. First, he or she must make the determination that home care is appropriate and feasible for a particular patient. Appropriate, meaning there is evidence that this patient is likely to benefit from home care. Feasible, meaning there are resources available in the community and family to safely care for the patient at home. “Often a house call will serve as the first step in developing a home-based-management plan.”32
Continue to: Second, the physician serves...
Second, the physician serves an important role in directing and coordinating the team of professionals involved. This primarily means helping the team to communicate with one another. Before home visits begin, the physician’s office should reach out not only to the patient and family, but also to any other health care personnel involved in the patient’s home care. Otherwise, many of the health care providers involved will never have face-to-face interaction with the physician. Creation of the coordinated health team minimizes duplication and miscommunication; it also builds a valuable bond.
How does one go about making a home visit?
Scheduling. What often works best in a busy practice is to schedule home visits for the end of the workday or to devote an entire afternoon to making home visits to several patients in one locale. Also important is scheduling times, if possible, when important family members or other caregivers are at home or when other members of the home care team can accompany you.
What to bring along. Carry a “home visit bag” that includes equipment you’re likely to need and that is not available away from your office. A minimally equipped visit bag would include different-sized blood pressure cuffs, a glucometer, a pulse oximeter, thermometers, and patient education materials. Other suggested contents are listed in TABLE 1.
Dos and don’ts. Take a few minutes when you first arrive to simply visit with the patient. Sit down and introduce yourself and any members of the home care team that the patient has not met. Take an interim history. While you’re doing this, be observant: Is the home neat or cluttered? Is the indoor temperature comfortable? Are there fall hazards? Is there a smell of cigarette smoke? Are there any indoor combustion sources (eg, wood stove or kerosene heater)? Ask questions such as: Who lives here with you? Can you show me where you keep your medicines? (If the patient keeps insulin or any other medicines in the refrigerator, ask to see it. Note any apparent food scarcity.)
During your exam, pay particular attention to whether vital signs are appreciably different than those measured in the office or hospital. Pay special attention to the patient’s functional abilities. “A subtle, but critical distinction between medical management in the home and medical management in the hospital, clinic, or office is the emphasis on the patient’s functional abilities, family assistance, and environmental factors.”33
Observe the patient’s use of any home technology, if possible; this can be as simple as home oxygenation or as complex as home hemodialysis. Assess for any apparent caregiver stress. Finally, don’t neglect to offer appropriate emotional and spiritual support to the patient and family and to schedule the next follow-up visit before you leave.
Continue to: Documentation and reimbursement.
Documentation and reimbursement. While individual electronic medical records may require use of particular forms of documentation, using a home visit template when possible can be extremely helpful (TABLE 2). A template not only assures thoroughness and consistency (pharmacy, home health contacts, billing information) but also serves as a prompt to survey the patient and the caregivers about nonmedical, but essential, social and well-being services. The document should be as simple and user-friendly as possible.
Not all assessments will be able to be done at each visit but seeing them listed in the template can be helpful. Billing follows the same principles as for office visits and has similar requirements for documentation. Codes for the most common types of home visits are listed in TABLE 3.
Where can I get help?
Graduates of family medicine residency programs are required to receive training in home visits by the Accreditation Council for Graduate Medical Education (ACGME). Current ACGME program requirements stipulate that “residents must demonstrate competence to independently diagnose, manage, and integrate the care of patients of all ages in various outpatient settings, including the FMP [family medicine practice] site and home environment,” and “residents must be primarily responsible for a panel of continuity patients, integrating each patient’s care across all settings, including the home ...” [emphasis added].34
For those already in practice, one of the hardest parts of doing home visits is feeling alone, especially if few other providers in your community engage in home care. As you run into questions and challenges with incorporating home care of patients into your practice, one excellent resource is the American Academy of Home Care Medicine (www.aahcm.org/). Founded in 1988 and headquartered in Chicago, it not only provides numerous helpful resources, but serves as a networking tool for physicians involved in home care.
This unprecedented pandemichas allowed home visits to shine
As depicted in our opening patient case, patients who have high-risk conditions and those who are older than 65 years of age may be cared for more appropriately in a home visit rather than having them come to the office. Home visits may also be a way for providers to “lay eyes” on patients who do not have technology available to participate in virtual visits.
Before performing a home visit, inquire as to whether the patient has symptoms of COVID-19. Adequate PPE should be donned at all times and social distancing should be practiced when appropriate. With adequate PPE, home visits may also allow providers to care for low-risk patients known to have COVID-19 and thereby minimize risks to staff and other patients in the office. JFP
CORRESPONDENCE
Curt Elliott, MD, Prisma Health USC Family Medicine Center, 3209 Colonial Drive, Columbia, SC 29203; [email protected].
1. Unwin BK, Tatum PE. House calls. Am Fam Physician. 2011;83:925-938.
3. Sairenji T, Jetty A, Peterson LE. Shifting patterns of physician home visits. J Prim Care Community Health. 2016;7:71-75.
4. Ornstein KA, Leff B, Covinsky K, et al. Epidemiology of the homebound population in the United States. JAMA Intern Med. 2015;175;1180-1186.
5. CMS. Current Procedural Terminology, Fourth Edition ("CPT®"). www.cms.gov/apps/physician-fee-schedule/license-agreement.aspx. Accessed November 30, 2020.
6. Elkan R, Kendrick D, Dewey M, et al. Effectiveness of home based support for older people: systematic review and meta-analysis. BMJ. 2001;323:719-725.
7. Stuck AE, Egger M, Hammer A, et al. Home visits to prevent nursing home admission and functional decline in elderly people: systematic review and meta-regression analysis. JAMA. 2002;287:1022-1028.
8. Stall N, Nowaczynski M, Sinha SK. Systematic review of outcomes from home-based primary care programs for homebound older adults. J Am Geriatr Soc. 2014;62:2243-2251.
9. Prosman GJ, Lo Fo Wong SH, van der Wouden JC, et al. Effectiveness of home visiting in reducing partner violence for families experiencing abuse: a systematic review. Fam Pract. 2015;32:247-256.
10. Han L, Ma Y, Wei S, et al. Are home visits an effective method for diabetes management? A quantitative systematic review and meta-analysis. J Diabetes Investig. 2017;8:701-708.
11. McWhinney IR. Fourth annual Nicholas J. Pisacano Lecture. The doctor, the patient, and the home: returning to our roots. J Am Board Fam Pract. 1997;10:430-435.
12. Kao H, Conant R, Soriano T, et al. The past, present, and future of house calls. Clin Geriatr Med. 2009;25:19-34.
13. American Public Health Association. Community health workers. www.apha.org/apha-communities/member-sections/community-health-workers. Accessed November 30, 2020.
14. Campbell JD, Brooks M, Hosokawa P, et al. Community health worker home visits for Medicaid-enrolled children with asthma: effects on asthma outcomes and costs. Am J Public Health. 2015;105:2366-2372.
15. Anugu M, Braksmajer A, Huang J, et al. Enriched medical home intervention using community health worker home visitation and ED use. Pediatrics. 2017;139:e20161849.
16. Reckrey JM, Gettenberg G, Ross H, et al. The critical role of social workers in home-based primary care. Soc Work in Health Care. 2014;53:330-343.
17. Cohen-Mansfield J, Shmotkin D, Hazan H. The effect of homebound status on older persons. J Am Geriatr Soc. 2010;58:2358-2362.
18. Mt. Sinai Visiting Doctors Program. www.mountsinai.org/care/primary-care/upper-east-side/visiting-doctors/about. Accessed November 30, 2020.
19. Ornstein K, Hernandez CR, DeCherrie LV, et al. The Mount Sinai (New York) Visiting Doctors Program: meeting the needs of the urban homebound population. Care Manag J. 2011;12:159-163.
20. Ornstein K, Smith K, Boal J. Understanding and improving the burden and unmet needs of informal caregivers of homebound patients enrolled in a home-based primary care program. J Appl Gerontol. 2009;28:482-503.
21. Novak M, Guest C. Application of a multidimensional caregiver burden inventory. Gerontologist. 1989;29:798-803.
22. Cruz J, Brooks D, Marques A. Home telemonitoring effectiveness in COPD: a systematic review. Int J Clin Pract. 2014;68:369-378.
23. Antoniades NC, Rochford PD, Pretto JJ, et al. Pilot study of remote telemonitoring in COPD. Telemed J E Health. 2012;18:634-640.
24. Koff PB, Jones RH, Cashman JM, et al. Proactive integrated care improves quality of life in patients with COPD. Eur Respir J. 2009;33:1031-1038.
25. Inglis SC, Clark RA, McAlister FA, et al. Which components of heart failure programmes are effective? A systematic review and meta-analysis of the outcomes of structured telephone support or telemonitoring as the primary component of chronic heart failure management in 8323 patients: abridged Cochrane review. Eur J Heart Fail. 2011;13:1028-1040.
26. Koehler F, Koehler K, Deckwart O, et al. Efficacy of telemedical interventional management in patients with heart failure (TIM-HF2): a randomised, controlled, parallel-group, unmasked trial. Lancet. 2018;392:1047-1057.
27. Ticona L, Schulman KA. Extreme home makeover–the role of intensive home health care. New Eng J Med. 2016;375:1707-1709.
28. Caplan GA. A meta-analysis of “hospital in the home.” Med J Aust. 2013;198:195-196.
29. Leff B, Burton L, Mader SL, et al. Hospital at home: feasibility and outcomes of a program to provide hospital-level care at home for acutely ill older patients. Ann Intern Med. 2005;143:798-808.
30. Shepperd S, Iliffe S, Doll HA, et al. Admission avoidance hospital at home. Cochrane Database Syst Rev. 2016;9:CD007491.
31. Levine DM, Ouchi K, Blanchfield B, et al. Hospital-level care at home for acutely ill adults: a randomized controlled trial. Ann Intern Med. 2020;172:77-85.
32. Cornwell T and Schwartzberg JG, eds. Medical Management of the Home Care Patient: Guidelines for Physicians. 4th ed. Chicago, IL: American Medical Association and American Academy of Home Care Physicians; 2012:p18.
33. Cornwell T and Schwartzberg JG, eds. Medical Management of the Home Care Patient: Guidelines for Physicians. 4th ed. Chicago, IL: American Medical Association and American Academy of Home Care Physicians; 2012:p19.
34. Accreditation Council for Graduate Medical Education. ACGME Program Requirements for Graduate Medical Education in Family Medicine. www.acgme.org/Portals/0/PFAssets/ProgramRequirements/120_FamilyMedicine_2020.pdf. (section IV.C.1.b). Accessed November 30, 2020.
CASE
Mr. A is a 30-year-old man with neurofibromatosis and myelopathy with associated quadriplegia, complicated by dysphasia and chronic hypercapnic respiratory failure requiring a tracheostomy. He is cared for at home by his very competent mother but requires regular visits with his medical providers for assistance with his complex care needs. Due to logistical challenges, he had been receiving regular home visits even before the COVID-19 pandemic.
After estimating the risk of exposure to the patient, Mr. A’s family and his physician’s office staff scheduled a home visit. Before the appointment, the doctor conducted a virtual visit with the patient and family members to screen for COVID-19 infection, which proved negative. The doctor arranged a visit to coincide with Mr. A’s regular appointment with the home health nurse. He invited the patient’s social worker to attend, as well.
The providers donned masks, face shields, and gloves before entering the home. Mr. A’s temperature was checked and was normal. The team completed a physical exam, assessed the patient’s current needs, and refilled prescriptions. The doctor, nurse, and social worker met afterward in the family’s driveway to coordinate plans for the patient’s future care.
This encounter allowed a vulnerable patient with special needs to have access to care while reducing his risk of undesirable exposure. Also, his health care team’s provision of care in the home setting reduced Mr. A’s anxiety and that of his family members.
Home visits have long been an integral part of what it means to be a family physician. In 1930, roughly 40% of all patient-physician encounters in the United States occurred in patients’ homes. By 1980, this number had dropped to < 1%.1 Still, a 1994 survey of American doctors in 3 primary care specialties revealed that 63% of family physicians, more than the other 2 specialties, still made house calls.2 A 2016 analysis of Medicare claims data showed that between 2006 and 2011, only 5% of American doctors overall made house calls on Medicare recipients, but interestingly, the total number of home visits was increasing.3
This resurgence of interest in home health care is due in part to the increasing number of homebound patients in America, which exceeds the number of those in nursing homes.4 Further, a growing body of evidence indicates that home visits improve patient outcomes. And finally, many family physicians whose work lives have been centered around a busy office or hospital practice have found satisfaction in once again seeing patients in their own homes.
The COVID-19 pandemic has of course presented unique challenges—and opportunities, too—for home visits, which we discuss at the end of the article.
Why aren’t more of us making home visits?
For most of us, the decision not to make home visits is simply a matter of time and money. Although Medicare reimbursement for a home visit is typically about 150% that of a comparable office visit,5 it’s difficult, if not impossible, to make 2 home visits in the time you could see 3 patients in the office. So, economically it’s a net loss. Furthermore, we tend to feel less comfortable in our patients’ homes than in our offices. We have less control outside our own environment, and what happens away from our office is often less predictable—sometimes to the point that we may be concerned for our safety.
Continue to: So why make home visits at all?
So why make home visits at all?
First and foremost, home visits improve patient outcomes. This is most evident in our more vulnerable patients: newborns and the elderly, those who have been recently hospitalized, and those at risk because of their particular home situation. Multiple studies have shown that, for elders, home visits reduce functional decline, nursing home admissions, and mortality by around 25% to 33%.6-8 For those at risk of abuse, a recent systematic review showed that home visits reduce intimate partner violence and child abuse.9 Another systematic review demonstrated that patients with diabetes who received home visits vs usual care were more likely to show improvements in quality of life.10 These patients were also more likely to have lower HbA1c levels and lower systolic blood pressure readings.10 A few caveats apply to these studies:
- all of them targeted “vulnerable” patients
- most studies enlisted interdisciplinary teams and had regular team meetings
- most findings reached significance only after multiple home visits.
A further reason for choosing to become involved in home care is that it builds relationships, understanding, and empathy with our patients. “There is deep symbolism in the home visit.... It says, ‘I care enough about you to leave my power base … to come and see you on your own ground.’”11 And this benefit is 2-way; we also grow to understand and appreciate our patients better, especially if they are different from us culturally or socioeconomically.
Home visits allow the medical team to see challenges the patient has grown accustomed to, and perhaps ones that the patient has deemed too insignificant to mention. For the patient, home visits foster a strong sense of trust with the individual doctor and our health delivery network, and they decrease the need to seek emergency services. Finally, it has been demonstrated that provider satisfaction improves when home visits are incorporated into the work week.12
What is the role of community health workers in home-based care?
Community health workers (CHWs), defined as “frontline public health workers who are trusted members of and/or have an unusually close understanding of the community they serve,”13 can be an integral part of the home-based care team. Although CHWs have variable amounts of formal training, they have a unique perspective on local health beliefs and practices, which can assist the home-care team in providing culturally competent health care services and reduce health care costs.
In a study of children with asthma in Seattle, Washington, patients were randomized to a group that had 4 home visits by CHWs and a group that received usual care. The group that received home visits demonstrated more asthma symptom–free days, improved quality-of-life scores, and fewer urgent care visits.14 Furthermore, the intervention was estimated to save approximately $1300 per patient, resulting in a return on investment of 190%. Similarly, in a study comparing inappropriate emergency department (ED) visits between children who received CHW visits and those who did not, patients in the intervention group were significantly less likely to visit the ED for ambulatory complaints (18.2% vs 35.1%; P = .004).15
Continue to: What is the role of social workersin home-based care?
What is the role of social workersin home-based care?
Social workers can help meet the complex medical and biopsychosocial needs of the homebound population.16 A study by Cohen et al based in Israel concluded that homebound participants had a significantly higher risk for mortality, higher rates of depression, and difficulty completing instrumental activities of daily living when compared with their non-homebound counterparts.17
The Mount Sinai (New York) Visiting Doctors Program (MSVD) is a home-based care team that uses social workers to meet the needs of their complex patients.18 The social workers in the MSVD program provide direct counseling, make referrals to government and community resources, and monitor caregiver burden. Using a combination of measurement tools to assess caregiver burden, Ornstein et al demonstrated that the MSVD program led to a decrease in unmet needs and in caregiver burden.19,20 Caregiver burnout can be assessed using the Caregiver Burden Inventory, a validated 24-item questionnaire.21
What electronic tools are availableto monitor patients at home?
Although expensive in terms of both dollars and personnel time, telemonitoring allows home care providers to receive real-time, updated information regarding their patients.
Chronic obstructive pulmonary disease (COPD). One systematic review showed that although telemonitoring of patients with COPD improved quality of life and decreased COPD exacerbations, it did not reduce the risk of hospitalization and, therefore, did not reduce health care costs.22 Telemonitoring in COPD can include transmission of data about spirometry parameters, weight, temperature, blood pressure, sputum color, and 6-minute walk distance.23,24
Congestive heart failure (CHF). A 2010 Cochrane review found that telemonitoring of patients with CHF reduced all-cause mortality (risk ratio [RR] = 0.66; P < .0001).25 The Telemedical Interventional Management in Heart Failure II (TIM-HF2) trial,conducted from 2013 to 2017, compared usual care for CHF patients with care incorporating daily transmission of body weight, blood pressure, heart rate, electrocardiogram tracings, pulse oximetry, and self-rated health status.26 This study showed that the average number of days lost per year due to hospital admission was less in the telemonitoring group than in the usual care group (17.8 days vs. 24.2 days; P = .046). All-cause mortality was also reduced in the telemonitoring group (hazard ratio = 0.70; P = .028).
Continue to: What role do “home hospitals” play?
What role do “home hospitals” play?
Home hospitals provide acute or subacute treatment in a patient’s home for a condition that would normally require hospitalization.27 In a meta-analysis of 61 studies evaluating the effectiveness of home hospitals, this option was more likely to reduce mortality (odds ratio [OR] = 0.81; P = .008) and to reduce readmission rates (OR = 0.75; P = .02).28 In a study of 455 older adults, Leff et al found that hospital-at-home was associated with a shorter length of stay (3.2 vs. 4.9 days; P = .004) and that the mean cost was lower for hospital-at-home vs traditional hospital care.29
However, a 2016 Cochrane review of 16 randomized controlled trials comparing hospital-at-home with traditional hospital care showed that while care in a hospital-at-home may decrease formal costs, if costs for caregivers are taken into account, any difference in cost may disappear.30
Although the evidence for cost saving is variable, hospital-at-home admission has been shown to reduce the likelihood of living in a residential care facility at 6 months (RR = 0.35; P < .0001).30 Further, the same Cochrane review showed that admission avoidance may increase patient satisfaction with the care provided.30
Finally, a recent randomized trial in a Boston-area hospital system showed that patients cared for in hospital-at-home were significantly less likely to be readmitted within 30 days and that adjusted cost was about two-thirds the cost of traditional hospital care.31
What is the physician’s rolein home health care?
While home health care is a team effort, the physician has several crucial roles. First, he or she must make the determination that home care is appropriate and feasible for a particular patient. Appropriate, meaning there is evidence that this patient is likely to benefit from home care. Feasible, meaning there are resources available in the community and family to safely care for the patient at home. “Often a house call will serve as the first step in developing a home-based-management plan.”32
Continue to: Second, the physician serves...
Second, the physician serves an important role in directing and coordinating the team of professionals involved. This primarily means helping the team to communicate with one another. Before home visits begin, the physician’s office should reach out not only to the patient and family, but also to any other health care personnel involved in the patient’s home care. Otherwise, many of the health care providers involved will never have face-to-face interaction with the physician. Creation of the coordinated health team minimizes duplication and miscommunication; it also builds a valuable bond.
How does one go about making a home visit?
Scheduling. What often works best in a busy practice is to schedule home visits for the end of the workday or to devote an entire afternoon to making home visits to several patients in one locale. Also important is scheduling times, if possible, when important family members or other caregivers are at home or when other members of the home care team can accompany you.
What to bring along. Carry a “home visit bag” that includes equipment you’re likely to need and that is not available away from your office. A minimally equipped visit bag would include different-sized blood pressure cuffs, a glucometer, a pulse oximeter, thermometers, and patient education materials. Other suggested contents are listed in TABLE 1.
Dos and don’ts. Take a few minutes when you first arrive to simply visit with the patient. Sit down and introduce yourself and any members of the home care team that the patient has not met. Take an interim history. While you’re doing this, be observant: Is the home neat or cluttered? Is the indoor temperature comfortable? Are there fall hazards? Is there a smell of cigarette smoke? Are there any indoor combustion sources (eg, wood stove or kerosene heater)? Ask questions such as: Who lives here with you? Can you show me where you keep your medicines? (If the patient keeps insulin or any other medicines in the refrigerator, ask to see it. Note any apparent food scarcity.)
During your exam, pay particular attention to whether vital signs are appreciably different than those measured in the office or hospital. Pay special attention to the patient’s functional abilities. “A subtle, but critical distinction between medical management in the home and medical management in the hospital, clinic, or office is the emphasis on the patient’s functional abilities, family assistance, and environmental factors.”33
Observe the patient’s use of any home technology, if possible; this can be as simple as home oxygenation or as complex as home hemodialysis. Assess for any apparent caregiver stress. Finally, don’t neglect to offer appropriate emotional and spiritual support to the patient and family and to schedule the next follow-up visit before you leave.
Continue to: Documentation and reimbursement.
Documentation and reimbursement. While individual electronic medical records may require use of particular forms of documentation, using a home visit template when possible can be extremely helpful (TABLE 2). A template not only assures thoroughness and consistency (pharmacy, home health contacts, billing information) but also serves as a prompt to survey the patient and the caregivers about nonmedical, but essential, social and well-being services. The document should be as simple and user-friendly as possible.
Not all assessments will be able to be done at each visit but seeing them listed in the template can be helpful. Billing follows the same principles as for office visits and has similar requirements for documentation. Codes for the most common types of home visits are listed in TABLE 3.
Where can I get help?
Graduates of family medicine residency programs are required to receive training in home visits by the Accreditation Council for Graduate Medical Education (ACGME). Current ACGME program requirements stipulate that “residents must demonstrate competence to independently diagnose, manage, and integrate the care of patients of all ages in various outpatient settings, including the FMP [family medicine practice] site and home environment,” and “residents must be primarily responsible for a panel of continuity patients, integrating each patient’s care across all settings, including the home ...” [emphasis added].34
For those already in practice, one of the hardest parts of doing home visits is feeling alone, especially if few other providers in your community engage in home care. As you run into questions and challenges with incorporating home care of patients into your practice, one excellent resource is the American Academy of Home Care Medicine (www.aahcm.org/). Founded in 1988 and headquartered in Chicago, it not only provides numerous helpful resources, but serves as a networking tool for physicians involved in home care.
This unprecedented pandemichas allowed home visits to shine
As depicted in our opening patient case, patients who have high-risk conditions and those who are older than 65 years of age may be cared for more appropriately in a home visit rather than having them come to the office. Home visits may also be a way for providers to “lay eyes” on patients who do not have technology available to participate in virtual visits.
Before performing a home visit, inquire as to whether the patient has symptoms of COVID-19. Adequate PPE should be donned at all times and social distancing should be practiced when appropriate. With adequate PPE, home visits may also allow providers to care for low-risk patients known to have COVID-19 and thereby minimize risks to staff and other patients in the office. JFP
CORRESPONDENCE
Curt Elliott, MD, Prisma Health USC Family Medicine Center, 3209 Colonial Drive, Columbia, SC 29203; [email protected].
CASE
Mr. A is a 30-year-old man with neurofibromatosis and myelopathy with associated quadriplegia, complicated by dysphasia and chronic hypercapnic respiratory failure requiring a tracheostomy. He is cared for at home by his very competent mother but requires regular visits with his medical providers for assistance with his complex care needs. Due to logistical challenges, he had been receiving regular home visits even before the COVID-19 pandemic.
After estimating the risk of exposure to the patient, Mr. A’s family and his physician’s office staff scheduled a home visit. Before the appointment, the doctor conducted a virtual visit with the patient and family members to screen for COVID-19 infection, which proved negative. The doctor arranged a visit to coincide with Mr. A’s regular appointment with the home health nurse. He invited the patient’s social worker to attend, as well.
The providers donned masks, face shields, and gloves before entering the home. Mr. A’s temperature was checked and was normal. The team completed a physical exam, assessed the patient’s current needs, and refilled prescriptions. The doctor, nurse, and social worker met afterward in the family’s driveway to coordinate plans for the patient’s future care.
This encounter allowed a vulnerable patient with special needs to have access to care while reducing his risk of undesirable exposure. Also, his health care team’s provision of care in the home setting reduced Mr. A’s anxiety and that of his family members.
Home visits have long been an integral part of what it means to be a family physician. In 1930, roughly 40% of all patient-physician encounters in the United States occurred in patients’ homes. By 1980, this number had dropped to < 1%.1 Still, a 1994 survey of American doctors in 3 primary care specialties revealed that 63% of family physicians, more than the other 2 specialties, still made house calls.2 A 2016 analysis of Medicare claims data showed that between 2006 and 2011, only 5% of American doctors overall made house calls on Medicare recipients, but interestingly, the total number of home visits was increasing.3
This resurgence of interest in home health care is due in part to the increasing number of homebound patients in America, which exceeds the number of those in nursing homes.4 Further, a growing body of evidence indicates that home visits improve patient outcomes. And finally, many family physicians whose work lives have been centered around a busy office or hospital practice have found satisfaction in once again seeing patients in their own homes.
The COVID-19 pandemic has of course presented unique challenges—and opportunities, too—for home visits, which we discuss at the end of the article.
Why aren’t more of us making home visits?
For most of us, the decision not to make home visits is simply a matter of time and money. Although Medicare reimbursement for a home visit is typically about 150% that of a comparable office visit,5 it’s difficult, if not impossible, to make 2 home visits in the time you could see 3 patients in the office. So, economically it’s a net loss. Furthermore, we tend to feel less comfortable in our patients’ homes than in our offices. We have less control outside our own environment, and what happens away from our office is often less predictable—sometimes to the point that we may be concerned for our safety.
Continue to: So why make home visits at all?
So why make home visits at all?
First and foremost, home visits improve patient outcomes. This is most evident in our more vulnerable patients: newborns and the elderly, those who have been recently hospitalized, and those at risk because of their particular home situation. Multiple studies have shown that, for elders, home visits reduce functional decline, nursing home admissions, and mortality by around 25% to 33%.6-8 For those at risk of abuse, a recent systematic review showed that home visits reduce intimate partner violence and child abuse.9 Another systematic review demonstrated that patients with diabetes who received home visits vs usual care were more likely to show improvements in quality of life.10 These patients were also more likely to have lower HbA1c levels and lower systolic blood pressure readings.10 A few caveats apply to these studies:
- all of them targeted “vulnerable” patients
- most studies enlisted interdisciplinary teams and had regular team meetings
- most findings reached significance only after multiple home visits.
A further reason for choosing to become involved in home care is that it builds relationships, understanding, and empathy with our patients. “There is deep symbolism in the home visit.... It says, ‘I care enough about you to leave my power base … to come and see you on your own ground.’”11 And this benefit is 2-way; we also grow to understand and appreciate our patients better, especially if they are different from us culturally or socioeconomically.
Home visits allow the medical team to see challenges the patient has grown accustomed to, and perhaps ones that the patient has deemed too insignificant to mention. For the patient, home visits foster a strong sense of trust with the individual doctor and our health delivery network, and they decrease the need to seek emergency services. Finally, it has been demonstrated that provider satisfaction improves when home visits are incorporated into the work week.12
What is the role of community health workers in home-based care?
Community health workers (CHWs), defined as “frontline public health workers who are trusted members of and/or have an unusually close understanding of the community they serve,”13 can be an integral part of the home-based care team. Although CHWs have variable amounts of formal training, they have a unique perspective on local health beliefs and practices, which can assist the home-care team in providing culturally competent health care services and reduce health care costs.
In a study of children with asthma in Seattle, Washington, patients were randomized to a group that had 4 home visits by CHWs and a group that received usual care. The group that received home visits demonstrated more asthma symptom–free days, improved quality-of-life scores, and fewer urgent care visits.14 Furthermore, the intervention was estimated to save approximately $1300 per patient, resulting in a return on investment of 190%. Similarly, in a study comparing inappropriate emergency department (ED) visits between children who received CHW visits and those who did not, patients in the intervention group were significantly less likely to visit the ED for ambulatory complaints (18.2% vs 35.1%; P = .004).15
Continue to: What is the role of social workersin home-based care?
What is the role of social workersin home-based care?
Social workers can help meet the complex medical and biopsychosocial needs of the homebound population.16 A study by Cohen et al based in Israel concluded that homebound participants had a significantly higher risk for mortality, higher rates of depression, and difficulty completing instrumental activities of daily living when compared with their non-homebound counterparts.17
The Mount Sinai (New York) Visiting Doctors Program (MSVD) is a home-based care team that uses social workers to meet the needs of their complex patients.18 The social workers in the MSVD program provide direct counseling, make referrals to government and community resources, and monitor caregiver burden. Using a combination of measurement tools to assess caregiver burden, Ornstein et al demonstrated that the MSVD program led to a decrease in unmet needs and in caregiver burden.19,20 Caregiver burnout can be assessed using the Caregiver Burden Inventory, a validated 24-item questionnaire.21
What electronic tools are availableto monitor patients at home?
Although expensive in terms of both dollars and personnel time, telemonitoring allows home care providers to receive real-time, updated information regarding their patients.
Chronic obstructive pulmonary disease (COPD). One systematic review showed that although telemonitoring of patients with COPD improved quality of life and decreased COPD exacerbations, it did not reduce the risk of hospitalization and, therefore, did not reduce health care costs.22 Telemonitoring in COPD can include transmission of data about spirometry parameters, weight, temperature, blood pressure, sputum color, and 6-minute walk distance.23,24
Congestive heart failure (CHF). A 2010 Cochrane review found that telemonitoring of patients with CHF reduced all-cause mortality (risk ratio [RR] = 0.66; P < .0001).25 The Telemedical Interventional Management in Heart Failure II (TIM-HF2) trial,conducted from 2013 to 2017, compared usual care for CHF patients with care incorporating daily transmission of body weight, blood pressure, heart rate, electrocardiogram tracings, pulse oximetry, and self-rated health status.26 This study showed that the average number of days lost per year due to hospital admission was less in the telemonitoring group than in the usual care group (17.8 days vs. 24.2 days; P = .046). All-cause mortality was also reduced in the telemonitoring group (hazard ratio = 0.70; P = .028).
Continue to: What role do “home hospitals” play?
What role do “home hospitals” play?
Home hospitals provide acute or subacute treatment in a patient’s home for a condition that would normally require hospitalization.27 In a meta-analysis of 61 studies evaluating the effectiveness of home hospitals, this option was more likely to reduce mortality (odds ratio [OR] = 0.81; P = .008) and to reduce readmission rates (OR = 0.75; P = .02).28 In a study of 455 older adults, Leff et al found that hospital-at-home was associated with a shorter length of stay (3.2 vs. 4.9 days; P = .004) and that the mean cost was lower for hospital-at-home vs traditional hospital care.29
However, a 2016 Cochrane review of 16 randomized controlled trials comparing hospital-at-home with traditional hospital care showed that while care in a hospital-at-home may decrease formal costs, if costs for caregivers are taken into account, any difference in cost may disappear.30
Although the evidence for cost saving is variable, hospital-at-home admission has been shown to reduce the likelihood of living in a residential care facility at 6 months (RR = 0.35; P < .0001).30 Further, the same Cochrane review showed that admission avoidance may increase patient satisfaction with the care provided.30
Finally, a recent randomized trial in a Boston-area hospital system showed that patients cared for in hospital-at-home were significantly less likely to be readmitted within 30 days and that adjusted cost was about two-thirds the cost of traditional hospital care.31
What is the physician’s rolein home health care?
While home health care is a team effort, the physician has several crucial roles. First, he or she must make the determination that home care is appropriate and feasible for a particular patient. Appropriate, meaning there is evidence that this patient is likely to benefit from home care. Feasible, meaning there are resources available in the community and family to safely care for the patient at home. “Often a house call will serve as the first step in developing a home-based-management plan.”32
Continue to: Second, the physician serves...
Second, the physician serves an important role in directing and coordinating the team of professionals involved. This primarily means helping the team to communicate with one another. Before home visits begin, the physician’s office should reach out not only to the patient and family, but also to any other health care personnel involved in the patient’s home care. Otherwise, many of the health care providers involved will never have face-to-face interaction with the physician. Creation of the coordinated health team minimizes duplication and miscommunication; it also builds a valuable bond.
How does one go about making a home visit?
Scheduling. What often works best in a busy practice is to schedule home visits for the end of the workday or to devote an entire afternoon to making home visits to several patients in one locale. Also important is scheduling times, if possible, when important family members or other caregivers are at home or when other members of the home care team can accompany you.
What to bring along. Carry a “home visit bag” that includes equipment you’re likely to need and that is not available away from your office. A minimally equipped visit bag would include different-sized blood pressure cuffs, a glucometer, a pulse oximeter, thermometers, and patient education materials. Other suggested contents are listed in TABLE 1.
Dos and don’ts. Take a few minutes when you first arrive to simply visit with the patient. Sit down and introduce yourself and any members of the home care team that the patient has not met. Take an interim history. While you’re doing this, be observant: Is the home neat or cluttered? Is the indoor temperature comfortable? Are there fall hazards? Is there a smell of cigarette smoke? Are there any indoor combustion sources (eg, wood stove or kerosene heater)? Ask questions such as: Who lives here with you? Can you show me where you keep your medicines? (If the patient keeps insulin or any other medicines in the refrigerator, ask to see it. Note any apparent food scarcity.)
During your exam, pay particular attention to whether vital signs are appreciably different than those measured in the office or hospital. Pay special attention to the patient’s functional abilities. “A subtle, but critical distinction between medical management in the home and medical management in the hospital, clinic, or office is the emphasis on the patient’s functional abilities, family assistance, and environmental factors.”33
Observe the patient’s use of any home technology, if possible; this can be as simple as home oxygenation or as complex as home hemodialysis. Assess for any apparent caregiver stress. Finally, don’t neglect to offer appropriate emotional and spiritual support to the patient and family and to schedule the next follow-up visit before you leave.
Continue to: Documentation and reimbursement.
Documentation and reimbursement. While individual electronic medical records may require use of particular forms of documentation, using a home visit template when possible can be extremely helpful (TABLE 2). A template not only assures thoroughness and consistency (pharmacy, home health contacts, billing information) but also serves as a prompt to survey the patient and the caregivers about nonmedical, but essential, social and well-being services. The document should be as simple and user-friendly as possible.
Not all assessments will be able to be done at each visit but seeing them listed in the template can be helpful. Billing follows the same principles as for office visits and has similar requirements for documentation. Codes for the most common types of home visits are listed in TABLE 3.
Where can I get help?
Graduates of family medicine residency programs are required to receive training in home visits by the Accreditation Council for Graduate Medical Education (ACGME). Current ACGME program requirements stipulate that “residents must demonstrate competence to independently diagnose, manage, and integrate the care of patients of all ages in various outpatient settings, including the FMP [family medicine practice] site and home environment,” and “residents must be primarily responsible for a panel of continuity patients, integrating each patient’s care across all settings, including the home ...” [emphasis added].34
For those already in practice, one of the hardest parts of doing home visits is feeling alone, especially if few other providers in your community engage in home care. As you run into questions and challenges with incorporating home care of patients into your practice, one excellent resource is the American Academy of Home Care Medicine (www.aahcm.org/). Founded in 1988 and headquartered in Chicago, it not only provides numerous helpful resources, but serves as a networking tool for physicians involved in home care.
This unprecedented pandemichas allowed home visits to shine
As depicted in our opening patient case, patients who have high-risk conditions and those who are older than 65 years of age may be cared for more appropriately in a home visit rather than having them come to the office. Home visits may also be a way for providers to “lay eyes” on patients who do not have technology available to participate in virtual visits.
Before performing a home visit, inquire as to whether the patient has symptoms of COVID-19. Adequate PPE should be donned at all times and social distancing should be practiced when appropriate. With adequate PPE, home visits may also allow providers to care for low-risk patients known to have COVID-19 and thereby minimize risks to staff and other patients in the office. JFP
CORRESPONDENCE
Curt Elliott, MD, Prisma Health USC Family Medicine Center, 3209 Colonial Drive, Columbia, SC 29203; [email protected].
1. Unwin BK, Tatum PE. House calls. Am Fam Physician. 2011;83:925-938.
3. Sairenji T, Jetty A, Peterson LE. Shifting patterns of physician home visits. J Prim Care Community Health. 2016;7:71-75.
4. Ornstein KA, Leff B, Covinsky K, et al. Epidemiology of the homebound population in the United States. JAMA Intern Med. 2015;175;1180-1186.
5. CMS. Current Procedural Terminology, Fourth Edition ("CPT®"). www.cms.gov/apps/physician-fee-schedule/license-agreement.aspx. Accessed November 30, 2020.
6. Elkan R, Kendrick D, Dewey M, et al. Effectiveness of home based support for older people: systematic review and meta-analysis. BMJ. 2001;323:719-725.
7. Stuck AE, Egger M, Hammer A, et al. Home visits to prevent nursing home admission and functional decline in elderly people: systematic review and meta-regression analysis. JAMA. 2002;287:1022-1028.
8. Stall N, Nowaczynski M, Sinha SK. Systematic review of outcomes from home-based primary care programs for homebound older adults. J Am Geriatr Soc. 2014;62:2243-2251.
9. Prosman GJ, Lo Fo Wong SH, van der Wouden JC, et al. Effectiveness of home visiting in reducing partner violence for families experiencing abuse: a systematic review. Fam Pract. 2015;32:247-256.
10. Han L, Ma Y, Wei S, et al. Are home visits an effective method for diabetes management? A quantitative systematic review and meta-analysis. J Diabetes Investig. 2017;8:701-708.
11. McWhinney IR. Fourth annual Nicholas J. Pisacano Lecture. The doctor, the patient, and the home: returning to our roots. J Am Board Fam Pract. 1997;10:430-435.
12. Kao H, Conant R, Soriano T, et al. The past, present, and future of house calls. Clin Geriatr Med. 2009;25:19-34.
13. American Public Health Association. Community health workers. www.apha.org/apha-communities/member-sections/community-health-workers. Accessed November 30, 2020.
14. Campbell JD, Brooks M, Hosokawa P, et al. Community health worker home visits for Medicaid-enrolled children with asthma: effects on asthma outcomes and costs. Am J Public Health. 2015;105:2366-2372.
15. Anugu M, Braksmajer A, Huang J, et al. Enriched medical home intervention using community health worker home visitation and ED use. Pediatrics. 2017;139:e20161849.
16. Reckrey JM, Gettenberg G, Ross H, et al. The critical role of social workers in home-based primary care. Soc Work in Health Care. 2014;53:330-343.
17. Cohen-Mansfield J, Shmotkin D, Hazan H. The effect of homebound status on older persons. J Am Geriatr Soc. 2010;58:2358-2362.
18. Mt. Sinai Visiting Doctors Program. www.mountsinai.org/care/primary-care/upper-east-side/visiting-doctors/about. Accessed November 30, 2020.
19. Ornstein K, Hernandez CR, DeCherrie LV, et al. The Mount Sinai (New York) Visiting Doctors Program: meeting the needs of the urban homebound population. Care Manag J. 2011;12:159-163.
20. Ornstein K, Smith K, Boal J. Understanding and improving the burden and unmet needs of informal caregivers of homebound patients enrolled in a home-based primary care program. J Appl Gerontol. 2009;28:482-503.
21. Novak M, Guest C. Application of a multidimensional caregiver burden inventory. Gerontologist. 1989;29:798-803.
22. Cruz J, Brooks D, Marques A. Home telemonitoring effectiveness in COPD: a systematic review. Int J Clin Pract. 2014;68:369-378.
23. Antoniades NC, Rochford PD, Pretto JJ, et al. Pilot study of remote telemonitoring in COPD. Telemed J E Health. 2012;18:634-640.
24. Koff PB, Jones RH, Cashman JM, et al. Proactive integrated care improves quality of life in patients with COPD. Eur Respir J. 2009;33:1031-1038.
25. Inglis SC, Clark RA, McAlister FA, et al. Which components of heart failure programmes are effective? A systematic review and meta-analysis of the outcomes of structured telephone support or telemonitoring as the primary component of chronic heart failure management in 8323 patients: abridged Cochrane review. Eur J Heart Fail. 2011;13:1028-1040.
26. Koehler F, Koehler K, Deckwart O, et al. Efficacy of telemedical interventional management in patients with heart failure (TIM-HF2): a randomised, controlled, parallel-group, unmasked trial. Lancet. 2018;392:1047-1057.
27. Ticona L, Schulman KA. Extreme home makeover–the role of intensive home health care. New Eng J Med. 2016;375:1707-1709.
28. Caplan GA. A meta-analysis of “hospital in the home.” Med J Aust. 2013;198:195-196.
29. Leff B, Burton L, Mader SL, et al. Hospital at home: feasibility and outcomes of a program to provide hospital-level care at home for acutely ill older patients. Ann Intern Med. 2005;143:798-808.
30. Shepperd S, Iliffe S, Doll HA, et al. Admission avoidance hospital at home. Cochrane Database Syst Rev. 2016;9:CD007491.
31. Levine DM, Ouchi K, Blanchfield B, et al. Hospital-level care at home for acutely ill adults: a randomized controlled trial. Ann Intern Med. 2020;172:77-85.
32. Cornwell T and Schwartzberg JG, eds. Medical Management of the Home Care Patient: Guidelines for Physicians. 4th ed. Chicago, IL: American Medical Association and American Academy of Home Care Physicians; 2012:p18.
33. Cornwell T and Schwartzberg JG, eds. Medical Management of the Home Care Patient: Guidelines for Physicians. 4th ed. Chicago, IL: American Medical Association and American Academy of Home Care Physicians; 2012:p19.
34. Accreditation Council for Graduate Medical Education. ACGME Program Requirements for Graduate Medical Education in Family Medicine. www.acgme.org/Portals/0/PFAssets/ProgramRequirements/120_FamilyMedicine_2020.pdf. (section IV.C.1.b). Accessed November 30, 2020.
1. Unwin BK, Tatum PE. House calls. Am Fam Physician. 2011;83:925-938.
3. Sairenji T, Jetty A, Peterson LE. Shifting patterns of physician home visits. J Prim Care Community Health. 2016;7:71-75.
4. Ornstein KA, Leff B, Covinsky K, et al. Epidemiology of the homebound population in the United States. JAMA Intern Med. 2015;175;1180-1186.
5. CMS. Current Procedural Terminology, Fourth Edition ("CPT®"). www.cms.gov/apps/physician-fee-schedule/license-agreement.aspx. Accessed November 30, 2020.
6. Elkan R, Kendrick D, Dewey M, et al. Effectiveness of home based support for older people: systematic review and meta-analysis. BMJ. 2001;323:719-725.
7. Stuck AE, Egger M, Hammer A, et al. Home visits to prevent nursing home admission and functional decline in elderly people: systematic review and meta-regression analysis. JAMA. 2002;287:1022-1028.
8. Stall N, Nowaczynski M, Sinha SK. Systematic review of outcomes from home-based primary care programs for homebound older adults. J Am Geriatr Soc. 2014;62:2243-2251.
9. Prosman GJ, Lo Fo Wong SH, van der Wouden JC, et al. Effectiveness of home visiting in reducing partner violence for families experiencing abuse: a systematic review. Fam Pract. 2015;32:247-256.
10. Han L, Ma Y, Wei S, et al. Are home visits an effective method for diabetes management? A quantitative systematic review and meta-analysis. J Diabetes Investig. 2017;8:701-708.
11. McWhinney IR. Fourth annual Nicholas J. Pisacano Lecture. The doctor, the patient, and the home: returning to our roots. J Am Board Fam Pract. 1997;10:430-435.
12. Kao H, Conant R, Soriano T, et al. The past, present, and future of house calls. Clin Geriatr Med. 2009;25:19-34.
13. American Public Health Association. Community health workers. www.apha.org/apha-communities/member-sections/community-health-workers. Accessed November 30, 2020.
14. Campbell JD, Brooks M, Hosokawa P, et al. Community health worker home visits for Medicaid-enrolled children with asthma: effects on asthma outcomes and costs. Am J Public Health. 2015;105:2366-2372.
15. Anugu M, Braksmajer A, Huang J, et al. Enriched medical home intervention using community health worker home visitation and ED use. Pediatrics. 2017;139:e20161849.
16. Reckrey JM, Gettenberg G, Ross H, et al. The critical role of social workers in home-based primary care. Soc Work in Health Care. 2014;53:330-343.
17. Cohen-Mansfield J, Shmotkin D, Hazan H. The effect of homebound status on older persons. J Am Geriatr Soc. 2010;58:2358-2362.
18. Mt. Sinai Visiting Doctors Program. www.mountsinai.org/care/primary-care/upper-east-side/visiting-doctors/about. Accessed November 30, 2020.
19. Ornstein K, Hernandez CR, DeCherrie LV, et al. The Mount Sinai (New York) Visiting Doctors Program: meeting the needs of the urban homebound population. Care Manag J. 2011;12:159-163.
20. Ornstein K, Smith K, Boal J. Understanding and improving the burden and unmet needs of informal caregivers of homebound patients enrolled in a home-based primary care program. J Appl Gerontol. 2009;28:482-503.
21. Novak M, Guest C. Application of a multidimensional caregiver burden inventory. Gerontologist. 1989;29:798-803.
22. Cruz J, Brooks D, Marques A. Home telemonitoring effectiveness in COPD: a systematic review. Int J Clin Pract. 2014;68:369-378.
23. Antoniades NC, Rochford PD, Pretto JJ, et al. Pilot study of remote telemonitoring in COPD. Telemed J E Health. 2012;18:634-640.
24. Koff PB, Jones RH, Cashman JM, et al. Proactive integrated care improves quality of life in patients with COPD. Eur Respir J. 2009;33:1031-1038.
25. Inglis SC, Clark RA, McAlister FA, et al. Which components of heart failure programmes are effective? A systematic review and meta-analysis of the outcomes of structured telephone support or telemonitoring as the primary component of chronic heart failure management in 8323 patients: abridged Cochrane review. Eur J Heart Fail. 2011;13:1028-1040.
26. Koehler F, Koehler K, Deckwart O, et al. Efficacy of telemedical interventional management in patients with heart failure (TIM-HF2): a randomised, controlled, parallel-group, unmasked trial. Lancet. 2018;392:1047-1057.
27. Ticona L, Schulman KA. Extreme home makeover–the role of intensive home health care. New Eng J Med. 2016;375:1707-1709.
28. Caplan GA. A meta-analysis of “hospital in the home.” Med J Aust. 2013;198:195-196.
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PRACTICE RECOMMENDATIONS
❯ Consider incorporating home visits into the primary care of select vulnerable patients because doing so improves clinical outcomes, including mortality rates in neonates and elders. A
❯ Employ team-based home care and include community health workers, nurses, pharmacists, social workers, chaplains, and others. B
Strength of recommendation (SOR)
A Good-quality patient-oriented evidence
B Inconsistent or limited-quality patient-oriented evidence
C Consensus, usual practice, opinion, disease-oriented evidence, case series
