Commentary

Does it seem strange to you that while on one hand we hear from multiple sources that a troubling number of adults and children are going hungry, but on the other hand data from the Centers for Disease Control and Prevention indicate that self reports of obesity by adults in 2014 in different ethnic groups ranged from 27% to 38% and approximately 17% of children and adolescents aged 2-19 years are obese per 2011-2012 data?

One might guess that this situation is simply that too many Americans can afford to overeat and their numbers overwhelm the data from a smaller segment of the population who are underweight because they can’t afford to feed themselves.

But this isn’t the case at all, because the obesity rates in our poorest counties are nearly 12% above the national median (“Obesity: The New Hunger” by Robert Paarlberg, Ph.D., The Wall Street Journal, May 10, 2016). So the question is why do we have so many overweight adults and children if we also have a hunger problem? The answer is very complicated and even more complicated because of how we define hunger.

While obesity is relatively easy to measure with a scale and a tape measure, hunger is a perception that is difficult, if not impossible, to quantify. Possibly in an attempt to create clarity for people like me who are confused by the coexistence of hunger and obesity, there has been a trend toward replacing “hunger” with the more techno-sounding buzz words, “food insecurity.”

According to Dr. Paarlberg, an adjunct professor of public policy at Harvard University, Cambridge, Mass., and author of “The United States of Excess: Gluttony and the Dark Side of American Exceptionalism” (New York, N.Y.: Oxford University Press, 2015), the United States Department of Agriculture calculates our national food insecurity quotient by way of an annual survey of a sample of households. Family members are asked questions such as whether “they had failed to eat or worried about running out of food for lack of money at any time in the previous 12 months.”

There are many reasons why a survey respondent might be concerned that he or she wouldn’t have enough to eat on a given day. It could have been poor planning on the part of the head of the household or a consequence of family chaos. And we have to assume that in some cases, it is simply because there wasn’t enough money to buy food that day. If it were only a matter of money, the solution would be easy. We could simply provide economically challenged families with more money to buy more food, but that is already being done through programs such as the Supplemental Nutrition Assistance Program (often referred to as food stamps or SNAP). But the coexistence of obesity and hunger suggests to me that more food isn’t the answer.

Part of the problem is that “food” is too broadly defined. Some foods are more likely to contribute to obesity than others, and some foods satiate more quickly than others. While some restrictions have been built into the SNAP program to encourage participants to eat a healthier diet, the fact that soda and candy can be bought with food stamps is a serious error that must be corrected. It may be time to take a harder look at tightening other guidelines to make the subsidized diet healthier.

Unfortunately, the last step in the process occurs in the home. A diet that discourages obesity often includes fresh fruits and vegetables that can be expensive and may not be appealing to a family accustomed to calorie-dense foods. And a healthy diet often requires preparation skills and time, both of which economically challenged families may not have.

All of this makes me wonder whether we should stop worrying so much about hunger in America and shift the focus of our nutritional support programs more toward obesity prevention. Of course, that is easy to say for someone like myself who is lean and can always find something in the refrigerator to eat. But let’s remember that while starvation and obesity can kill, hunger doesn’t.

The problem is that “hunger” and the less emotionally charged term “food insecurity” are potent motivators for legislators who control the funding of our critical nutritional support programs. It still makes sense politically to continue to talk about eliminating hunger. But we need to craft our programs so that they address the larger problem of obesity.

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics including “How to Say No to Your Toddler.”

Does it seem strange to you that while on one hand we hear from multiple sources that a troubling number of adults and children are going hungry, but on the other hand data from the Centers for Disease Control and Prevention indicate that self reports of obesity by adults in 2014 in different ethnic groups ranged from 27% to 38% and approximately 17% of children and adolescents aged 2-19 years are obese per 2011-2012 data?

One might guess that this situation is simply that too many Americans can afford to overeat and their numbers overwhelm the data from a smaller segment of the population who are underweight because they can’t afford to feed themselves.

But this isn’t the case at all, because the obesity rates in our poorest counties are nearly 12% above the national median (“Obesity: The New Hunger” by Robert Paarlberg, Ph.D., The Wall Street Journal, May 10, 2016). So the question is why do we have so many overweight adults and children if we also have a hunger problem? The answer is very complicated and even more complicated because of how we define hunger.

While obesity is relatively easy to measure with a scale and a tape measure, hunger is a perception that is difficult, if not impossible, to quantify. Possibly in an attempt to create clarity for people like me who are confused by the coexistence of hunger and obesity, there has been a trend toward replacing “hunger” with the more techno-sounding buzz words, “food insecurity.”

According to Dr. Paarlberg, an adjunct professor of public policy at Harvard University, Cambridge, Mass., and author of “The United States of Excess: Gluttony and the Dark Side of American Exceptionalism” (New York, N.Y.: Oxford University Press, 2015), the United States Department of Agriculture calculates our national food insecurity quotient by way of an annual survey of a sample of households. Family members are asked questions such as whether “they had failed to eat or worried about running out of food for lack of money at any time in the previous 12 months.”

There are many reasons why a survey respondent might be concerned that he or she wouldn’t have enough to eat on a given day. It could have been poor planning on the part of the head of the household or a consequence of family chaos. And we have to assume that in some cases, it is simply because there wasn’t enough money to buy food that day. If it were only a matter of money, the solution would be easy. We could simply provide economically challenged families with more money to buy more food, but that is already being done through programs such as the Supplemental Nutrition Assistance Program (often referred to as food stamps or SNAP). But the coexistence of obesity and hunger suggests to me that more food isn’t the answer.

Part of the problem is that “food” is too broadly defined. Some foods are more likely to contribute to obesity than others, and some foods satiate more quickly than others. While some restrictions have been built into the SNAP program to encourage participants to eat a healthier diet, the fact that soda and candy can be bought with food stamps is a serious error that must be corrected. It may be time to take a harder look at tightening other guidelines to make the subsidized diet healthier.

Unfortunately, the last step in the process occurs in the home. A diet that discourages obesity often includes fresh fruits and vegetables that can be expensive and may not be appealing to a family accustomed to calorie-dense foods. And a healthy diet often requires preparation skills and time, both of which economically challenged families may not have.

All of this makes me wonder whether we should stop worrying so much about hunger in America and shift the focus of our nutritional support programs more toward obesity prevention. Of course, that is easy to say for someone like myself who is lean and can always find something in the refrigerator to eat. But let’s remember that while starvation and obesity can kill, hunger doesn’t.

The problem is that “hunger” and the less emotionally charged term “food insecurity” are potent motivators for legislators who control the funding of our critical nutritional support programs. It still makes sense politically to continue to talk about eliminating hunger. But we need to craft our programs so that they address the larger problem of obesity.

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics including “How to Say No to Your Toddler.”

Does it seem strange to you that while on one hand we hear from multiple sources that a troubling number of adults and children are going hungry, but on the other hand data from the Centers for Disease Control and Prevention indicate that self reports of obesity by adults in 2014 in different ethnic groups ranged from 27% to 38% and approximately 17% of children and adolescents aged 2-19 years are obese per 2011-2012 data?

One might guess that this situation is simply that too many Americans can afford to overeat and their numbers overwhelm the data from a smaller segment of the population who are underweight because they can’t afford to feed themselves.

But this isn’t the case at all, because the obesity rates in our poorest counties are nearly 12% above the national median (“Obesity: The New Hunger” by Robert Paarlberg, Ph.D., The Wall Street Journal, May 10, 2016). So the question is why do we have so many overweight adults and children if we also have a hunger problem? The answer is very complicated and even more complicated because of how we define hunger.

While obesity is relatively easy to measure with a scale and a tape measure, hunger is a perception that is difficult, if not impossible, to quantify. Possibly in an attempt to create clarity for people like me who are confused by the coexistence of hunger and obesity, there has been a trend toward replacing “hunger” with the more techno-sounding buzz words, “food insecurity.”

According to Dr. Paarlberg, an adjunct professor of public policy at Harvard University, Cambridge, Mass., and author of “The United States of Excess: Gluttony and the Dark Side of American Exceptionalism” (New York, N.Y.: Oxford University Press, 2015), the United States Department of Agriculture calculates our national food insecurity quotient by way of an annual survey of a sample of households. Family members are asked questions such as whether “they had failed to eat or worried about running out of food for lack of money at any time in the previous 12 months.”

There are many reasons why a survey respondent might be concerned that he or she wouldn’t have enough to eat on a given day. It could have been poor planning on the part of the head of the household or a consequence of family chaos. And we have to assume that in some cases, it is simply because there wasn’t enough money to buy food that day. If it were only a matter of money, the solution would be easy. We could simply provide economically challenged families with more money to buy more food, but that is already being done through programs such as the Supplemental Nutrition Assistance Program (often referred to as food stamps or SNAP). But the coexistence of obesity and hunger suggests to me that more food isn’t the answer.

Part of the problem is that “food” is too broadly defined. Some foods are more likely to contribute to obesity than others, and some foods satiate more quickly than others. While some restrictions have been built into the SNAP program to encourage participants to eat a healthier diet, the fact that soda and candy can be bought with food stamps is a serious error that must be corrected. It may be time to take a harder look at tightening other guidelines to make the subsidized diet healthier.

Unfortunately, the last step in the process occurs in the home. A diet that discourages obesity often includes fresh fruits and vegetables that can be expensive and may not be appealing to a family accustomed to calorie-dense foods. And a healthy diet often requires preparation skills and time, both of which economically challenged families may not have.

All of this makes me wonder whether we should stop worrying so much about hunger in America and shift the focus of our nutritional support programs more toward obesity prevention. Of course, that is easy to say for someone like myself who is lean and can always find something in the refrigerator to eat. But let’s remember that while starvation and obesity can kill, hunger doesn’t.

The problem is that “hunger” and the less emotionally charged term “food insecurity” are potent motivators for legislators who control the funding of our critical nutritional support programs. It still makes sense politically to continue to talk about eliminating hunger. But we need to craft our programs so that they address the larger problem of obesity.

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics including “How to Say No to Your Toddler.”

With great pleasure I announce a partnership with the Association of Military Dermatologists (AMD) whereby Cutis^® is the official journal of the organization. We welcome the AMD President Nicholas Logemann, DO, and the active members of the AMD—dermatologists in the Army, Navy, Air Force, and US Public Health Service—who provide laudable care to their charges in the United States and around the world.

The AMD strives to “[k]eep our troops fit to fight, take care of our wounded warriors on the field and back home, and provide quality Dermatologic care to their dependents, our retirees, and others in need of humanitarian assistance throughout the world when duty calls.” In addition to their clinical mission, members of the AMD have an educational mission by which they, at any one time, are training approximately 50 young active-duty physicians in dermatology residency training programs at their 3 sites in Bethesda, Maryland; San Antonio, Texas; and San Diego, California.

The value of this collaboration for the readers of Cutis is illustrated by the inaugural Military Dermatology column, “Managing Residual Limb Hyperhidrosis in Wounded Warriors: What Have We Learned?” This topic and others that will be featured in this new column, which will be published quarterly, will focus on an important area of skin disease that we may all see in our practices but an area in which AMD physicians have extensive expertise that they will share with us.

On a personal note, my dermatology training was in the US Public Health Service and I am an (inactive) member of the organization. I would urge all of our readers to consider supporting the mission of the AMD by visiting their website (http://www.militaryderm.org) and consider joining the organization, which accepts civilian members.

Vincent A. DeLeo, MD
Editor-in-Chief, Cutis

With great pleasure I announce a partnership with the Association of Military Dermatologists (AMD) whereby Cutis^® is the official journal of the organization. We welcome the AMD President Nicholas Logemann, DO, and the active members of the AMD—dermatologists in the Army, Navy, Air Force, and US Public Health Service—who provide laudable care to their charges in the United States and around the world.

The AMD strives to “[k]eep our troops fit to fight, take care of our wounded warriors on the field and back home, and provide quality Dermatologic care to their dependents, our retirees, and others in need of humanitarian assistance throughout the world when duty calls.” In addition to their clinical mission, members of the AMD have an educational mission by which they, at any one time, are training approximately 50 young active-duty physicians in dermatology residency training programs at their 3 sites in Bethesda, Maryland; San Antonio, Texas; and San Diego, California.

The value of this collaboration for the readers of Cutis is illustrated by the inaugural Military Dermatology column, “Managing Residual Limb Hyperhidrosis in Wounded Warriors: What Have We Learned?” This topic and others that will be featured in this new column, which will be published quarterly, will focus on an important area of skin disease that we may all see in our practices but an area in which AMD physicians have extensive expertise that they will share with us.

On a personal note, my dermatology training was in the US Public Health Service and I am an (inactive) member of the organization. I would urge all of our readers to consider supporting the mission of the AMD by visiting their website (http://www.militaryderm.org) and consider joining the organization, which accepts civilian members.

Vincent A. DeLeo, MD
Editor-in-Chief, Cutis

With great pleasure I announce a partnership with the Association of Military Dermatologists (AMD) whereby Cutis^® is the official journal of the organization. We welcome the AMD President Nicholas Logemann, DO, and the active members of the AMD—dermatologists in the Army, Navy, Air Force, and US Public Health Service—who provide laudable care to their charges in the United States and around the world.

The AMD strives to “[k]eep our troops fit to fight, take care of our wounded warriors on the field and back home, and provide quality Dermatologic care to their dependents, our retirees, and others in need of humanitarian assistance throughout the world when duty calls.” In addition to their clinical mission, members of the AMD have an educational mission by which they, at any one time, are training approximately 50 young active-duty physicians in dermatology residency training programs at their 3 sites in Bethesda, Maryland; San Antonio, Texas; and San Diego, California.

The value of this collaboration for the readers of Cutis is illustrated by the inaugural Military Dermatology column, “Managing Residual Limb Hyperhidrosis in Wounded Warriors: What Have We Learned?” This topic and others that will be featured in this new column, which will be published quarterly, will focus on an important area of skin disease that we may all see in our practices but an area in which AMD physicians have extensive expertise that they will share with us.

On a personal note, my dermatology training was in the US Public Health Service and I am an (inactive) member of the organization. I would urge all of our readers to consider supporting the mission of the AMD by visiting their website (http://www.militaryderm.org) and consider joining the organization, which accepts civilian members.

Vincent A. DeLeo, MD
Editor-in-Chief, Cutis

“START OFFERING ASPIRIN TO PREGNANT WOMEN AT HIGH RISK FOR PREECLAMPSIA”
ROBERT L. BARBIERI, MD (EDITORIAL; MAY 2016)

When should we stop aspirin during pregnancy?
In his Editorial, Dr. Barbieri discusses the ideal time to start aspirin in women at high risk for preeclampsia, but does not identify when to stop this medication. At our community health center, we have been stopping oral aspirin 81 mg at 36 weeks’ gestation because of the “potential” for postpartum hemorrhage or intrapartum hemorrhage after this time. Is there any literature regarding the evidence behind this date?

Tammy R. Gruenberg, MD, MPH
Bronx, New York

Dr. Barbieri responds
I appreciate Dr. Gruenberg’s important advice for our readers. Although low-dose aspirin is not known to be a major risk factor for adverse maternal or fetal outcomes, it is wise to stop the therapy a week prior to delivery, to reduce the theoretical risk of postpartum hemorrhage. Stopping aspirin at 36 or 37 weeks’ gestation will ensure that the majority of women are not taking aspirin at delivery.

“INTRACTABLE SHOULDER DYSTOCIA: A POSTERIOR AXILLA MANEUVER MAY SAVE THE DAY”
ROBERT L. BARBIERI, MD (EDITORIAL; APRIL 2016)

Another shoulder dystocia maneuver?
An additional technique that I use for managing shoulder dystocia is to simply track upward with the baby’s head, delivering the posterior shoulder without injury to the arm. Once the posterior shoulder clears the plane of the pubis and the anterior shoulder is mobilized, the posterior shoulder is rotated anterior in front of the pubic plane and the body unscrews itself from the pelvis. I also described this technique in a published letter to the editor in August 2013.

Dr. Barbieri’s suggestions in his April 2016 article are complicated for the less experienced ObGyn and could be dangerous for the baby (with potential fractures, nerve, and vascular injuries). Think about the described Gaskin maneuver: you flip the patient over on all fours, pull the baby’s head down, and deliver the superior shoulder (formerly the posterior shoulder).

Many obese and exhausted patients with epidurals will not be able to flip over for the Gaskin maneuver. The beauty of what I suggest is that this repositioning is not needed, and pulling on arms and axillae can endanger the baby. 

Robert Graebe, MD
Long Branch, New Jersey

Dr. Barbieri responds
I thank Dr. Graebe for describing his approach to resolving an intractable shoulder dystocia. Personally, I try to avoid applying force to the fetal head once a shoulder dystocia has been diagnosed.

QUICK POLL RESULTS
Preferred approaches to resolving the difficult shoulder dystocia
In his article, "Intractable shoulder dystocia: A posterior axilla maneuver may save the day," which appeared in the April 2016 issue of OBG Management, Editor in Chief Robert L. Barbieri, MD, offered several posterior axilla maneuvers to use when initial shoulder dystocia management steps are not enough.

He indicated his preferred maneuver as the Menticoglou, and asked readers: "What is your preferred approach to resolving the difficult shoulder dystocia?"

More than 100 readers weighed in:

• 33.6% (38 readers) prefer the Menicoglou maneuver
• 21.2% (24 readers) prefer the Schramm maneuver
• 19.5% (22 readers) prefer the Holman maneuver
• 15% (17 readers) prefer the Willughby maneuver
• 10.6% (12 readers) prefer the Hofmeyr-Cluver maneuver.

Share your thoughts! Send your Letter to the Editor to [email protected]. Please include your name and the city and state in which you practice.

“START OFFERING ASPIRIN TO PREGNANT WOMEN AT HIGH RISK FOR PREECLAMPSIA”
ROBERT L. BARBIERI, MD (EDITORIAL; MAY 2016)

When should we stop aspirin during pregnancy?
In his Editorial, Dr. Barbieri discusses the ideal time to start aspirin in women at high risk for preeclampsia, but does not identify when to stop this medication. At our community health center, we have been stopping oral aspirin 81 mg at 36 weeks’ gestation because of the “potential” for postpartum hemorrhage or intrapartum hemorrhage after this time. Is there any literature regarding the evidence behind this date?

Tammy R. Gruenberg, MD, MPH
Bronx, New York

Dr. Barbieri responds
I appreciate Dr. Gruenberg’s important advice for our readers. Although low-dose aspirin is not known to be a major risk factor for adverse maternal or fetal outcomes, it is wise to stop the therapy a week prior to delivery, to reduce the theoretical risk of postpartum hemorrhage. Stopping aspirin at 36 or 37 weeks’ gestation will ensure that the majority of women are not taking aspirin at delivery.

“INTRACTABLE SHOULDER DYSTOCIA: A POSTERIOR AXILLA MANEUVER MAY SAVE THE DAY”
ROBERT L. BARBIERI, MD (EDITORIAL; APRIL 2016)

Another shoulder dystocia maneuver?
An additional technique that I use for managing shoulder dystocia is to simply track upward with the baby’s head, delivering the posterior shoulder without injury to the arm. Once the posterior shoulder clears the plane of the pubis and the anterior shoulder is mobilized, the posterior shoulder is rotated anterior in front of the pubic plane and the body unscrews itself from the pelvis. I also described this technique in a published letter to the editor in August 2013.

Dr. Barbieri’s suggestions in his April 2016 article are complicated for the less experienced ObGyn and could be dangerous for the baby (with potential fractures, nerve, and vascular injuries). Think about the described Gaskin maneuver: you flip the patient over on all fours, pull the baby’s head down, and deliver the superior shoulder (formerly the posterior shoulder).

Many obese and exhausted patients with epidurals will not be able to flip over for the Gaskin maneuver. The beauty of what I suggest is that this repositioning is not needed, and pulling on arms and axillae can endanger the baby. 

Robert Graebe, MD
Long Branch, New Jersey

Dr. Barbieri responds
I thank Dr. Graebe for describing his approach to resolving an intractable shoulder dystocia. Personally, I try to avoid applying force to the fetal head once a shoulder dystocia has been diagnosed.

QUICK POLL RESULTS
Preferred approaches to resolving the difficult shoulder dystocia
In his article, "Intractable shoulder dystocia: A posterior axilla maneuver may save the day," which appeared in the April 2016 issue of OBG Management, Editor in Chief Robert L. Barbieri, MD, offered several posterior axilla maneuvers to use when initial shoulder dystocia management steps are not enough.

He indicated his preferred maneuver as the Menticoglou, and asked readers: "What is your preferred approach to resolving the difficult shoulder dystocia?"

More than 100 readers weighed in:

• 33.6% (38 readers) prefer the Menicoglou maneuver
• 21.2% (24 readers) prefer the Schramm maneuver
• 19.5% (22 readers) prefer the Holman maneuver
• 15% (17 readers) prefer the Willughby maneuver
• 10.6% (12 readers) prefer the Hofmeyr-Cluver maneuver.

Share your thoughts! Send your Letter to the Editor to [email protected]. Please include your name and the city and state in which you practice.

“START OFFERING ASPIRIN TO PREGNANT WOMEN AT HIGH RISK FOR PREECLAMPSIA”
ROBERT L. BARBIERI, MD (EDITORIAL; MAY 2016)

When should we stop aspirin during pregnancy?
In his Editorial, Dr. Barbieri discusses the ideal time to start aspirin in women at high risk for preeclampsia, but does not identify when to stop this medication. At our community health center, we have been stopping oral aspirin 81 mg at 36 weeks’ gestation because of the “potential” for postpartum hemorrhage or intrapartum hemorrhage after this time. Is there any literature regarding the evidence behind this date?

Tammy R. Gruenberg, MD, MPH
Bronx, New York

Dr. Barbieri responds
I appreciate Dr. Gruenberg’s important advice for our readers. Although low-dose aspirin is not known to be a major risk factor for adverse maternal or fetal outcomes, it is wise to stop the therapy a week prior to delivery, to reduce the theoretical risk of postpartum hemorrhage. Stopping aspirin at 36 or 37 weeks’ gestation will ensure that the majority of women are not taking aspirin at delivery.

“INTRACTABLE SHOULDER DYSTOCIA: A POSTERIOR AXILLA MANEUVER MAY SAVE THE DAY”
ROBERT L. BARBIERI, MD (EDITORIAL; APRIL 2016)

Another shoulder dystocia maneuver?
An additional technique that I use for managing shoulder dystocia is to simply track upward with the baby’s head, delivering the posterior shoulder without injury to the arm. Once the posterior shoulder clears the plane of the pubis and the anterior shoulder is mobilized, the posterior shoulder is rotated anterior in front of the pubic plane and the body unscrews itself from the pelvis. I also described this technique in a published letter to the editor in August 2013.

Dr. Barbieri’s suggestions in his April 2016 article are complicated for the less experienced ObGyn and could be dangerous for the baby (with potential fractures, nerve, and vascular injuries). Think about the described Gaskin maneuver: you flip the patient over on all fours, pull the baby’s head down, and deliver the superior shoulder (formerly the posterior shoulder).

Many obese and exhausted patients with epidurals will not be able to flip over for the Gaskin maneuver. The beauty of what I suggest is that this repositioning is not needed, and pulling on arms and axillae can endanger the baby. 

Robert Graebe, MD
Long Branch, New Jersey

Dr. Barbieri responds
I thank Dr. Graebe for describing his approach to resolving an intractable shoulder dystocia. Personally, I try to avoid applying force to the fetal head once a shoulder dystocia has been diagnosed.

QUICK POLL RESULTS
Preferred approaches to resolving the difficult shoulder dystocia
In his article, "Intractable shoulder dystocia: A posterior axilla maneuver may save the day," which appeared in the April 2016 issue of OBG Management, Editor in Chief Robert L. Barbieri, MD, offered several posterior axilla maneuvers to use when initial shoulder dystocia management steps are not enough.

He indicated his preferred maneuver as the Menticoglou, and asked readers: "What is your preferred approach to resolving the difficult shoulder dystocia?"

More than 100 readers weighed in:

• 33.6% (38 readers) prefer the Menicoglou maneuver
• 21.2% (24 readers) prefer the Schramm maneuver
• 19.5% (22 readers) prefer the Holman maneuver
• 15% (17 readers) prefer the Willughby maneuver
• 10.6% (12 readers) prefer the Hofmeyr-Cluver maneuver.

Share your thoughts! Send your Letter to the Editor to [email protected]. Please include your name and the city and state in which you practice.

Recently published guidelines for the pharmacologic management of heart failure in patients with reduced ejection fraction (HFrEF) focus on two drugs – both of which have been approved by the Food and Drug Administration – that have shown promise in managing heart failure patients.

The guideline committee has deemed that the combination drug sacubitril-valsartan (Entresto, Novartis) and ivabradine (Corlanor, Amgen) as “milestone” achievements. In this reader’s mind, compared with the mortality and morbidity effect of beta-blockers and ACE inhibitors, they really don’t make it to that status. They do, however, reach the threshold of important adjuncts to the care for heart failure treatment.

Ivabradine was shown to improve the combination of rehospitalization and mortality when added to conventional therapy, including beta-blockers, by decreasing heart rate. Unfortunately, many of the patients in the trial were not adequately treated with beta-blockers. Sacubitril-valsartan, a drug we have commented about in previous columns, is interesting and adds an additional effect on mortality and morbidity when compared with enalapril alone. In the PARADIGM-HF trial, it showed a significant 20% decrease in rehospitalization and total mortality. A strong case can be made that it should be used instead of an ACE inhibitor, although it is associated with some increased hypotension and angioneurotic edema.

Sacubitril-valsartan poses a significant social issue in regard to its pricing. Most of the drugs we use for the treatment of heart failure cost less than a dollar a day when introduced, and pennies now, and they are immensely effective. Sacubitril-valsartan on average moves the mortality needle a bit, but at a cost of 20 times its competitor, enalapril. It doesn’t do it in all patients, so that it might be reasonable to use it just in those patients who are failing with an ACE inhibitor alone. This is the first time heart failure doctors have had to grapple with the problem of drug pricing, whereas the oncologist and the lipid specialists have been facing this issue for some time. Is it worth $500 a month, compared to $25 a month, to possibly move the mortality index, which has already been modified with the previous ACE inhibitors, down a bit? I suppose that the decision is up to all of us to make.

Reading the guidelines, however, provided me with some insight that I have missed in the past. Of the 17 members of the guideline writing team representing the American College of Cardiology, American Heart Association, and the Heart Failure Society of America, eight had “significant relationships” with the two pharmaceutical companies in question. Committee members were advised not to vote if they had a relevant relationship with industry. How they functioned in the committee proceeding it’s impossible to tell, but the potential for bias is there. I would imagine that eight other heart failure specialists who did not have a conflict could have been found to serve on the writing committee. As guidelines have become such a major part of the construct of the pharmacopoeia, potential bias like this should and easily can be avoided.

Dr. Goldstein, medical editor of Cardiology News, is professor of medicine at Wayne State University and division head emeritus of cardiovascular medicine at Henry Ford Hospital, both in Detroit. He is on data safety monitoring committees for the National Institutes of Health and several pharmaceutical companies.

Recently published guidelines for the pharmacologic management of heart failure in patients with reduced ejection fraction (HFrEF) focus on two drugs – both of which have been approved by the Food and Drug Administration – that have shown promise in managing heart failure patients.

The guideline committee has deemed that the combination drug sacubitril-valsartan (Entresto, Novartis) and ivabradine (Corlanor, Amgen) as “milestone” achievements. In this reader’s mind, compared with the mortality and morbidity effect of beta-blockers and ACE inhibitors, they really don’t make it to that status. They do, however, reach the threshold of important adjuncts to the care for heart failure treatment.

Ivabradine was shown to improve the combination of rehospitalization and mortality when added to conventional therapy, including beta-blockers, by decreasing heart rate. Unfortunately, many of the patients in the trial were not adequately treated with beta-blockers. Sacubitril-valsartan, a drug we have commented about in previous columns, is interesting and adds an additional effect on mortality and morbidity when compared with enalapril alone. In the PARADIGM-HF trial, it showed a significant 20% decrease in rehospitalization and total mortality. A strong case can be made that it should be used instead of an ACE inhibitor, although it is associated with some increased hypotension and angioneurotic edema.

Sacubitril-valsartan poses a significant social issue in regard to its pricing. Most of the drugs we use for the treatment of heart failure cost less than a dollar a day when introduced, and pennies now, and they are immensely effective. Sacubitril-valsartan on average moves the mortality needle a bit, but at a cost of 20 times its competitor, enalapril. It doesn’t do it in all patients, so that it might be reasonable to use it just in those patients who are failing with an ACE inhibitor alone. This is the first time heart failure doctors have had to grapple with the problem of drug pricing, whereas the oncologist and the lipid specialists have been facing this issue for some time. Is it worth $500 a month, compared to $25 a month, to possibly move the mortality index, which has already been modified with the previous ACE inhibitors, down a bit? I suppose that the decision is up to all of us to make.

Reading the guidelines, however, provided me with some insight that I have missed in the past. Of the 17 members of the guideline writing team representing the American College of Cardiology, American Heart Association, and the Heart Failure Society of America, eight had “significant relationships” with the two pharmaceutical companies in question. Committee members were advised not to vote if they had a relevant relationship with industry. How they functioned in the committee proceeding it’s impossible to tell, but the potential for bias is there. I would imagine that eight other heart failure specialists who did not have a conflict could have been found to serve on the writing committee. As guidelines have become such a major part of the construct of the pharmacopoeia, potential bias like this should and easily can be avoided.

Dr. Goldstein, medical editor of Cardiology News, is professor of medicine at Wayne State University and division head emeritus of cardiovascular medicine at Henry Ford Hospital, both in Detroit. He is on data safety monitoring committees for the National Institutes of Health and several pharmaceutical companies.

Recently published guidelines for the pharmacologic management of heart failure in patients with reduced ejection fraction (HFrEF) focus on two drugs – both of which have been approved by the Food and Drug Administration – that have shown promise in managing heart failure patients.

The guideline committee has deemed that the combination drug sacubitril-valsartan (Entresto, Novartis) and ivabradine (Corlanor, Amgen) as “milestone” achievements. In this reader’s mind, compared with the mortality and morbidity effect of beta-blockers and ACE inhibitors, they really don’t make it to that status. They do, however, reach the threshold of important adjuncts to the care for heart failure treatment.

Ivabradine was shown to improve the combination of rehospitalization and mortality when added to conventional therapy, including beta-blockers, by decreasing heart rate. Unfortunately, many of the patients in the trial were not adequately treated with beta-blockers. Sacubitril-valsartan, a drug we have commented about in previous columns, is interesting and adds an additional effect on mortality and morbidity when compared with enalapril alone. In the PARADIGM-HF trial, it showed a significant 20% decrease in rehospitalization and total mortality. A strong case can be made that it should be used instead of an ACE inhibitor, although it is associated with some increased hypotension and angioneurotic edema.

Sacubitril-valsartan poses a significant social issue in regard to its pricing. Most of the drugs we use for the treatment of heart failure cost less than a dollar a day when introduced, and pennies now, and they are immensely effective. Sacubitril-valsartan on average moves the mortality needle a bit, but at a cost of 20 times its competitor, enalapril. It doesn’t do it in all patients, so that it might be reasonable to use it just in those patients who are failing with an ACE inhibitor alone. This is the first time heart failure doctors have had to grapple with the problem of drug pricing, whereas the oncologist and the lipid specialists have been facing this issue for some time. Is it worth $500 a month, compared to $25 a month, to possibly move the mortality index, which has already been modified with the previous ACE inhibitors, down a bit? I suppose that the decision is up to all of us to make.

Reading the guidelines, however, provided me with some insight that I have missed in the past. Of the 17 members of the guideline writing team representing the American College of Cardiology, American Heart Association, and the Heart Failure Society of America, eight had “significant relationships” with the two pharmaceutical companies in question. Committee members were advised not to vote if they had a relevant relationship with industry. How they functioned in the committee proceeding it’s impossible to tell, but the potential for bias is there. I would imagine that eight other heart failure specialists who did not have a conflict could have been found to serve on the writing committee. As guidelines have become such a major part of the construct of the pharmacopoeia, potential bias like this should and easily can be avoided.

Dr. Goldstein, medical editor of Cardiology News, is professor of medicine at Wayne State University and division head emeritus of cardiovascular medicine at Henry Ford Hospital, both in Detroit. He is on data safety monitoring committees for the National Institutes of Health and several pharmaceutical companies.

Roughly 1%-2% of pregnancies are complicated by an adnexal mass, and prenatal ultrasound for fetal evaluation has detected more asymptomatic ovarian masses as a result.

The differential diagnosis for adnexal mass is broad and includes follicular or corpus luteum cysts, mature teratoma, theca lutein cyst, hydrosalpinx, endometrioma, cystadenoma, pedunculated leiomyoma, luteoma, as well as malignant neoplasms of epithelial, germ cell, and sex cord–stromal origin (J Ultrasound Med. 2004 Jun;23[6]:805-19). Most masses will be benign neoplasms, with a fraction identified as malignancies.

In 2013, Baser et al. performed a retrospective study of 151 women who underwent surgery of an adnexal mass at time of cesarean delivery. Of the 151 cases reviewed, 148 (98%) of the masses were benign (Int J Gynaecol Obstet. 2013 Nov;123[2]:124-6). Additionally, if the patient presents with pain, diagnoses such as ectopic pregnancy, heterotopic pregnancy, degenerating fibroid, and torsion should also be considered.

Diagnostic evaluation and management

The majority of adnexal masses identified in pregnancy are benign simple cysts measuring less than 5 cm in diameter. Approximately 70% of cystic masses detected in the first trimester will spontaneously resolve by the second trimester (Clin Obstet Gynecol. 2006 Sep;49[3]:492-505). However, for some masses, surgical resection is warranted.

Masses present after the first trimester and that are (1) greater than 10cm in diameter or (2) are solid or contain solid and cystic areas or have septated or papillary areas, are generally managed surgically as these features increase the risk of malignancy or complications such as adnexal torsion, rupture, or labor dystocia (Gynecol Oncol. 2006 May;101(2):315-21).

Adnexal masses without these features often resolve during pregnancy and can be expectantly managed (Obstet Gynecol. 2005 May;105[5 Pt 1]:1098-103). The optimal time for surgical intervention is after the first trimester as organogenesis is largely complete, therefore minimizing the risk of drug-induced teratogenesis, and any necessary cystectomy or oophorectomy will not disrupt the required progesterone production of the corpus luteum as this has been replaced by the placenta.

Preoperative assessment

For most cases, imaging with ultrasound is adequate for preoperative evaluation; however, in some cases, further imaging is needed for appropriate characterization of the mass. In this situation, further imaging with MRI is preferred as this modality has good resolution for visualization of soft tissue pathology and does not expose the patient and fetus to ionizing radiation. Of note, Gadolinium-based contrast should be avoided as effects have not been well established in pregnancy (AJR Am J Roentgenol. 2008 Aug;191[2]:364-70).

If there is concern for malignancy during pregnancy, drawing serum tumor markers preoperatively is typically not suggested. Oncofetal antigens, including alpha fetoprotein (AFP), human chorionic gonadotropin (hCG), carcinoembryonic antigen (CEA), and cancer antigen 125 (CA-125), are elevated during gestation, making them poor markers for malignancy. If malignancy is ultimately diagnosed, then tumor markers can be obtained immediately postoperatively.

Surgical approach and prognosis

If there is low suspicion for malignancy, a laparoscopic approach is preferable and reasonable at all stages of pregnancy, although early second trimester is ideal. Entry at Palmer’s point in the left upper quadrant versus the umbilicus is preferable in order to minimize risk of uterine injury.

If malignancy is suspected, maximum exposure should be obtained with a midline vertical incision. Peritoneal washings should be obtained on immediate entry of the peritoneal cavity, and the contralateral ovary should also be adequately examined along with a general abdominopelvic survey. If the mass demonstrates concerning features, such as solid features or presence of ascites, then the specimen should be sent for intraoperative frozen pathology, and the pathologist should be made aware of the concurrent pregnancy. If malignancy is confirmed on frozen pathology, a full staging procedure should be performed and a gynecologic oncologist consulted.

Roughly three-quarters of invasive ovarian cancers diagnosed in pregnancy are early stage disease, and the 5-year survival of ovarian cancers associated with pregnancy is between 72% and 90% (Int J Gynecol Cancer. 2006 Jan-Feb;16[1]:8-15).

In a retrospective cohort study of 101 pregnant women, 31% of adnexal masses resected in pregnant women greater than 14 weeks gestation were teratomas. In total, 23% of masses were luteal cysts. Less commonly, patients were diagnosed with serous cystadenoma (14%), endometrioma (8%), mucinous cystadenoma (7%), benign cyst (6%), tumor of low malignant potential (5%), and paratubal cyst (3%).

In this study, approximately half of the women underwent minimally invasive surgery and half had surgery via laparotomy. There were more complications in the women undergoing laparotomy (ileus) and there were no differences between the groups with regards to pregnancy and neonatal outcomes (J Minim Invasive Gynecol. 2011 Nov-Dec;18[6]:720-5).

In general, characteristics that are favorable for spontaneous resolution include masses that are simple in nature by ultrasound and less than 5 cm to 6 cm in diameter.

For women with simple-appearing masses on ultrasound, reimaging can occur during the remainder of the pregnancy at the discretion of the physician or during the postpartum period. All women should be provided with torsion and rupture precautions during the pregnancy (Am J Obstet Gynecol. 2011 Aug;205[2]:97-102). For women with more concerning features on ultrasound, referral to a gynecologic oncologist is warranted. If the decision for surgical management is made, minimally invasive surgery should be strongly considered due to minimal maternal and perinatal morbidity.

Dr. Staley is a resident physician in the department of obstetrics and gynecology at the University of North Carolina at Chapel Hill. Dr. Gehrig is professor and director of gynecologic oncology at the university. They reported having no relevant financial disclosures.

Roughly 1%-2% of pregnancies are complicated by an adnexal mass, and prenatal ultrasound for fetal evaluation has detected more asymptomatic ovarian masses as a result.

The differential diagnosis for adnexal mass is broad and includes follicular or corpus luteum cysts, mature teratoma, theca lutein cyst, hydrosalpinx, endometrioma, cystadenoma, pedunculated leiomyoma, luteoma, as well as malignant neoplasms of epithelial, germ cell, and sex cord–stromal origin (J Ultrasound Med. 2004 Jun;23[6]:805-19). Most masses will be benign neoplasms, with a fraction identified as malignancies.

In 2013, Baser et al. performed a retrospective study of 151 women who underwent surgery of an adnexal mass at time of cesarean delivery. Of the 151 cases reviewed, 148 (98%) of the masses were benign (Int J Gynaecol Obstet. 2013 Nov;123[2]:124-6). Additionally, if the patient presents with pain, diagnoses such as ectopic pregnancy, heterotopic pregnancy, degenerating fibroid, and torsion should also be considered.

Diagnostic evaluation and management

The majority of adnexal masses identified in pregnancy are benign simple cysts measuring less than 5 cm in diameter. Approximately 70% of cystic masses detected in the first trimester will spontaneously resolve by the second trimester (Clin Obstet Gynecol. 2006 Sep;49[3]:492-505). However, for some masses, surgical resection is warranted.

Masses present after the first trimester and that are (1) greater than 10cm in diameter or (2) are solid or contain solid and cystic areas or have septated or papillary areas, are generally managed surgically as these features increase the risk of malignancy or complications such as adnexal torsion, rupture, or labor dystocia (Gynecol Oncol. 2006 May;101(2):315-21).

Adnexal masses without these features often resolve during pregnancy and can be expectantly managed (Obstet Gynecol. 2005 May;105[5 Pt 1]:1098-103). The optimal time for surgical intervention is after the first trimester as organogenesis is largely complete, therefore minimizing the risk of drug-induced teratogenesis, and any necessary cystectomy or oophorectomy will not disrupt the required progesterone production of the corpus luteum as this has been replaced by the placenta.

Preoperative assessment

For most cases, imaging with ultrasound is adequate for preoperative evaluation; however, in some cases, further imaging is needed for appropriate characterization of the mass. In this situation, further imaging with MRI is preferred as this modality has good resolution for visualization of soft tissue pathology and does not expose the patient and fetus to ionizing radiation. Of note, Gadolinium-based contrast should be avoided as effects have not been well established in pregnancy (AJR Am J Roentgenol. 2008 Aug;191[2]:364-70).

If there is concern for malignancy during pregnancy, drawing serum tumor markers preoperatively is typically not suggested. Oncofetal antigens, including alpha fetoprotein (AFP), human chorionic gonadotropin (hCG), carcinoembryonic antigen (CEA), and cancer antigen 125 (CA-125), are elevated during gestation, making them poor markers for malignancy. If malignancy is ultimately diagnosed, then tumor markers can be obtained immediately postoperatively.

Surgical approach and prognosis

If there is low suspicion for malignancy, a laparoscopic approach is preferable and reasonable at all stages of pregnancy, although early second trimester is ideal. Entry at Palmer’s point in the left upper quadrant versus the umbilicus is preferable in order to minimize risk of uterine injury.

If malignancy is suspected, maximum exposure should be obtained with a midline vertical incision. Peritoneal washings should be obtained on immediate entry of the peritoneal cavity, and the contralateral ovary should also be adequately examined along with a general abdominopelvic survey. If the mass demonstrates concerning features, such as solid features or presence of ascites, then the specimen should be sent for intraoperative frozen pathology, and the pathologist should be made aware of the concurrent pregnancy. If malignancy is confirmed on frozen pathology, a full staging procedure should be performed and a gynecologic oncologist consulted.

Roughly three-quarters of invasive ovarian cancers diagnosed in pregnancy are early stage disease, and the 5-year survival of ovarian cancers associated with pregnancy is between 72% and 90% (Int J Gynecol Cancer. 2006 Jan-Feb;16[1]:8-15).

In a retrospective cohort study of 101 pregnant women, 31% of adnexal masses resected in pregnant women greater than 14 weeks gestation were teratomas. In total, 23% of masses were luteal cysts. Less commonly, patients were diagnosed with serous cystadenoma (14%), endometrioma (8%), mucinous cystadenoma (7%), benign cyst (6%), tumor of low malignant potential (5%), and paratubal cyst (3%).

In this study, approximately half of the women underwent minimally invasive surgery and half had surgery via laparotomy. There were more complications in the women undergoing laparotomy (ileus) and there were no differences between the groups with regards to pregnancy and neonatal outcomes (J Minim Invasive Gynecol. 2011 Nov-Dec;18[6]:720-5).

In general, characteristics that are favorable for spontaneous resolution include masses that are simple in nature by ultrasound and less than 5 cm to 6 cm in diameter.

For women with simple-appearing masses on ultrasound, reimaging can occur during the remainder of the pregnancy at the discretion of the physician or during the postpartum period. All women should be provided with torsion and rupture precautions during the pregnancy (Am J Obstet Gynecol. 2011 Aug;205[2]:97-102). For women with more concerning features on ultrasound, referral to a gynecologic oncologist is warranted. If the decision for surgical management is made, minimally invasive surgery should be strongly considered due to minimal maternal and perinatal morbidity.

Dr. Staley is a resident physician in the department of obstetrics and gynecology at the University of North Carolina at Chapel Hill. Dr. Gehrig is professor and director of gynecologic oncology at the university. They reported having no relevant financial disclosures.

Roughly 1%-2% of pregnancies are complicated by an adnexal mass, and prenatal ultrasound for fetal evaluation has detected more asymptomatic ovarian masses as a result.

The differential diagnosis for adnexal mass is broad and includes follicular or corpus luteum cysts, mature teratoma, theca lutein cyst, hydrosalpinx, endometrioma, cystadenoma, pedunculated leiomyoma, luteoma, as well as malignant neoplasms of epithelial, germ cell, and sex cord–stromal origin (J Ultrasound Med. 2004 Jun;23[6]:805-19). Most masses will be benign neoplasms, with a fraction identified as malignancies.

In 2013, Baser et al. performed a retrospective study of 151 women who underwent surgery of an adnexal mass at time of cesarean delivery. Of the 151 cases reviewed, 148 (98%) of the masses were benign (Int J Gynaecol Obstet. 2013 Nov;123[2]:124-6). Additionally, if the patient presents with pain, diagnoses such as ectopic pregnancy, heterotopic pregnancy, degenerating fibroid, and torsion should also be considered.

Diagnostic evaluation and management

The majority of adnexal masses identified in pregnancy are benign simple cysts measuring less than 5 cm in diameter. Approximately 70% of cystic masses detected in the first trimester will spontaneously resolve by the second trimester (Clin Obstet Gynecol. 2006 Sep;49[3]:492-505). However, for some masses, surgical resection is warranted.

Masses present after the first trimester and that are (1) greater than 10cm in diameter or (2) are solid or contain solid and cystic areas or have septated or papillary areas, are generally managed surgically as these features increase the risk of malignancy or complications such as adnexal torsion, rupture, or labor dystocia (Gynecol Oncol. 2006 May;101(2):315-21).

Adnexal masses without these features often resolve during pregnancy and can be expectantly managed (Obstet Gynecol. 2005 May;105[5 Pt 1]:1098-103). The optimal time for surgical intervention is after the first trimester as organogenesis is largely complete, therefore minimizing the risk of drug-induced teratogenesis, and any necessary cystectomy or oophorectomy will not disrupt the required progesterone production of the corpus luteum as this has been replaced by the placenta.

Preoperative assessment

For most cases, imaging with ultrasound is adequate for preoperative evaluation; however, in some cases, further imaging is needed for appropriate characterization of the mass. In this situation, further imaging with MRI is preferred as this modality has good resolution for visualization of soft tissue pathology and does not expose the patient and fetus to ionizing radiation. Of note, Gadolinium-based contrast should be avoided as effects have not been well established in pregnancy (AJR Am J Roentgenol. 2008 Aug;191[2]:364-70).

If there is concern for malignancy during pregnancy, drawing serum tumor markers preoperatively is typically not suggested. Oncofetal antigens, including alpha fetoprotein (AFP), human chorionic gonadotropin (hCG), carcinoembryonic antigen (CEA), and cancer antigen 125 (CA-125), are elevated during gestation, making them poor markers for malignancy. If malignancy is ultimately diagnosed, then tumor markers can be obtained immediately postoperatively.

Surgical approach and prognosis

If there is low suspicion for malignancy, a laparoscopic approach is preferable and reasonable at all stages of pregnancy, although early second trimester is ideal. Entry at Palmer’s point in the left upper quadrant versus the umbilicus is preferable in order to minimize risk of uterine injury.

If malignancy is suspected, maximum exposure should be obtained with a midline vertical incision. Peritoneal washings should be obtained on immediate entry of the peritoneal cavity, and the contralateral ovary should also be adequately examined along with a general abdominopelvic survey. If the mass demonstrates concerning features, such as solid features or presence of ascites, then the specimen should be sent for intraoperative frozen pathology, and the pathologist should be made aware of the concurrent pregnancy. If malignancy is confirmed on frozen pathology, a full staging procedure should be performed and a gynecologic oncologist consulted.

Roughly three-quarters of invasive ovarian cancers diagnosed in pregnancy are early stage disease, and the 5-year survival of ovarian cancers associated with pregnancy is between 72% and 90% (Int J Gynecol Cancer. 2006 Jan-Feb;16[1]:8-15).

In a retrospective cohort study of 101 pregnant women, 31% of adnexal masses resected in pregnant women greater than 14 weeks gestation were teratomas. In total, 23% of masses were luteal cysts. Less commonly, patients were diagnosed with serous cystadenoma (14%), endometrioma (8%), mucinous cystadenoma (7%), benign cyst (6%), tumor of low malignant potential (5%), and paratubal cyst (3%).

In this study, approximately half of the women underwent minimally invasive surgery and half had surgery via laparotomy. There were more complications in the women undergoing laparotomy (ileus) and there were no differences between the groups with regards to pregnancy and neonatal outcomes (J Minim Invasive Gynecol. 2011 Nov-Dec;18[6]:720-5).

In general, characteristics that are favorable for spontaneous resolution include masses that are simple in nature by ultrasound and less than 5 cm to 6 cm in diameter.

For women with simple-appearing masses on ultrasound, reimaging can occur during the remainder of the pregnancy at the discretion of the physician or during the postpartum period. All women should be provided with torsion and rupture precautions during the pregnancy (Am J Obstet Gynecol. 2011 Aug;205[2]:97-102). For women with more concerning features on ultrasound, referral to a gynecologic oncologist is warranted. If the decision for surgical management is made, minimally invasive surgery should be strongly considered due to minimal maternal and perinatal morbidity.

Dr. Staley is a resident physician in the department of obstetrics and gynecology at the University of North Carolina at Chapel Hill. Dr. Gehrig is professor and director of gynecologic oncology at the university. They reported having no relevant financial disclosures.

When I was growing up, my mother frequently told me that it was rude to interrupt. Although she was referring to conversations, she may have been onto something bigger.

In the nearly three quarters of a century since their discovery, vitamin K antagonist anticoagulant drugs have been used by millions of patients to prevent heart attack and stroke. Before these patients undergo surgery, a decision to continue or interrupt anticoagulation must be made, weighing the risks of postsurgical hemorrhage with continuation of anticoagulation against the risks of stroke or other embolic complications with interruption of anticoagulation. Bleeding after dental surgery when anticoagulation is continued is rarely or never life-threatening. On the other hand, embolic complications of interrupting anticoagulation are almost always consequential and often lead to death or disability. Although consideration may be different for other types of surgery, there is no need to interrupt lifesaving anticoagulation for dental surgery.

EVIDENCE THAT SUPPORTS CONTINUING ANTICOAGULATION

As early as 1957, there were reports of prolonged postoperative bleeding after dental extractions in patients taking anticoagulants. But there were also reports of embolic complications in patients whose anticoagulation was interrupted for dental procedures. Since then, there has been a plethora of literature in this area.

A review published in 2000 showed that of more than 950 anticoagulated patients undergoing more than 2,400 dental surgical procedures (including simple and surgical extraction, alveoplasty, and gingival surgery), only 12 (< 1.3%) required more than local measures for hemostasis (eg, fresh-frozen plasma, vitamin K), and no patient died,¹ leading to the conclusion that the bleeding risk was not significant in anticoagulated dental patients. Other studies and systematic reviews have also concluded that anticoagulation for dental procedures should not be interrupted.^2,3 In a recent review of 83 studies, only 31 (0.6%) of 5,431 patients taking warfarin suffered bleeding complications requiring more than local measures for hemostasis; there were no fatalities.⁴

The risk of embolism

There have been many reports of embolic complications in patients whose anticoagulation was interrupted for dental procedures. A 2000 review of 575 cases in 526 patients whose anticoagulation was interrupted for dental procedures showed that 5 patients (0.9%) had a serious embolic complication, and 4 died.¹ In a more recent review of 64 studies and more than 2,673 patients whose anticoagulation was interrupted for dental procedures, 22 patients (0.8%) suffered embolic complications, and 6 (0.2%) died of the complications.⁴ Of those with embolic complications, the interruption period was often not reported; however; the interruption ranged from 1 to 4 days. A 2003 systematic review by Dunn and Turpie found a 0.4% embolic complication rate when anticoagulation was interrupted for dental surgery.²

BLEEDING AFTER DENTAL SURGERY

Bleeding after dental surgery can occur with either anticoagulation continuation or interruption, and minor postoperative bleeding requiring additional local hemostatic methods occurs at about the same rate in anticoagulated patients as in those whose anticoagulation is interrupted.

In our recent literature review,⁴ about 6% of patients in whom anticoagulation was interrupted (and 7% in whom it was not interrupted) had minor bleeding requiring additional local hemostasis, and only 0.2% of patients required more than hemostatic measures (eg, vitamin K injection, plasma transfusion), the same rate found by Dunn and Turpie.² All patients who required more than local hemostatic measures presumably made a full recovery, while at least 6 who suffered postoperative embolic complications died, and the rest may have had permanent disabilities.

Although bridging therapy with low-molecular-weight heparin can decrease the time without anticoagulation for a dental procedure to only 12 hours, it can be complicated to implement, and there appears to be no benefit in terms of the rates of bleeding or embolic complications. Of the 64 anticoagulation interruption studies,⁴ 17 used heparin or low-molecular-weight heparin in conjunction with temporary warfarin interruption. In 210 instances of bridging therapy in 202 patients undergoing dental procedures, there were 2 embolic complications (1% of bridging cases) and 20 bleeding complications, with 3 (1.4%) requiring hemostasis beyond local measures.⁴

Many of the studies analyzed independently showed there was no significant difference in postoperative bleeding with:

• Anticoagulation continuation vs interruption for a few days
• Lower vs higher international normalized ratio (INR), including some over 4.0
• Surgical vs nonsurgical extraction
• Few vs many extractions.⁴

Some studies of anticoagulation and anticoagulation interruption for dental surgery had important limitations. Many of the anticoagulation studies excluded patients at high risk of bleeding, those with a high INR (> 4.0), and those with severe liver or kidney disease, and their exclusion could have lowered the incidence of bleeding complications. Many studies of anticoagulation interruption excluded patients at high risk of embolism, including patients with a previous embolic event and patients with an artificial heart valve, and this could have skewed the results lower for embolic complications.

WHY DO SOME CLINICIANS STILL RECOMMEND INTERRUPTION?

The choice seems clear: for dental surgery in anticoagulated patients, the small risk of a nonfatal bleeding complication in anticoagulated patients is outweighed by the small risk of a disabling or fatal embolic complication when anticoagulation is interrupted. Most authors have concluded that anticoagulation should be continued for dental surgery. Yet surveys of dentists and physicians have shown that many still recommend interrupting anticoagulation for dental surgery.^5,6

Medical and dental association positions

The American Academy of Neurology⁷ and the American Dental Association⁸ recommend continuing anticoagulant medications for dental surgery. The American College of Chest Physicians also recommends continuing anticoagulation but in 2012 added an option to interrupt or decrease anticoagulation for 2 to 3 days for dental surgery.⁹ Their recommendation was based partly on the results of four controlled prospective studies^10–13 comparing anticoagulated dental surgical patients with patients whose anticoagulation was interrupted. In each study, there were no embolic or bleeding complications requiring more than local methods for hemostasis in the interruption groups, leading the American College of Chest Physicians to conclude that brief anticoagulation interruption for dental surgery is safe and effective.

But the results of these studies actually argue against interrupting anticoagulation for dental surgery. In each study, rates of postoperative bleeding complications and blood loss were similar in both groups, and there were no embolic complications. The authors of each study independently concluded that anticoagulation should not be interrupted for dental surgery.

The optimal INR range for anticoagulation therapy is widely accepted as 2.0 to 3.0, and 2.5 to 3.5 for patients with a mechanical mitral valve.¹⁴ Interrupting warfarin anticoagulation for 2 or 3 days leads to a suboptimal INR. Patel et al¹⁵ studied the incidence of embolic complications (including stroke, non-central nervous system embolism, myocardial infarction, and vascular death) within 30 days in 7,082 patients taking warfarin with and without an interruption of therapy of at least 3 days (median 6 days). The observed rate of embolic events in those with temporary interruption (10.75 events per 100 patient-years) was more than double the rate in those without interruption (4.03 per 100 patient-years).¹⁵ However, this study was designed to compare rivaroxaban vs warfarin, not interrupting vs not interrupting warfarin.

A DECISION-TREE REANALYSIS

In 2010, Balevi published a decision-tree analysis that slightly favored withdrawing warfarin for dental surgery, but he stated that the analysis “can be updated in the future as more accurate and up-to-date data for each of the variables in the model become available.”¹⁶ Now that there are more accurate and up-to-date data, it is time to revisit this decision-tree analysis.

In Balevi’s analysis, major bleeding is not defined. But major bleeding after dental surgery should be defined as any bleeding requiring more than local measures for hemostasis. In calculating probabilities for the analysis, Balevi cited studies allegedly showing high incidences of major bleeding after dental extractions with warfarin continuation.^17,18 There were some minor bleeding complications necessitating additional local measures for hemostasis in these studies, but no major bleeding complications at all in the warfarin- continuation or warfarin-interruption group. There were no significant bleeding events in either study, and the differences in bleeding rates were not significantly different between the two groups. In both studies, the authors concluded that warfarin interruption for dental surgery should be reconsidered.

Similarly, Balevi accurately asserted that there has never been a reported case of fatal bleeding after a dental procedure in an anticoagulated patient, but “for the sake of creating balance,”¹⁶ his decision-tree analysis uses a fatal bleeding probability of 1%, based on an estimated 1% risk for nondental procedures (eg, colorectal surgery, major abdominal surgery). It is unclear how a 1% incidence creates “balance,” but dental surgery is unlike other types of surgery, and that is one reason there has never been a documented postdental fatal hemorrhage in an anticoagulated patient. Major vessels are unlikely to be encountered, and bleeding sites are easily accessible to local hemostatic methods.

Balevi used an embolic complication incidence of 0.059% with warfarin interruption of 3 days. Perhaps he used such a low embolic probability because of his incorrect assertion that “there has been no reported case of a dental extraction causing a cardiovascular accident in a patient whose warfarin was temporarily discontinued.”¹⁶ In fact, our group has now identified at least 22 reported cases of embolic complications after temporary interruption of warfarin therapy in patients undergoing dental surgery.⁴ These included 12 embolic complications (3 fatal) after interruption periods from 1 to 5 days.^19,20 In addition, there are numerous cases of embolic complications reported in patients whose warfarin was temporarily interrupted for other types of surgery.^21,22

The literature shows that embolic complications after temporary warfarin interruption occur at a much higher rate than 0.059%. Many documented embolic complications have occurred after relatively long warfarin interruption periods (greater than 5 days), but many have occurred with much shorter interruptions. Wysokinski et al²¹ showed that there was a 1.1% incidence of thromboembolic events, more than 18 times greater than Balevi’s incidence, in patients whose warfarin was interrupted for 4 or 5 days with or without bridging therapy. One of these patients developed an occipital infarct within 3 days after stopping warfarin without bridging (for a nondental procedure). Garcia et al²² showed that of 984 warfarin therapy interruptions of 5 days or less, there were 4 embolic complications, a rate (0.4%) more than 6 times greater than that reported by Balevi.

Even if one were to accept a 0.059% embolic risk from interruption of warfarin, that would mean for every 1,700 warfarin interruptions for dental procedures, there would be one possibly fatal embolic complication. On the other hand, if 1,700 dental surgeries were performed without warfarin interruption, based on the literature, there may be some bleeding complications, but none would be fatal. If airline flights had a 0.059% chance of crashing, far fewer people would choose to fly. (There are 87,000 airline flights in the US per day. A 0.059% crash rate would mean there would be 51 crashes per day in the United States alone.)

But regardless of whether the embolic risk is 0.059% or 1%, the question comes down to whether an anticoagulated patient should be subjected to a small but significant risk of death or permanent disability (if anticoagulation is interrupted) or to a small risk of a bleeding complication (if anticoagulation is continued), when 100% of cases up until now have apparently resulted in a full recovery.

As a result, the decision-tree analysis was fatally flawed by grossly overestimating the incidence of fatal bleeding when warfarin is continued, and by grossly underestimating the incidence of embolic complications when warfarin is interrupted.

IS WARFARIN CONTINUATION ‘TROUBLESOME’?

An oral surgeon stated, “My experience and that of many of my colleagues is that even though bleeding is never life-threatening [emphasis mine], it can be difficult to control at therapeutic levels of anticoagulation and can be troublesome, especially for elderly patients.”²³ The American College of Chest Physicians stated that postoperative bleeding after dental procedures can cause “anxiety and distress.”³ Patients with even minor postoperative bleeding can be anxious, but surely, postoperative stroke is almost always far more troublesome than postoperative bleeding, which has never been life-threatening. Although other types of surgery may be different, there is no need to interrupt lifesaving anticoagulation for innocuous dental surgery.

My mother was right—it can be rude to interrupt. Anticoagulation should not be interrupted for dental surgery.

When I was growing up, my mother frequently told me that it was rude to interrupt. Although she was referring to conversations, she may have been onto something bigger.

In the nearly three quarters of a century since their discovery, vitamin K antagonist anticoagulant drugs have been used by millions of patients to prevent heart attack and stroke. Before these patients undergo surgery, a decision to continue or interrupt anticoagulation must be made, weighing the risks of postsurgical hemorrhage with continuation of anticoagulation against the risks of stroke or other embolic complications with interruption of anticoagulation. Bleeding after dental surgery when anticoagulation is continued is rarely or never life-threatening. On the other hand, embolic complications of interrupting anticoagulation are almost always consequential and often lead to death or disability. Although consideration may be different for other types of surgery, there is no need to interrupt lifesaving anticoagulation for dental surgery.

EVIDENCE THAT SUPPORTS CONTINUING ANTICOAGULATION

As early as 1957, there were reports of prolonged postoperative bleeding after dental extractions in patients taking anticoagulants. But there were also reports of embolic complications in patients whose anticoagulation was interrupted for dental procedures. Since then, there has been a plethora of literature in this area.

A review published in 2000 showed that of more than 950 anticoagulated patients undergoing more than 2,400 dental surgical procedures (including simple and surgical extraction, alveoplasty, and gingival surgery), only 12 (< 1.3%) required more than local measures for hemostasis (eg, fresh-frozen plasma, vitamin K), and no patient died,¹ leading to the conclusion that the bleeding risk was not significant in anticoagulated dental patients. Other studies and systematic reviews have also concluded that anticoagulation for dental procedures should not be interrupted.^2,3 In a recent review of 83 studies, only 31 (0.6%) of 5,431 patients taking warfarin suffered bleeding complications requiring more than local measures for hemostasis; there were no fatalities.⁴

The risk of embolism

There have been many reports of embolic complications in patients whose anticoagulation was interrupted for dental procedures. A 2000 review of 575 cases in 526 patients whose anticoagulation was interrupted for dental procedures showed that 5 patients (0.9%) had a serious embolic complication, and 4 died.¹ In a more recent review of 64 studies and more than 2,673 patients whose anticoagulation was interrupted for dental procedures, 22 patients (0.8%) suffered embolic complications, and 6 (0.2%) died of the complications.⁴ Of those with embolic complications, the interruption period was often not reported; however; the interruption ranged from 1 to 4 days. A 2003 systematic review by Dunn and Turpie found a 0.4% embolic complication rate when anticoagulation was interrupted for dental surgery.²

BLEEDING AFTER DENTAL SURGERY

Bleeding after dental surgery can occur with either anticoagulation continuation or interruption, and minor postoperative bleeding requiring additional local hemostatic methods occurs at about the same rate in anticoagulated patients as in those whose anticoagulation is interrupted.

In our recent literature review,⁴ about 6% of patients in whom anticoagulation was interrupted (and 7% in whom it was not interrupted) had minor bleeding requiring additional local hemostasis, and only 0.2% of patients required more than hemostatic measures (eg, vitamin K injection, plasma transfusion), the same rate found by Dunn and Turpie.² All patients who required more than local hemostatic measures presumably made a full recovery, while at least 6 who suffered postoperative embolic complications died, and the rest may have had permanent disabilities.

Although bridging therapy with low-molecular-weight heparin can decrease the time without anticoagulation for a dental procedure to only 12 hours, it can be complicated to implement, and there appears to be no benefit in terms of the rates of bleeding or embolic complications. Of the 64 anticoagulation interruption studies,⁴ 17 used heparin or low-molecular-weight heparin in conjunction with temporary warfarin interruption. In 210 instances of bridging therapy in 202 patients undergoing dental procedures, there were 2 embolic complications (1% of bridging cases) and 20 bleeding complications, with 3 (1.4%) requiring hemostasis beyond local measures.⁴

Many of the studies analyzed independently showed there was no significant difference in postoperative bleeding with:

• Anticoagulation continuation vs interruption for a few days
• Lower vs higher international normalized ratio (INR), including some over 4.0
• Surgical vs nonsurgical extraction
• Few vs many extractions.⁴

Some studies of anticoagulation and anticoagulation interruption for dental surgery had important limitations. Many of the anticoagulation studies excluded patients at high risk of bleeding, those with a high INR (> 4.0), and those with severe liver or kidney disease, and their exclusion could have lowered the incidence of bleeding complications. Many studies of anticoagulation interruption excluded patients at high risk of embolism, including patients with a previous embolic event and patients with an artificial heart valve, and this could have skewed the results lower for embolic complications.

WHY DO SOME CLINICIANS STILL RECOMMEND INTERRUPTION?

The choice seems clear: for dental surgery in anticoagulated patients, the small risk of a nonfatal bleeding complication in anticoagulated patients is outweighed by the small risk of a disabling or fatal embolic complication when anticoagulation is interrupted. Most authors have concluded that anticoagulation should be continued for dental surgery. Yet surveys of dentists and physicians have shown that many still recommend interrupting anticoagulation for dental surgery.^5,6

Medical and dental association positions

The American Academy of Neurology⁷ and the American Dental Association⁸ recommend continuing anticoagulant medications for dental surgery. The American College of Chest Physicians also recommends continuing anticoagulation but in 2012 added an option to interrupt or decrease anticoagulation for 2 to 3 days for dental surgery.⁹ Their recommendation was based partly on the results of four controlled prospective studies^10–13 comparing anticoagulated dental surgical patients with patients whose anticoagulation was interrupted. In each study, there were no embolic or bleeding complications requiring more than local methods for hemostasis in the interruption groups, leading the American College of Chest Physicians to conclude that brief anticoagulation interruption for dental surgery is safe and effective.

But the results of these studies actually argue against interrupting anticoagulation for dental surgery. In each study, rates of postoperative bleeding complications and blood loss were similar in both groups, and there were no embolic complications. The authors of each study independently concluded that anticoagulation should not be interrupted for dental surgery.

The optimal INR range for anticoagulation therapy is widely accepted as 2.0 to 3.0, and 2.5 to 3.5 for patients with a mechanical mitral valve.¹⁴ Interrupting warfarin anticoagulation for 2 or 3 days leads to a suboptimal INR. Patel et al¹⁵ studied the incidence of embolic complications (including stroke, non-central nervous system embolism, myocardial infarction, and vascular death) within 30 days in 7,082 patients taking warfarin with and without an interruption of therapy of at least 3 days (median 6 days). The observed rate of embolic events in those with temporary interruption (10.75 events per 100 patient-years) was more than double the rate in those without interruption (4.03 per 100 patient-years).¹⁵ However, this study was designed to compare rivaroxaban vs warfarin, not interrupting vs not interrupting warfarin.

A DECISION-TREE REANALYSIS

In 2010, Balevi published a decision-tree analysis that slightly favored withdrawing warfarin for dental surgery, but he stated that the analysis “can be updated in the future as more accurate and up-to-date data for each of the variables in the model become available.”¹⁶ Now that there are more accurate and up-to-date data, it is time to revisit this decision-tree analysis.

In Balevi’s analysis, major bleeding is not defined. But major bleeding after dental surgery should be defined as any bleeding requiring more than local measures for hemostasis. In calculating probabilities for the analysis, Balevi cited studies allegedly showing high incidences of major bleeding after dental extractions with warfarin continuation.^17,18 There were some minor bleeding complications necessitating additional local measures for hemostasis in these studies, but no major bleeding complications at all in the warfarin- continuation or warfarin-interruption group. There were no significant bleeding events in either study, and the differences in bleeding rates were not significantly different between the two groups. In both studies, the authors concluded that warfarin interruption for dental surgery should be reconsidered.

Similarly, Balevi accurately asserted that there has never been a reported case of fatal bleeding after a dental procedure in an anticoagulated patient, but “for the sake of creating balance,”¹⁶ his decision-tree analysis uses a fatal bleeding probability of 1%, based on an estimated 1% risk for nondental procedures (eg, colorectal surgery, major abdominal surgery). It is unclear how a 1% incidence creates “balance,” but dental surgery is unlike other types of surgery, and that is one reason there has never been a documented postdental fatal hemorrhage in an anticoagulated patient. Major vessels are unlikely to be encountered, and bleeding sites are easily accessible to local hemostatic methods.

Balevi used an embolic complication incidence of 0.059% with warfarin interruption of 3 days. Perhaps he used such a low embolic probability because of his incorrect assertion that “there has been no reported case of a dental extraction causing a cardiovascular accident in a patient whose warfarin was temporarily discontinued.”¹⁶ In fact, our group has now identified at least 22 reported cases of embolic complications after temporary interruption of warfarin therapy in patients undergoing dental surgery.⁴ These included 12 embolic complications (3 fatal) after interruption periods from 1 to 5 days.^19,20 In addition, there are numerous cases of embolic complications reported in patients whose warfarin was temporarily interrupted for other types of surgery.^21,22

The literature shows that embolic complications after temporary warfarin interruption occur at a much higher rate than 0.059%. Many documented embolic complications have occurred after relatively long warfarin interruption periods (greater than 5 days), but many have occurred with much shorter interruptions. Wysokinski et al²¹ showed that there was a 1.1% incidence of thromboembolic events, more than 18 times greater than Balevi’s incidence, in patients whose warfarin was interrupted for 4 or 5 days with or without bridging therapy. One of these patients developed an occipital infarct within 3 days after stopping warfarin without bridging (for a nondental procedure). Garcia et al²² showed that of 984 warfarin therapy interruptions of 5 days or less, there were 4 embolic complications, a rate (0.4%) more than 6 times greater than that reported by Balevi.

Even if one were to accept a 0.059% embolic risk from interruption of warfarin, that would mean for every 1,700 warfarin interruptions for dental procedures, there would be one possibly fatal embolic complication. On the other hand, if 1,700 dental surgeries were performed without warfarin interruption, based on the literature, there may be some bleeding complications, but none would be fatal. If airline flights had a 0.059% chance of crashing, far fewer people would choose to fly. (There are 87,000 airline flights in the US per day. A 0.059% crash rate would mean there would be 51 crashes per day in the United States alone.)

But regardless of whether the embolic risk is 0.059% or 1%, the question comes down to whether an anticoagulated patient should be subjected to a small but significant risk of death or permanent disability (if anticoagulation is interrupted) or to a small risk of a bleeding complication (if anticoagulation is continued), when 100% of cases up until now have apparently resulted in a full recovery.

As a result, the decision-tree analysis was fatally flawed by grossly overestimating the incidence of fatal bleeding when warfarin is continued, and by grossly underestimating the incidence of embolic complications when warfarin is interrupted.

IS WARFARIN CONTINUATION ‘TROUBLESOME’?

An oral surgeon stated, “My experience and that of many of my colleagues is that even though bleeding is never life-threatening [emphasis mine], it can be difficult to control at therapeutic levels of anticoagulation and can be troublesome, especially for elderly patients.”²³ The American College of Chest Physicians stated that postoperative bleeding after dental procedures can cause “anxiety and distress.”³ Patients with even minor postoperative bleeding can be anxious, but surely, postoperative stroke is almost always far more troublesome than postoperative bleeding, which has never been life-threatening. Although other types of surgery may be different, there is no need to interrupt lifesaving anticoagulation for innocuous dental surgery.

My mother was right—it can be rude to interrupt. Anticoagulation should not be interrupted for dental surgery.

When I was growing up, my mother frequently told me that it was rude to interrupt. Although she was referring to conversations, she may have been onto something bigger.

In the nearly three quarters of a century since their discovery, vitamin K antagonist anticoagulant drugs have been used by millions of patients to prevent heart attack and stroke. Before these patients undergo surgery, a decision to continue or interrupt anticoagulation must be made, weighing the risks of postsurgical hemorrhage with continuation of anticoagulation against the risks of stroke or other embolic complications with interruption of anticoagulation. Bleeding after dental surgery when anticoagulation is continued is rarely or never life-threatening. On the other hand, embolic complications of interrupting anticoagulation are almost always consequential and often lead to death or disability. Although consideration may be different for other types of surgery, there is no need to interrupt lifesaving anticoagulation for dental surgery.

EVIDENCE THAT SUPPORTS CONTINUING ANTICOAGULATION

As early as 1957, there were reports of prolonged postoperative bleeding after dental extractions in patients taking anticoagulants. But there were also reports of embolic complications in patients whose anticoagulation was interrupted for dental procedures. Since then, there has been a plethora of literature in this area.

A review published in 2000 showed that of more than 950 anticoagulated patients undergoing more than 2,400 dental surgical procedures (including simple and surgical extraction, alveoplasty, and gingival surgery), only 12 (< 1.3%) required more than local measures for hemostasis (eg, fresh-frozen plasma, vitamin K), and no patient died,¹ leading to the conclusion that the bleeding risk was not significant in anticoagulated dental patients. Other studies and systematic reviews have also concluded that anticoagulation for dental procedures should not be interrupted.^2,3 In a recent review of 83 studies, only 31 (0.6%) of 5,431 patients taking warfarin suffered bleeding complications requiring more than local measures for hemostasis; there were no fatalities.⁴

The risk of embolism

There have been many reports of embolic complications in patients whose anticoagulation was interrupted for dental procedures. A 2000 review of 575 cases in 526 patients whose anticoagulation was interrupted for dental procedures showed that 5 patients (0.9%) had a serious embolic complication, and 4 died.¹ In a more recent review of 64 studies and more than 2,673 patients whose anticoagulation was interrupted for dental procedures, 22 patients (0.8%) suffered embolic complications, and 6 (0.2%) died of the complications.⁴ Of those with embolic complications, the interruption period was often not reported; however; the interruption ranged from 1 to 4 days. A 2003 systematic review by Dunn and Turpie found a 0.4% embolic complication rate when anticoagulation was interrupted for dental surgery.²

BLEEDING AFTER DENTAL SURGERY

Bleeding after dental surgery can occur with either anticoagulation continuation or interruption, and minor postoperative bleeding requiring additional local hemostatic methods occurs at about the same rate in anticoagulated patients as in those whose anticoagulation is interrupted.

In our recent literature review,⁴ about 6% of patients in whom anticoagulation was interrupted (and 7% in whom it was not interrupted) had minor bleeding requiring additional local hemostasis, and only 0.2% of patients required more than hemostatic measures (eg, vitamin K injection, plasma transfusion), the same rate found by Dunn and Turpie.² All patients who required more than local hemostatic measures presumably made a full recovery, while at least 6 who suffered postoperative embolic complications died, and the rest may have had permanent disabilities.

Although bridging therapy with low-molecular-weight heparin can decrease the time without anticoagulation for a dental procedure to only 12 hours, it can be complicated to implement, and there appears to be no benefit in terms of the rates of bleeding or embolic complications. Of the 64 anticoagulation interruption studies,⁴ 17 used heparin or low-molecular-weight heparin in conjunction with temporary warfarin interruption. In 210 instances of bridging therapy in 202 patients undergoing dental procedures, there were 2 embolic complications (1% of bridging cases) and 20 bleeding complications, with 3 (1.4%) requiring hemostasis beyond local measures.⁴

Many of the studies analyzed independently showed there was no significant difference in postoperative bleeding with:

• Anticoagulation continuation vs interruption for a few days
• Lower vs higher international normalized ratio (INR), including some over 4.0
• Surgical vs nonsurgical extraction
• Few vs many extractions.⁴

Some studies of anticoagulation and anticoagulation interruption for dental surgery had important limitations. Many of the anticoagulation studies excluded patients at high risk of bleeding, those with a high INR (> 4.0), and those with severe liver or kidney disease, and their exclusion could have lowered the incidence of bleeding complications. Many studies of anticoagulation interruption excluded patients at high risk of embolism, including patients with a previous embolic event and patients with an artificial heart valve, and this could have skewed the results lower for embolic complications.

WHY DO SOME CLINICIANS STILL RECOMMEND INTERRUPTION?

The choice seems clear: for dental surgery in anticoagulated patients, the small risk of a nonfatal bleeding complication in anticoagulated patients is outweighed by the small risk of a disabling or fatal embolic complication when anticoagulation is interrupted. Most authors have concluded that anticoagulation should be continued for dental surgery. Yet surveys of dentists and physicians have shown that many still recommend interrupting anticoagulation for dental surgery.^5,6

Medical and dental association positions

The American Academy of Neurology⁷ and the American Dental Association⁸ recommend continuing anticoagulant medications for dental surgery. The American College of Chest Physicians also recommends continuing anticoagulation but in 2012 added an option to interrupt or decrease anticoagulation for 2 to 3 days for dental surgery.⁹ Their recommendation was based partly on the results of four controlled prospective studies^10–13 comparing anticoagulated dental surgical patients with patients whose anticoagulation was interrupted. In each study, there were no embolic or bleeding complications requiring more than local methods for hemostasis in the interruption groups, leading the American College of Chest Physicians to conclude that brief anticoagulation interruption for dental surgery is safe and effective.

But the results of these studies actually argue against interrupting anticoagulation for dental surgery. In each study, rates of postoperative bleeding complications and blood loss were similar in both groups, and there were no embolic complications. The authors of each study independently concluded that anticoagulation should not be interrupted for dental surgery.

The optimal INR range for anticoagulation therapy is widely accepted as 2.0 to 3.0, and 2.5 to 3.5 for patients with a mechanical mitral valve.¹⁴ Interrupting warfarin anticoagulation for 2 or 3 days leads to a suboptimal INR. Patel et al¹⁵ studied the incidence of embolic complications (including stroke, non-central nervous system embolism, myocardial infarction, and vascular death) within 30 days in 7,082 patients taking warfarin with and without an interruption of therapy of at least 3 days (median 6 days). The observed rate of embolic events in those with temporary interruption (10.75 events per 100 patient-years) was more than double the rate in those without interruption (4.03 per 100 patient-years).¹⁵ However, this study was designed to compare rivaroxaban vs warfarin, not interrupting vs not interrupting warfarin.

A DECISION-TREE REANALYSIS

In 2010, Balevi published a decision-tree analysis that slightly favored withdrawing warfarin for dental surgery, but he stated that the analysis “can be updated in the future as more accurate and up-to-date data for each of the variables in the model become available.”¹⁶ Now that there are more accurate and up-to-date data, it is time to revisit this decision-tree analysis.

In Balevi’s analysis, major bleeding is not defined. But major bleeding after dental surgery should be defined as any bleeding requiring more than local measures for hemostasis. In calculating probabilities for the analysis, Balevi cited studies allegedly showing high incidences of major bleeding after dental extractions with warfarin continuation.^17,18 There were some minor bleeding complications necessitating additional local measures for hemostasis in these studies, but no major bleeding complications at all in the warfarin- continuation or warfarin-interruption group. There were no significant bleeding events in either study, and the differences in bleeding rates were not significantly different between the two groups. In both studies, the authors concluded that warfarin interruption for dental surgery should be reconsidered.

Similarly, Balevi accurately asserted that there has never been a reported case of fatal bleeding after a dental procedure in an anticoagulated patient, but “for the sake of creating balance,”¹⁶ his decision-tree analysis uses a fatal bleeding probability of 1%, based on an estimated 1% risk for nondental procedures (eg, colorectal surgery, major abdominal surgery). It is unclear how a 1% incidence creates “balance,” but dental surgery is unlike other types of surgery, and that is one reason there has never been a documented postdental fatal hemorrhage in an anticoagulated patient. Major vessels are unlikely to be encountered, and bleeding sites are easily accessible to local hemostatic methods.

Balevi used an embolic complication incidence of 0.059% with warfarin interruption of 3 days. Perhaps he used such a low embolic probability because of his incorrect assertion that “there has been no reported case of a dental extraction causing a cardiovascular accident in a patient whose warfarin was temporarily discontinued.”¹⁶ In fact, our group has now identified at least 22 reported cases of embolic complications after temporary interruption of warfarin therapy in patients undergoing dental surgery.⁴ These included 12 embolic complications (3 fatal) after interruption periods from 1 to 5 days.^19,20 In addition, there are numerous cases of embolic complications reported in patients whose warfarin was temporarily interrupted for other types of surgery.^21,22

The literature shows that embolic complications after temporary warfarin interruption occur at a much higher rate than 0.059%. Many documented embolic complications have occurred after relatively long warfarin interruption periods (greater than 5 days), but many have occurred with much shorter interruptions. Wysokinski et al²¹ showed that there was a 1.1% incidence of thromboembolic events, more than 18 times greater than Balevi’s incidence, in patients whose warfarin was interrupted for 4 or 5 days with or without bridging therapy. One of these patients developed an occipital infarct within 3 days after stopping warfarin without bridging (for a nondental procedure). Garcia et al²² showed that of 984 warfarin therapy interruptions of 5 days or less, there were 4 embolic complications, a rate (0.4%) more than 6 times greater than that reported by Balevi.

Even if one were to accept a 0.059% embolic risk from interruption of warfarin, that would mean for every 1,700 warfarin interruptions for dental procedures, there would be one possibly fatal embolic complication. On the other hand, if 1,700 dental surgeries were performed without warfarin interruption, based on the literature, there may be some bleeding complications, but none would be fatal. If airline flights had a 0.059% chance of crashing, far fewer people would choose to fly. (There are 87,000 airline flights in the US per day. A 0.059% crash rate would mean there would be 51 crashes per day in the United States alone.)

But regardless of whether the embolic risk is 0.059% or 1%, the question comes down to whether an anticoagulated patient should be subjected to a small but significant risk of death or permanent disability (if anticoagulation is interrupted) or to a small risk of a bleeding complication (if anticoagulation is continued), when 100% of cases up until now have apparently resulted in a full recovery.

As a result, the decision-tree analysis was fatally flawed by grossly overestimating the incidence of fatal bleeding when warfarin is continued, and by grossly underestimating the incidence of embolic complications when warfarin is interrupted.

IS WARFARIN CONTINUATION ‘TROUBLESOME’?

An oral surgeon stated, “My experience and that of many of my colleagues is that even though bleeding is never life-threatening [emphasis mine], it can be difficult to control at therapeutic levels of anticoagulation and can be troublesome, especially for elderly patients.”²³ The American College of Chest Physicians stated that postoperative bleeding after dental procedures can cause “anxiety and distress.”³ Patients with even minor postoperative bleeding can be anxious, but surely, postoperative stroke is almost always far more troublesome than postoperative bleeding, which has never been life-threatening. Although other types of surgery may be different, there is no need to interrupt lifesaving anticoagulation for innocuous dental surgery.

My mother was right—it can be rude to interrupt. Anticoagulation should not be interrupted for dental surgery.

In 2009, the US Preventive Services Task Force issued an I statement for routine skin cancer screening, noting a lack of evidence to support the balance of benefits and harms from screening,¹ a recommendation that is likely to be upheld this year. As dermatologists and melanoma specialists, we have abundant anecdotal evidence of the value of screening; however, population-based screening performed exclusively by dermatologists is not practical. There are approximately 170,000,000 adults 35 years and older and only 9600 practicing dermatologists in the United States, requiring each dermatologist to screen nearly 18,000 individuals per year to meet the needs of the population.

Only 8% to 15% of people in the United States report having received a recent skin examination by a physician.^2,3 Partnering with our primary care provider (PCP) colleagues has the potential to reach more patients and to improve skin cancer screening rates more rapidly. The workforce in primary care is substantially larger than dermatology by approximately 30-fold, and PCPs are more likely than dermatologists to practice in rural areas, thus reaching patients with limited access to dermatologists. Skin cancer screening can be included in the routine PCP visit, reducing the need for an additional physician visit for the patient. Patients visit their PCP more frequently as they age, which parallels the risk for developing and dying from melanoma and also provides an opportunity to introduce skin cancer education and screening to a population at higher risk who may not otherwise seek it on their own.⁴ Providing PCPs with the training and tools to perform melanoma screening shifts the responsibility of initiating screening from the patient alone to a shared responsibility of patient and provider. Dermatologists, in turn, need to be available to examine those patients found to have a suspicious lesion, treat newly diagnosed skin cancer, and follow those patients at highest risk of developing skin cancer, including those who are immunosuppressed, have multiple atypical moles, or have a personal or family history of melanoma.

Evidence from the SCREEN (Skin Cancer Research to provide Evidence for Effectiveness of Screening in Northern Germany) project supports PCP-based screening. In the 5 years following a 1-year pilot screening program, there was nearly a 50% reduction in melanoma mortality.⁵ Unfortunately, these encouraging results were not confirmed once the pilot project was translated into a national skin cancer screening program.⁶ However, there are lessons to be learned from the German project and we propose that PCP-led screening is feasible and practical in the United States and we currently have a pilot program in our institution, the University of Pittsburgh Medical Center (Pittsburgh, Pennsylvania).

In the SCREEN project and in routine practice across the United States, screening is primarily driven by patients. Generally, higher-risk patients such as men and the elderly are the least likely group to seek skin cancer screening. In our program, PCPs are offered training in skin cancer screening using a validated web-based program and alerted through the electronic health record to offer skin cancer screening annually to patients 35 years and older who present for routine primary care visits.⁷ This approach reduces self-referral bias by promoting physician initiation rather than patient initiation of screening, which can occur while the patient is already in the PCP’s office.

Melanoma thickness can be measured among screened patients, unscreened patients, and historic controls and compared to determine if this approach is effective. Health care utilization data can help to inform us if this approach leads to more skin biopsies and procedures or to an increased rate of dermatology referrals. As health care payment and delivery models evolve, there is greater emphasis on outcomes and team-based care. We believe that this approach will allow us to form effective teams of PCPs, dermatologists, and other experts in melanoma, public health, and informatics to reduce melanoma mortality in a cost-effective manner.

In 2009, the US Preventive Services Task Force issued an I statement for routine skin cancer screening, noting a lack of evidence to support the balance of benefits and harms from screening,¹ a recommendation that is likely to be upheld this year. As dermatologists and melanoma specialists, we have abundant anecdotal evidence of the value of screening; however, population-based screening performed exclusively by dermatologists is not practical. There are approximately 170,000,000 adults 35 years and older and only 9600 practicing dermatologists in the United States, requiring each dermatologist to screen nearly 18,000 individuals per year to meet the needs of the population.

Only 8% to 15% of people in the United States report having received a recent skin examination by a physician.^2,3 Partnering with our primary care provider (PCP) colleagues has the potential to reach more patients and to improve skin cancer screening rates more rapidly. The workforce in primary care is substantially larger than dermatology by approximately 30-fold, and PCPs are more likely than dermatologists to practice in rural areas, thus reaching patients with limited access to dermatologists. Skin cancer screening can be included in the routine PCP visit, reducing the need for an additional physician visit for the patient. Patients visit their PCP more frequently as they age, which parallels the risk for developing and dying from melanoma and also provides an opportunity to introduce skin cancer education and screening to a population at higher risk who may not otherwise seek it on their own.⁴ Providing PCPs with the training and tools to perform melanoma screening shifts the responsibility of initiating screening from the patient alone to a shared responsibility of patient and provider. Dermatologists, in turn, need to be available to examine those patients found to have a suspicious lesion, treat newly diagnosed skin cancer, and follow those patients at highest risk of developing skin cancer, including those who are immunosuppressed, have multiple atypical moles, or have a personal or family history of melanoma.

Evidence from the SCREEN (Skin Cancer Research to provide Evidence for Effectiveness of Screening in Northern Germany) project supports PCP-based screening. In the 5 years following a 1-year pilot screening program, there was nearly a 50% reduction in melanoma mortality.⁵ Unfortunately, these encouraging results were not confirmed once the pilot project was translated into a national skin cancer screening program.⁶ However, there are lessons to be learned from the German project and we propose that PCP-led screening is feasible and practical in the United States and we currently have a pilot program in our institution, the University of Pittsburgh Medical Center (Pittsburgh, Pennsylvania).

In the SCREEN project and in routine practice across the United States, screening is primarily driven by patients. Generally, higher-risk patients such as men and the elderly are the least likely group to seek skin cancer screening. In our program, PCPs are offered training in skin cancer screening using a validated web-based program and alerted through the electronic health record to offer skin cancer screening annually to patients 35 years and older who present for routine primary care visits.⁷ This approach reduces self-referral bias by promoting physician initiation rather than patient initiation of screening, which can occur while the patient is already in the PCP’s office.

Melanoma thickness can be measured among screened patients, unscreened patients, and historic controls and compared to determine if this approach is effective. Health care utilization data can help to inform us if this approach leads to more skin biopsies and procedures or to an increased rate of dermatology referrals. As health care payment and delivery models evolve, there is greater emphasis on outcomes and team-based care. We believe that this approach will allow us to form effective teams of PCPs, dermatologists, and other experts in melanoma, public health, and informatics to reduce melanoma mortality in a cost-effective manner.

In 2009, the US Preventive Services Task Force issued an I statement for routine skin cancer screening, noting a lack of evidence to support the balance of benefits and harms from screening,¹ a recommendation that is likely to be upheld this year. As dermatologists and melanoma specialists, we have abundant anecdotal evidence of the value of screening; however, population-based screening performed exclusively by dermatologists is not practical. There are approximately 170,000,000 adults 35 years and older and only 9600 practicing dermatologists in the United States, requiring each dermatologist to screen nearly 18,000 individuals per year to meet the needs of the population.

Only 8% to 15% of people in the United States report having received a recent skin examination by a physician.^2,3 Partnering with our primary care provider (PCP) colleagues has the potential to reach more patients and to improve skin cancer screening rates more rapidly. The workforce in primary care is substantially larger than dermatology by approximately 30-fold, and PCPs are more likely than dermatologists to practice in rural areas, thus reaching patients with limited access to dermatologists. Skin cancer screening can be included in the routine PCP visit, reducing the need for an additional physician visit for the patient. Patients visit their PCP more frequently as they age, which parallels the risk for developing and dying from melanoma and also provides an opportunity to introduce skin cancer education and screening to a population at higher risk who may not otherwise seek it on their own.⁴ Providing PCPs with the training and tools to perform melanoma screening shifts the responsibility of initiating screening from the patient alone to a shared responsibility of patient and provider. Dermatologists, in turn, need to be available to examine those patients found to have a suspicious lesion, treat newly diagnosed skin cancer, and follow those patients at highest risk of developing skin cancer, including those who are immunosuppressed, have multiple atypical moles, or have a personal or family history of melanoma.

Evidence from the SCREEN (Skin Cancer Research to provide Evidence for Effectiveness of Screening in Northern Germany) project supports PCP-based screening. In the 5 years following a 1-year pilot screening program, there was nearly a 50% reduction in melanoma mortality.⁵ Unfortunately, these encouraging results were not confirmed once the pilot project was translated into a national skin cancer screening program.⁶ However, there are lessons to be learned from the German project and we propose that PCP-led screening is feasible and practical in the United States and we currently have a pilot program in our institution, the University of Pittsburgh Medical Center (Pittsburgh, Pennsylvania).

In the SCREEN project and in routine practice across the United States, screening is primarily driven by patients. Generally, higher-risk patients such as men and the elderly are the least likely group to seek skin cancer screening. In our program, PCPs are offered training in skin cancer screening using a validated web-based program and alerted through the electronic health record to offer skin cancer screening annually to patients 35 years and older who present for routine primary care visits.⁷ This approach reduces self-referral bias by promoting physician initiation rather than patient initiation of screening, which can occur while the patient is already in the PCP’s office.

Melanoma thickness can be measured among screened patients, unscreened patients, and historic controls and compared to determine if this approach is effective. Health care utilization data can help to inform us if this approach leads to more skin biopsies and procedures or to an increased rate of dermatology referrals. As health care payment and delivery models evolve, there is greater emphasis on outcomes and team-based care. We believe that this approach will allow us to form effective teams of PCPs, dermatologists, and other experts in melanoma, public health, and informatics to reduce melanoma mortality in a cost-effective manner.

Early in my career, an attorney asked me to review a malpractice case. “The question,” he said, “is whether liquid nitrogen is the standard of care for treating warts.”

Come again?

A young woman had visited an academic center, where a physician froze her warts. These blistered and turned purple. Alarmed, she went to an ER, where doctors admitted her for cellulitis and gave her intravenous antibiotics for several days.

I later submitted an essay based on this case to my malpractice insurer’s Risk Management Contest, in which I called for better communication between treating doctors and those who follow up. I placed second and got a check from my malpractice insurer. How cool is that?

I hadn’t thought about that case in years, until last month. Earvin is a late-middle-aged gent with psoriasis on his elbows and liver spots on his chest. He asked me to freeze them, as I had done before.

After lunch 2 days later, my secretary buzzed me. “The man on the phone is very unhappy,” she said. “He says he called this morning and no one called back. He says if he doesn’t hear from you, his next call will be to his attorney.”

I phoned Earvin. My apology for not having gotten the message before was met with frigid hostility. “That’s unconscionable,” he said.

“My skin swelled up like a balloon,” he told me. “I know what to expect with freezing, and this never happened before. I think this time you froze me with a heavy hand. When I didn’t hear from you, I went to an urgent care clinic down the street. They said it was infected and prescribed an antibiotic ointment. I had to wait an hour, and the ointment cost $49.”

I held my breath. “Actually,” I said, “I don’t think it’s infected.”

“They said it was infected,” said Earvin. “It is swollen. I’m afraid it is going to scar. The cream cost $49.”

Straining to keep my voice even, I replied, “Would you like me to have a look at it?”

“I live too far,” he said. “I don’t have a ride. Maybe I will come tomorrow if someone can take me.”

Later that day I called him back. “I live the next town over from you,” I said. “I will stop by on my way home.” He agreed, and told me the color of his house.

Earvin let me in looking less angry than fearful. One glance at his chest told me what I needed to know: There was no infection. His skin looked like what skin looks like after it’s been frozen. Other treated areas – the ones Earvin wasn’t worried about – looked the same to me, though clearly not to him. “This one was worse,” he said. “It’s gone down since this morning.”

After examining Earvin with my cell phone flashlight, I sat down across from him. “Let me be clear,” I said. “You are not infected. Some areas frozen at the same time in the same way blister more briskly than others. In the end they heal fine, and so will yours. You’re not going to scar.”

Earvin relaxed a little. “I was afraid I’d done something I didn’t need to. My mother had skin cancer on her chest, not far from where this one is. My skin was discolored and swollen. The doctor at urgent care said it was infected.” There was a pause, as Earvin slumped in his chair. “I feel better,” he allowed.

There it was, the whole package – thinking that was full of hopelessly muddled categories. Infection? Scarring? Skin cancer? Yes to all? And there was moral anxiety – disappointment in himself for doing something needless and now having to pay the price – as well as anger at me as the instrument of retribution. Who knows what else? There were so many strands, hopelessly coiled, impossible to disentangle.

And all wrapped up in elemental terror. What have I done? What has he done?

Earvin did not need treatment. He needed a hug. Metaphorically, that is what I gave him.

So much angst, so much anger, so much fear, so little time. To be frank, it gets tiring.

People like to quote the philosopher George Santayana. He said that those who cannot remember the past are condemned to repeat it.

I like to paraphrase the even greater philosopher Bill Murray of “Groundhog Day”: Those who do remember the past are condemned to repeat it anyway.

Dr. Rockoff practices dermatology in Brookline, Mass., and is a longtime contributor to Dermatology News. He serves on the clinical faculty at Tufts University, Boston, and has taught senior medical students and other trainees for 30 years.

Early in my career, an attorney asked me to review a malpractice case. “The question,” he said, “is whether liquid nitrogen is the standard of care for treating warts.”

Come again?

A young woman had visited an academic center, where a physician froze her warts. These blistered and turned purple. Alarmed, she went to an ER, where doctors admitted her for cellulitis and gave her intravenous antibiotics for several days.

I later submitted an essay based on this case to my malpractice insurer’s Risk Management Contest, in which I called for better communication between treating doctors and those who follow up. I placed second and got a check from my malpractice insurer. How cool is that?

I hadn’t thought about that case in years, until last month. Earvin is a late-middle-aged gent with psoriasis on his elbows and liver spots on his chest. He asked me to freeze them, as I had done before.

After lunch 2 days later, my secretary buzzed me. “The man on the phone is very unhappy,” she said. “He says he called this morning and no one called back. He says if he doesn’t hear from you, his next call will be to his attorney.”

I phoned Earvin. My apology for not having gotten the message before was met with frigid hostility. “That’s unconscionable,” he said.

“My skin swelled up like a balloon,” he told me. “I know what to expect with freezing, and this never happened before. I think this time you froze me with a heavy hand. When I didn’t hear from you, I went to an urgent care clinic down the street. They said it was infected and prescribed an antibiotic ointment. I had to wait an hour, and the ointment cost $49.”

I held my breath. “Actually,” I said, “I don’t think it’s infected.”

“They said it was infected,” said Earvin. “It is swollen. I’m afraid it is going to scar. The cream cost $49.”

Straining to keep my voice even, I replied, “Would you like me to have a look at it?”

“I live too far,” he said. “I don’t have a ride. Maybe I will come tomorrow if someone can take me.”

Later that day I called him back. “I live the next town over from you,” I said. “I will stop by on my way home.” He agreed, and told me the color of his house.

Earvin let me in looking less angry than fearful. One glance at his chest told me what I needed to know: There was no infection. His skin looked like what skin looks like after it’s been frozen. Other treated areas – the ones Earvin wasn’t worried about – looked the same to me, though clearly not to him. “This one was worse,” he said. “It’s gone down since this morning.”

After examining Earvin with my cell phone flashlight, I sat down across from him. “Let me be clear,” I said. “You are not infected. Some areas frozen at the same time in the same way blister more briskly than others. In the end they heal fine, and so will yours. You’re not going to scar.”

Earvin relaxed a little. “I was afraid I’d done something I didn’t need to. My mother had skin cancer on her chest, not far from where this one is. My skin was discolored and swollen. The doctor at urgent care said it was infected.” There was a pause, as Earvin slumped in his chair. “I feel better,” he allowed.

There it was, the whole package – thinking that was full of hopelessly muddled categories. Infection? Scarring? Skin cancer? Yes to all? And there was moral anxiety – disappointment in himself for doing something needless and now having to pay the price – as well as anger at me as the instrument of retribution. Who knows what else? There were so many strands, hopelessly coiled, impossible to disentangle.

And all wrapped up in elemental terror. What have I done? What has he done?

Earvin did not need treatment. He needed a hug. Metaphorically, that is what I gave him.

So much angst, so much anger, so much fear, so little time. To be frank, it gets tiring.

People like to quote the philosopher George Santayana. He said that those who cannot remember the past are condemned to repeat it.

I like to paraphrase the even greater philosopher Bill Murray of “Groundhog Day”: Those who do remember the past are condemned to repeat it anyway.

Dr. Rockoff practices dermatology in Brookline, Mass., and is a longtime contributor to Dermatology News. He serves on the clinical faculty at Tufts University, Boston, and has taught senior medical students and other trainees for 30 years.

Early in my career, an attorney asked me to review a malpractice case. “The question,” he said, “is whether liquid nitrogen is the standard of care for treating warts.”

Come again?

A young woman had visited an academic center, where a physician froze her warts. These blistered and turned purple. Alarmed, she went to an ER, where doctors admitted her for cellulitis and gave her intravenous antibiotics for several days.

I later submitted an essay based on this case to my malpractice insurer’s Risk Management Contest, in which I called for better communication between treating doctors and those who follow up. I placed second and got a check from my malpractice insurer. How cool is that?

I hadn’t thought about that case in years, until last month. Earvin is a late-middle-aged gent with psoriasis on his elbows and liver spots on his chest. He asked me to freeze them, as I had done before.

After lunch 2 days later, my secretary buzzed me. “The man on the phone is very unhappy,” she said. “He says he called this morning and no one called back. He says if he doesn’t hear from you, his next call will be to his attorney.”

I phoned Earvin. My apology for not having gotten the message before was met with frigid hostility. “That’s unconscionable,” he said.

“My skin swelled up like a balloon,” he told me. “I know what to expect with freezing, and this never happened before. I think this time you froze me with a heavy hand. When I didn’t hear from you, I went to an urgent care clinic down the street. They said it was infected and prescribed an antibiotic ointment. I had to wait an hour, and the ointment cost $49.”

I held my breath. “Actually,” I said, “I don’t think it’s infected.”

“They said it was infected,” said Earvin. “It is swollen. I’m afraid it is going to scar. The cream cost $49.”

Straining to keep my voice even, I replied, “Would you like me to have a look at it?”

“I live too far,” he said. “I don’t have a ride. Maybe I will come tomorrow if someone can take me.”

Later that day I called him back. “I live the next town over from you,” I said. “I will stop by on my way home.” He agreed, and told me the color of his house.

Earvin let me in looking less angry than fearful. One glance at his chest told me what I needed to know: There was no infection. His skin looked like what skin looks like after it’s been frozen. Other treated areas – the ones Earvin wasn’t worried about – looked the same to me, though clearly not to him. “This one was worse,” he said. “It’s gone down since this morning.”

After examining Earvin with my cell phone flashlight, I sat down across from him. “Let me be clear,” I said. “You are not infected. Some areas frozen at the same time in the same way blister more briskly than others. In the end they heal fine, and so will yours. You’re not going to scar.”

Earvin relaxed a little. “I was afraid I’d done something I didn’t need to. My mother had skin cancer on her chest, not far from where this one is. My skin was discolored and swollen. The doctor at urgent care said it was infected.” There was a pause, as Earvin slumped in his chair. “I feel better,” he allowed.

There it was, the whole package – thinking that was full of hopelessly muddled categories. Infection? Scarring? Skin cancer? Yes to all? And there was moral anxiety – disappointment in himself for doing something needless and now having to pay the price – as well as anger at me as the instrument of retribution. Who knows what else? There were so many strands, hopelessly coiled, impossible to disentangle.

And all wrapped up in elemental terror. What have I done? What has he done?

Earvin did not need treatment. He needed a hug. Metaphorically, that is what I gave him.

So much angst, so much anger, so much fear, so little time. To be frank, it gets tiring.

People like to quote the philosopher George Santayana. He said that those who cannot remember the past are condemned to repeat it.

I like to paraphrase the even greater philosopher Bill Murray of “Groundhog Day”: Those who do remember the past are condemned to repeat it anyway.

Dr. Rockoff practices dermatology in Brookline, Mass., and is a longtime contributor to Dermatology News. He serves on the clinical faculty at Tufts University, Boston, and has taught senior medical students and other trainees for 30 years.