User login
Reye’s syndrome: Time to remind the parents
It is that time of year again. We are in the midst of flu season, which means that it is time to remind our patients’ parents about the importance of using acetaminophen instead of aspirin. This fact became evident when several guardians of our patients came in within a few days of each other in late November to early December unaware of the dangers of giving their children aspirin and other salicylate medications.
Case 1: A 4-year-old boy presented with mild diarrhea, but otherwise was clinically well. The diarrhea started while visiting family in Mexico. The mother took out a small bottle of Pepto-Bismol (bismuth subsalicylate) liquid, which she gave him 2 days previously. The bottle did have, in small font, a warning about Reye’s syndrome on the label, which the mother did not notice. She also did not think it pertained to her son anyway. During the visit, she was counseled on this being early influenza season and the avoidance of salicylate products since the 1980s in children, with the exception of cardiac uses.
Case 2: A 16-year-old male presented with his grandmother with a few scattered vesicles and low-grade fever. He had plans to go to Florida in a few days with friends and wished to know if he would be able to go. He had one dose of varicella vaccine when he was a toddler. Varicella IgM and IgG were ordered. When asked, the grandmother stated that she did not remember the warning signs about Reye’s syndrome posted in the pharmacies 30 years ago. In addition, she vaguely remembered baby aspirin not being made anymore, but she could not remember the reason why.
Case 3: An 18-year-old female with a medical history of occasional migraines controlled with over-the-counter products presented for a school form. Her mother mentioned that a relative had influenza symptoms. When we looked up the migraine medication, it was a generic aspirin/caffeine product. When counseled on Reye’s syndrome, the mother did not remember it at all, even though she was a teenager in the 1980s; she stated that she did remember her mom using only Tylenol for her illnesses.
Reye’s syndrome, a rare but serious condition causing liver degeneration and encephalopathy presenting in children younger than 18 years, was first described in 1963.1 Symptoms include mental confusion, vomiting, and even coma. The cause is unknown; however, salicylates have been implicated as a possible causative agent.
Products containing salicylate include but are not limited to aspirin and Pepto-Bismol. Studies linked Reye’s syndrome epidemiologically to recent illness with influenza or varicella and the use of aspirin. In 1978, the Centers for Disease Control and Prevention was informed that several children developed Reye’s syndrome during an influenza outbreak, and by 1980, the CDC demonstrated a link between those patients and the administration of salicylate-containing medications.2 Around the same time, more studies came out to support these findings. In 1980, 555 cases of Reye’s syndrome were reported in the United States. To decrease the occurrence, the CDC, American Academy of Pediatrics, and the U.S. Surgeon General tried to raise awareness of the association between Reye’s syndrome and aspirin by publishing journals, releasing warning statements, and including a “Black Box” warning in 1986 informing parents to not give aspirin to children and teenagers with influenza or chicken pox. Baby aspirin was removed from use for routine fevers in the mid-1980s and large warning signs would be found in every pharmacy for about 10 years. These warning signs are gone now.
As pediatricians and other primary care physicians, we have so many topics that we must address in the limited time we have allotted for each patient. However, we need to remind our patients and their parents about Reye’s syndrome and the importance of avoiding aspirin and salicylate products in children. Due to the public awareness of Reye’s syndrome in the 1980s and into the 1990s, the incidence decreased.2 From 1987 to 1993, fewer than 37 cases were reported in the United States and from 1994 to 1997, fewer than 2 cases were reported.
This demonstrates the importance of educating our patients and their parents about this syndrome and ways to avoid it. Based on the three clinical cases presented, it is clear that at least some of our patient’s guardians are unaware of this threat to their children. As physicians, it is our responsibility to educate our patient populations, but we should also ask our friends at our local supermarkets and pharmacies to dust off those old warning signs and help spread the word. While we are in flu season, let’s not forget to take a few minutes to inform our patients about this awful, but preventable syndrome.
References
1. Pediatrics. 1980 Dec;66(6):859-64.
2. J Gen Intern Med. 2012 Dec;27(12):1697-703.
Rachel Masia is a third-year medical student at Rowan University School of Osteopathic Medicine, Stratford, N.J. Dr. Alan Masia, Ms. Masia’s father, has a practice in Toms River, N.J. They said they had no relevant financial disclosures.
It is that time of year again. We are in the midst of flu season, which means that it is time to remind our patients’ parents about the importance of using acetaminophen instead of aspirin. This fact became evident when several guardians of our patients came in within a few days of each other in late November to early December unaware of the dangers of giving their children aspirin and other salicylate medications.
Case 1: A 4-year-old boy presented with mild diarrhea, but otherwise was clinically well. The diarrhea started while visiting family in Mexico. The mother took out a small bottle of Pepto-Bismol (bismuth subsalicylate) liquid, which she gave him 2 days previously. The bottle did have, in small font, a warning about Reye’s syndrome on the label, which the mother did not notice. She also did not think it pertained to her son anyway. During the visit, she was counseled on this being early influenza season and the avoidance of salicylate products since the 1980s in children, with the exception of cardiac uses.
Case 2: A 16-year-old male presented with his grandmother with a few scattered vesicles and low-grade fever. He had plans to go to Florida in a few days with friends and wished to know if he would be able to go. He had one dose of varicella vaccine when he was a toddler. Varicella IgM and IgG were ordered. When asked, the grandmother stated that she did not remember the warning signs about Reye’s syndrome posted in the pharmacies 30 years ago. In addition, she vaguely remembered baby aspirin not being made anymore, but she could not remember the reason why.
Case 3: An 18-year-old female with a medical history of occasional migraines controlled with over-the-counter products presented for a school form. Her mother mentioned that a relative had influenza symptoms. When we looked up the migraine medication, it was a generic aspirin/caffeine product. When counseled on Reye’s syndrome, the mother did not remember it at all, even though she was a teenager in the 1980s; she stated that she did remember her mom using only Tylenol for her illnesses.
Reye’s syndrome, a rare but serious condition causing liver degeneration and encephalopathy presenting in children younger than 18 years, was first described in 1963.1 Symptoms include mental confusion, vomiting, and even coma. The cause is unknown; however, salicylates have been implicated as a possible causative agent.
Products containing salicylate include but are not limited to aspirin and Pepto-Bismol. Studies linked Reye’s syndrome epidemiologically to recent illness with influenza or varicella and the use of aspirin. In 1978, the Centers for Disease Control and Prevention was informed that several children developed Reye’s syndrome during an influenza outbreak, and by 1980, the CDC demonstrated a link between those patients and the administration of salicylate-containing medications.2 Around the same time, more studies came out to support these findings. In 1980, 555 cases of Reye’s syndrome were reported in the United States. To decrease the occurrence, the CDC, American Academy of Pediatrics, and the U.S. Surgeon General tried to raise awareness of the association between Reye’s syndrome and aspirin by publishing journals, releasing warning statements, and including a “Black Box” warning in 1986 informing parents to not give aspirin to children and teenagers with influenza or chicken pox. Baby aspirin was removed from use for routine fevers in the mid-1980s and large warning signs would be found in every pharmacy for about 10 years. These warning signs are gone now.
As pediatricians and other primary care physicians, we have so many topics that we must address in the limited time we have allotted for each patient. However, we need to remind our patients and their parents about Reye’s syndrome and the importance of avoiding aspirin and salicylate products in children. Due to the public awareness of Reye’s syndrome in the 1980s and into the 1990s, the incidence decreased.2 From 1987 to 1993, fewer than 37 cases were reported in the United States and from 1994 to 1997, fewer than 2 cases were reported.
This demonstrates the importance of educating our patients and their parents about this syndrome and ways to avoid it. Based on the three clinical cases presented, it is clear that at least some of our patient’s guardians are unaware of this threat to their children. As physicians, it is our responsibility to educate our patient populations, but we should also ask our friends at our local supermarkets and pharmacies to dust off those old warning signs and help spread the word. While we are in flu season, let’s not forget to take a few minutes to inform our patients about this awful, but preventable syndrome.
References
1. Pediatrics. 1980 Dec;66(6):859-64.
2. J Gen Intern Med. 2012 Dec;27(12):1697-703.
Rachel Masia is a third-year medical student at Rowan University School of Osteopathic Medicine, Stratford, N.J. Dr. Alan Masia, Ms. Masia’s father, has a practice in Toms River, N.J. They said they had no relevant financial disclosures.
It is that time of year again. We are in the midst of flu season, which means that it is time to remind our patients’ parents about the importance of using acetaminophen instead of aspirin. This fact became evident when several guardians of our patients came in within a few days of each other in late November to early December unaware of the dangers of giving their children aspirin and other salicylate medications.
Case 1: A 4-year-old boy presented with mild diarrhea, but otherwise was clinically well. The diarrhea started while visiting family in Mexico. The mother took out a small bottle of Pepto-Bismol (bismuth subsalicylate) liquid, which she gave him 2 days previously. The bottle did have, in small font, a warning about Reye’s syndrome on the label, which the mother did not notice. She also did not think it pertained to her son anyway. During the visit, she was counseled on this being early influenza season and the avoidance of salicylate products since the 1980s in children, with the exception of cardiac uses.
Case 2: A 16-year-old male presented with his grandmother with a few scattered vesicles and low-grade fever. He had plans to go to Florida in a few days with friends and wished to know if he would be able to go. He had one dose of varicella vaccine when he was a toddler. Varicella IgM and IgG were ordered. When asked, the grandmother stated that she did not remember the warning signs about Reye’s syndrome posted in the pharmacies 30 years ago. In addition, she vaguely remembered baby aspirin not being made anymore, but she could not remember the reason why.
Case 3: An 18-year-old female with a medical history of occasional migraines controlled with over-the-counter products presented for a school form. Her mother mentioned that a relative had influenza symptoms. When we looked up the migraine medication, it was a generic aspirin/caffeine product. When counseled on Reye’s syndrome, the mother did not remember it at all, even though she was a teenager in the 1980s; she stated that she did remember her mom using only Tylenol for her illnesses.
Reye’s syndrome, a rare but serious condition causing liver degeneration and encephalopathy presenting in children younger than 18 years, was first described in 1963.1 Symptoms include mental confusion, vomiting, and even coma. The cause is unknown; however, salicylates have been implicated as a possible causative agent.
Products containing salicylate include but are not limited to aspirin and Pepto-Bismol. Studies linked Reye’s syndrome epidemiologically to recent illness with influenza or varicella and the use of aspirin. In 1978, the Centers for Disease Control and Prevention was informed that several children developed Reye’s syndrome during an influenza outbreak, and by 1980, the CDC demonstrated a link between those patients and the administration of salicylate-containing medications.2 Around the same time, more studies came out to support these findings. In 1980, 555 cases of Reye’s syndrome were reported in the United States. To decrease the occurrence, the CDC, American Academy of Pediatrics, and the U.S. Surgeon General tried to raise awareness of the association between Reye’s syndrome and aspirin by publishing journals, releasing warning statements, and including a “Black Box” warning in 1986 informing parents to not give aspirin to children and teenagers with influenza or chicken pox. Baby aspirin was removed from use for routine fevers in the mid-1980s and large warning signs would be found in every pharmacy for about 10 years. These warning signs are gone now.
As pediatricians and other primary care physicians, we have so many topics that we must address in the limited time we have allotted for each patient. However, we need to remind our patients and their parents about Reye’s syndrome and the importance of avoiding aspirin and salicylate products in children. Due to the public awareness of Reye’s syndrome in the 1980s and into the 1990s, the incidence decreased.2 From 1987 to 1993, fewer than 37 cases were reported in the United States and from 1994 to 1997, fewer than 2 cases were reported.
This demonstrates the importance of educating our patients and their parents about this syndrome and ways to avoid it. Based on the three clinical cases presented, it is clear that at least some of our patient’s guardians are unaware of this threat to their children. As physicians, it is our responsibility to educate our patient populations, but we should also ask our friends at our local supermarkets and pharmacies to dust off those old warning signs and help spread the word. While we are in flu season, let’s not forget to take a few minutes to inform our patients about this awful, but preventable syndrome.
References
1. Pediatrics. 1980 Dec;66(6):859-64.
2. J Gen Intern Med. 2012 Dec;27(12):1697-703.
Rachel Masia is a third-year medical student at Rowan University School of Osteopathic Medicine, Stratford, N.J. Dr. Alan Masia, Ms. Masia’s father, has a practice in Toms River, N.J. They said they had no relevant financial disclosures.
Distinguishing Dependence From Addiction
Four years ago, I left my career at a large urban VA hospital due to cancer; residual effects of my treatment have prevented my return. I share this as it reflects my personal experience with pain management.
As a Certified Addiction Registered Nurse–Advance Practice, I worked in a substance abuse clinic for 15 years, providing everything from primary care to detoxification and opiate replacement maintenance. I also consulted on cases throughout the facility and advocated for patients with substance abuse histories in regard to care management concerns, including pain. I spent a great deal of time educating staff from all areas on proper care for patients with a variety of substance abuse and addiction concerns.
In order to better address the conundrum of appropriate pain management, a fine distinction needs to be made between dependence and addiction. Chemical dependence is a physiologic status and a medical diagnosis; reduction or discontinuation of a culprit drug will result in symptoms of physiologic withdrawal. Addiction, on the other hand, is a legitimate brain disease that might be better thought of as a mental health disorder. It manifests signs and symptoms very similar to those of chemical dependence.
Perhaps the distinction is best revealed by example: A 65-year-old woman who is on opioid-based pain management for two weeks due to a complicated orthopedic injury will need to be tapered off to avoid physiologic symptoms of withdrawal. Yet, she is not considered a drug addict.
The behavioral characteristics of addiction are familiar: drug-seeking, illicit use, presentation with unexplained withdrawal symptoms, etc. Additionally, process addictions involve the same neurochemical pathways as chemical addictions. When they abstain, gamblers, sex addicts, and television addicts manifest the same anxiety and psychologic or even physical symptoms of withdrawal. The pathophysiology of the addiction process is established in addiction medicine literature.
The problem is that this knowledge has not been extended to practice. In my experience, poorly managed pain has a much greater risk for unintended negative consequences than aggressive management with opiods and adjuncts in a patient with a history of heroin addiction. Pseudo-addiction is real, and patients present with signs and symptoms similar to those of addiction: demanding, making specific requests, history of multiple providers (doctor shopping), and elevated anxiety.
Anyone who has experienced poorly managed severe pain will share stories of the drive to get relief at almost any cost. These people are not drug addicts. They are patients in need of informed, aggressive, and compassionate care.
Fear-based inadequate pain management creates instability and desperation in patients. Their intensive search for relief is nothing but rational. A clinician’s withholding of adequate care due to social prejudice, fear (of the DEA), and/or ignorance in a field where knowledge and tools are widely available is bad care at best and negligent incompetence at worst. Ultimately, it is the patient who suffers the consequences.
The well-known but often denied chasm between medicine and mental health has gone on too long. Medical practitioners need to
- Be better able to identify and distinguish between potential and current chemical dependence and true addiction.
- Be willing to treat pain aggressively in patients with a known history of addiction in order to prevent relapse or exacerbation of their addictive use.
- Develop a working knowledge of strategies to treat pain while minimizing risk for addiction and dependence.
- Commit to the intensity of practice that is required for effective pain management in any population.
Yes, my suggestions imply a labor-intensive approach. But there are no 20-minute appointments with a heroin addict. And time spent appropriately assessing patient risk for substance abuse, treating legitimate pain management needs, and intensively following up will reduce the medical and mental health costs associated with poorly managed pain in low-risk patients, and the hugely expensive and potentially tragic outcomes associated with poorly treated drug addicts.
L. Henry Beazlie, RN, CCRN, CARN-AP, MSN, MA (retired)
Akron, OH
Four years ago, I left my career at a large urban VA hospital due to cancer; residual effects of my treatment have prevented my return. I share this as it reflects my personal experience with pain management.
As a Certified Addiction Registered Nurse–Advance Practice, I worked in a substance abuse clinic for 15 years, providing everything from primary care to detoxification and opiate replacement maintenance. I also consulted on cases throughout the facility and advocated for patients with substance abuse histories in regard to care management concerns, including pain. I spent a great deal of time educating staff from all areas on proper care for patients with a variety of substance abuse and addiction concerns.
In order to better address the conundrum of appropriate pain management, a fine distinction needs to be made between dependence and addiction. Chemical dependence is a physiologic status and a medical diagnosis; reduction or discontinuation of a culprit drug will result in symptoms of physiologic withdrawal. Addiction, on the other hand, is a legitimate brain disease that might be better thought of as a mental health disorder. It manifests signs and symptoms very similar to those of chemical dependence.
Perhaps the distinction is best revealed by example: A 65-year-old woman who is on opioid-based pain management for two weeks due to a complicated orthopedic injury will need to be tapered off to avoid physiologic symptoms of withdrawal. Yet, she is not considered a drug addict.
The behavioral characteristics of addiction are familiar: drug-seeking, illicit use, presentation with unexplained withdrawal symptoms, etc. Additionally, process addictions involve the same neurochemical pathways as chemical addictions. When they abstain, gamblers, sex addicts, and television addicts manifest the same anxiety and psychologic or even physical symptoms of withdrawal. The pathophysiology of the addiction process is established in addiction medicine literature.
The problem is that this knowledge has not been extended to practice. In my experience, poorly managed pain has a much greater risk for unintended negative consequences than aggressive management with opiods and adjuncts in a patient with a history of heroin addiction. Pseudo-addiction is real, and patients present with signs and symptoms similar to those of addiction: demanding, making specific requests, history of multiple providers (doctor shopping), and elevated anxiety.
Anyone who has experienced poorly managed severe pain will share stories of the drive to get relief at almost any cost. These people are not drug addicts. They are patients in need of informed, aggressive, and compassionate care.
Fear-based inadequate pain management creates instability and desperation in patients. Their intensive search for relief is nothing but rational. A clinician’s withholding of adequate care due to social prejudice, fear (of the DEA), and/or ignorance in a field where knowledge and tools are widely available is bad care at best and negligent incompetence at worst. Ultimately, it is the patient who suffers the consequences.
The well-known but often denied chasm between medicine and mental health has gone on too long. Medical practitioners need to
- Be better able to identify and distinguish between potential and current chemical dependence and true addiction.
- Be willing to treat pain aggressively in patients with a known history of addiction in order to prevent relapse or exacerbation of their addictive use.
- Develop a working knowledge of strategies to treat pain while minimizing risk for addiction and dependence.
- Commit to the intensity of practice that is required for effective pain management in any population.
Yes, my suggestions imply a labor-intensive approach. But there are no 20-minute appointments with a heroin addict. And time spent appropriately assessing patient risk for substance abuse, treating legitimate pain management needs, and intensively following up will reduce the medical and mental health costs associated with poorly managed pain in low-risk patients, and the hugely expensive and potentially tragic outcomes associated with poorly treated drug addicts.
L. Henry Beazlie, RN, CCRN, CARN-AP, MSN, MA (retired)
Akron, OH
Four years ago, I left my career at a large urban VA hospital due to cancer; residual effects of my treatment have prevented my return. I share this as it reflects my personal experience with pain management.
As a Certified Addiction Registered Nurse–Advance Practice, I worked in a substance abuse clinic for 15 years, providing everything from primary care to detoxification and opiate replacement maintenance. I also consulted on cases throughout the facility and advocated for patients with substance abuse histories in regard to care management concerns, including pain. I spent a great deal of time educating staff from all areas on proper care for patients with a variety of substance abuse and addiction concerns.
In order to better address the conundrum of appropriate pain management, a fine distinction needs to be made between dependence and addiction. Chemical dependence is a physiologic status and a medical diagnosis; reduction or discontinuation of a culprit drug will result in symptoms of physiologic withdrawal. Addiction, on the other hand, is a legitimate brain disease that might be better thought of as a mental health disorder. It manifests signs and symptoms very similar to those of chemical dependence.
Perhaps the distinction is best revealed by example: A 65-year-old woman who is on opioid-based pain management for two weeks due to a complicated orthopedic injury will need to be tapered off to avoid physiologic symptoms of withdrawal. Yet, she is not considered a drug addict.
The behavioral characteristics of addiction are familiar: drug-seeking, illicit use, presentation with unexplained withdrawal symptoms, etc. Additionally, process addictions involve the same neurochemical pathways as chemical addictions. When they abstain, gamblers, sex addicts, and television addicts manifest the same anxiety and psychologic or even physical symptoms of withdrawal. The pathophysiology of the addiction process is established in addiction medicine literature.
The problem is that this knowledge has not been extended to practice. In my experience, poorly managed pain has a much greater risk for unintended negative consequences than aggressive management with opiods and adjuncts in a patient with a history of heroin addiction. Pseudo-addiction is real, and patients present with signs and symptoms similar to those of addiction: demanding, making specific requests, history of multiple providers (doctor shopping), and elevated anxiety.
Anyone who has experienced poorly managed severe pain will share stories of the drive to get relief at almost any cost. These people are not drug addicts. They are patients in need of informed, aggressive, and compassionate care.
Fear-based inadequate pain management creates instability and desperation in patients. Their intensive search for relief is nothing but rational. A clinician’s withholding of adequate care due to social prejudice, fear (of the DEA), and/or ignorance in a field where knowledge and tools are widely available is bad care at best and negligent incompetence at worst. Ultimately, it is the patient who suffers the consequences.
The well-known but often denied chasm between medicine and mental health has gone on too long. Medical practitioners need to
- Be better able to identify and distinguish between potential and current chemical dependence and true addiction.
- Be willing to treat pain aggressively in patients with a known history of addiction in order to prevent relapse or exacerbation of their addictive use.
- Develop a working knowledge of strategies to treat pain while minimizing risk for addiction and dependence.
- Commit to the intensity of practice that is required for effective pain management in any population.
Yes, my suggestions imply a labor-intensive approach. But there are no 20-minute appointments with a heroin addict. And time spent appropriately assessing patient risk for substance abuse, treating legitimate pain management needs, and intensively following up will reduce the medical and mental health costs associated with poorly managed pain in low-risk patients, and the hugely expensive and potentially tragic outcomes associated with poorly treated drug addicts.
L. Henry Beazlie, RN, CCRN, CARN-AP, MSN, MA (retired)
Akron, OH
Keeping Pain A Priority
Before pain was introduced as the “fifth vital sign” and the Joint Commission issued its standards, more than a decade’s worth of international research indicated that pain was largely ignored, untreated, or undertreated. The best tools available to treat pain (opioids) were reserved for patients on their deathbed. The horrific results of the SUPPORT study at the nation’s leading hospitals revealed that most patients had severe, uncontrolled pain up until their final days of life.1 Unfortunately, research suggests we are still reserving opioids for the last days or weeks of life.2
In 1992 and 1994, the Department of Health and Human Services issued clinical practice guidelines highlighting the huge gap between the availability of evidence-based pain control methods and the lack of pain assessment and treatment in practice.3 When these guidelines failed to change practice, the Joint Commission added “attending to pain” to its standards—the first effort to require that evidence-based practices be utilized. Twenty years later, the National Academy of Science issued a report stating that, despite transient improvements, the current state is inadequate since pain is the leading reason people seek health care. Patients with pain report an inability to get help, which is “viewed worldwide as poor medicine, unethical practice, and an abrogation of a fundamental human right.”4 Since I started working as an NP in 1983, I have never seen as many patients with pain stigmatized, ignored, labeled, and denied access to treatment as I have in the past year.
Pain afflicts more than 100 million Americans and is the leading cause of disability worldwide.5 Acute pain that is not effectively treated progresses to chronic pain in 51% of cases.6 An estimated 23 million Americans report frequent intense pain, 25 million endure daily chronic pain, and 40 million adults have high-impact, disabling, chronic pain that degrades health and requires health care intervention.6,7 The most notable damage is to the structure and function of the central nervous system.8 Brain remodeling and loss of gray matter occurs, producing changes in the brain similar to those observed with 10 to 20 years of aging; this explains why some of the learning, memory, and emotional difficulties endured by many with ongoing pain can be partially reversed with effective treatment.9 Left untreated, pain can result in significant biopsychosocial problems, frailty, financial ruin, and premature death.10-14
Prescription drug misuse and addiction also affect millions and have been a largely ignored public health problem for decades. Trying to fix the pain problem without attending equally to the problems of nonmedical drug use, addiction, and overdose deaths has contributed to the escalation of health problems to “epidemic” and “crisis” proportions. Although most patients who are prescribed medically indicated opioids for pain do not misuse their medications or become addicted, the failure to subsequently identify and properly treat an emergent substance use disorder is a problem in our current system.15 Unfortunately, making prescription opioids inaccessible to patients forces some to abuse alcohol or seek drugs from illicit sources, which only exacerbates the situation.16 A national study performed over a five-year period revealed that only 10% of patients admitted for prescription opioid treatment were referred from their health care providers.17 So, health care providers may have been part of the problem but have not been fully engaged in the solution.
Although opioids are neither the firstline, nor only, treatment option in our current evidence-based treatment toolbox, their prudent use does not cause addiction. Only 1% of patients who receive postoperative opioids go on to develop chronic opioid use, and adolescents treated with medically necessary opioids have no greater risk for future addiction than unexposed children. It is the nonmedical use of opioids, rather than proper medical use, that predisposes people to addiction.18,19 Discharging or not treating patients suspected of “drug-seeking” exacerbates the problem. Rates of opioid prescription have declined, while overdoses of illicitly manufactured fentanyl increased by 79% in 27 states from 2013 to 2014.20 In Massachusetts, only 8% of people who fatally overdosed had a prescription, while illicit fentanyl accounted for 54% of overdose deaths in 2015 and more than 74% in the third quarter of 2016.21 We need to screen for nonmedical use, drug misuse, and addiction before, during, and after we treat with this particular tool.
Unfortunately, the prevalence of pain and addiction are both increasing, especially for women and minorities—but there are safe, effective medications and non-drug approaches available to combat this.22-24 These problems will not go away on their own, and every health care professional must choose to be part of the solution rather than perpetuate the problem. A good place to start is to become familiar with the Surgeon General’s Report and the National Pain Strategy. Educate your patients, colleagues, and policy makers about the true nature of these problems. Take a public health approach to primary, secondary, and tertiary prevention by recognizing and treating these conditions in an expedient and effective matter. When problems persist, expand the treatment team to include specialists who can develop a patient-centered, multimodal treatment plan that treats co-occurring conditions. If we continue to ignore these problems, or focus on one at the expense of the other, both problems will worsen and our patients will suffer serious consequences.
Paul Arnstein, PhD, NP-C, FAAN, FNP-C
Boston, MA
1. Lynn J, Teno JM, Phillips RS, et al; SUPPORT Investigators. Perceptions by family members of the dying experience of older and seriously ill patients. Study to Understand Prognoses and Preferences for Outcomes and Risks of Treatments. Ann Intern Med. 1997;126(2):97-106.
2. Ziegler L, Mulvey M, Blenkinsopp A, et al. Opioid prescribing for patients with cancer in the last year of life: a longitudinal population cohort study. Pain. 2016;157(11):2445-2451.
3. Agency for Health Care Policy and Research [AHCPR]. Acute Pain Management: Operative or Medical Procedures and Trauma. Rockville, MD: US Department of Health and Human Services, Public Health Service; 1992.
4. Institute of Medicine (IOM). Relieving Pain in America: A Blueprint for Transforming Prevention, Care, Education, and Research. Washington DC: The National Academies Press; 2011.
5. GBD 2015 Disease and Injury Incidence and Prevalence Collaborators. Global, regional, and national incidence, prevalence, and years lived with disability for 310 diseases and injuries, 1990–2015: a systematic analysis for the Global Burden of Disease Study 2015. Lancet. 2016; 388(10053):1545-1602.
6. Macfarlane GJ. The epidemiology of chronic pain. Pain. 2016;157(10):2158-2159.
7. Nahin RL. Estimates of pain prevalence and severity in adults: United States, 2012. J Pain. 2015;16(8):769-780.
8. Pozek JP, Beausang D, Baratta JL, Viscusi ER. The acute to chronic pain transition: can chronic pain be prevented? Med Clin North Am. 2016;100(1):17-30.
9. Seminowicz DA, Wideman TH, Naso L, et al. Effective treatment of chronic low back pain in humans reverses abnormal brain anatomy and function. J Neurosci. 2011; 31(20):7540-7550.
10. Wade KF, Lee DM, McBeth J, et al. Chronic widespread pain is associated with worsening frailty in European men. Age Ageing. 2016;45(2):268-274.
11. Torrance N, Elliott A, Lee AJ, Smith BH. Severe chronic pain is associated with increased 10 year mortality. A cohort record linkage study. Eur J Pain. 2010;14(4):380-386.
12. Tang NK, Beckwith P, Ashworth P. Mental defeat is associated with suicide intent in patients with chronic pain. Clin J Pain. 2016;32(5):411-419.
13. Schaefer C, Sadosky A, Mann R, et al. Pain severity and the economic burden of neuropathic pain in the United States: BEAT Neuropathic Pain Observational Study. Clinicoecon Outcomes Res. 2014;6:483-496.
14. Schofield D, Kelly S, Shrestha R, et al. The impact of back problems on retirement wealth. Pain. 2012;153(1):203-210.
15. Chou R, Deyo R, Devine B, et al. The effectiveness and risks of long-term opioid treatment of chronic pain. AHRQ Report No. 218. Agency for Healthcare Research and Quality; September 2014. www.effectivehealthcare.ahrq.gov/ehc/products/557/1988/chronic-pain-opioid-treat ment-executive-141022.pdf. Accessed December 2, 2016.
16. Alford DP, German JS, Samet JH, et al. Primary care patients with drug use report chronic pain and self-medicate with alcohol and other drugs. J Gen Intern Med. 2016;31(5):486-491.
17. St. Marie BJ, Sahker E, Arndt S. Referrals and treatment completion for prescription opioid admissions: five years of national data. J Subst Abus Treat. 2015;59:109-114.
18. Sun EC, Darnall B, Baker LC, et al. Incidence of and risk factors for chronic opioid use among opioid-naive patients in the postoperative period. JAMA Intern Med. 2016; 176(9):1286-1293.
19. McCabe SE, Veliz P, Schulenberg JE. Adolescent context of exposure to prescription opioids and substance use disorder (SUD) symptoms at age 35: a national longitudinal study. Pain. 2016;157(10):2171-2178.
20. Gladden RM, Martinez P, Seth P. Fentanyl law enforcement submissions and increases in synthetic opioid-involved overdose deaths—27 states, 2013-2014. MMWR Morb Mortal Wkly Rep. 2016;65(33):837-843.
21. Massachusetts Department of Public Health. Data Brief: Opioid-related Overdose Deaths Among Massachusetts Residents. www.mass.gov/eohhs/docs/dph/quality/drugcontrol/county-level-pmp/data-brief-overdose-deaths-may-2016.pdf. Accessed December 2, 2016.
22. Barbour KE, Boring M, Helmick CG, et al. Prevalence of severe joint pain among adults with doctor-diagnosed arthritis—United States, 2002–2014. MMWR Morb Mortal Wkly Rep. 2016;65(39):1052-1056.
23. US Department of Health and Human Services (HHS), Office of the Surgeon General. Facing Addiction in America: The Surgeon General’s Report on Alcohol, Drugs, and Health, Executive Summary. Washington, DC: HHS; 2016. https://addiction.surgeongeneral.gov/executive-summary.pdf. Accessed December 2, 2016.
24. Herndon CM, Arnstein P, Darnall B, et al. Principles of Analgesic Use. 7th ed. Chicago, IL: American Pain Society Press; 2016.
Before pain was introduced as the “fifth vital sign” and the Joint Commission issued its standards, more than a decade’s worth of international research indicated that pain was largely ignored, untreated, or undertreated. The best tools available to treat pain (opioids) were reserved for patients on their deathbed. The horrific results of the SUPPORT study at the nation’s leading hospitals revealed that most patients had severe, uncontrolled pain up until their final days of life.1 Unfortunately, research suggests we are still reserving opioids for the last days or weeks of life.2
In 1992 and 1994, the Department of Health and Human Services issued clinical practice guidelines highlighting the huge gap between the availability of evidence-based pain control methods and the lack of pain assessment and treatment in practice.3 When these guidelines failed to change practice, the Joint Commission added “attending to pain” to its standards—the first effort to require that evidence-based practices be utilized. Twenty years later, the National Academy of Science issued a report stating that, despite transient improvements, the current state is inadequate since pain is the leading reason people seek health care. Patients with pain report an inability to get help, which is “viewed worldwide as poor medicine, unethical practice, and an abrogation of a fundamental human right.”4 Since I started working as an NP in 1983, I have never seen as many patients with pain stigmatized, ignored, labeled, and denied access to treatment as I have in the past year.
Pain afflicts more than 100 million Americans and is the leading cause of disability worldwide.5 Acute pain that is not effectively treated progresses to chronic pain in 51% of cases.6 An estimated 23 million Americans report frequent intense pain, 25 million endure daily chronic pain, and 40 million adults have high-impact, disabling, chronic pain that degrades health and requires health care intervention.6,7 The most notable damage is to the structure and function of the central nervous system.8 Brain remodeling and loss of gray matter occurs, producing changes in the brain similar to those observed with 10 to 20 years of aging; this explains why some of the learning, memory, and emotional difficulties endured by many with ongoing pain can be partially reversed with effective treatment.9 Left untreated, pain can result in significant biopsychosocial problems, frailty, financial ruin, and premature death.10-14
Prescription drug misuse and addiction also affect millions and have been a largely ignored public health problem for decades. Trying to fix the pain problem without attending equally to the problems of nonmedical drug use, addiction, and overdose deaths has contributed to the escalation of health problems to “epidemic” and “crisis” proportions. Although most patients who are prescribed medically indicated opioids for pain do not misuse their medications or become addicted, the failure to subsequently identify and properly treat an emergent substance use disorder is a problem in our current system.15 Unfortunately, making prescription opioids inaccessible to patients forces some to abuse alcohol or seek drugs from illicit sources, which only exacerbates the situation.16 A national study performed over a five-year period revealed that only 10% of patients admitted for prescription opioid treatment were referred from their health care providers.17 So, health care providers may have been part of the problem but have not been fully engaged in the solution.
Although opioids are neither the firstline, nor only, treatment option in our current evidence-based treatment toolbox, their prudent use does not cause addiction. Only 1% of patients who receive postoperative opioids go on to develop chronic opioid use, and adolescents treated with medically necessary opioids have no greater risk for future addiction than unexposed children. It is the nonmedical use of opioids, rather than proper medical use, that predisposes people to addiction.18,19 Discharging or not treating patients suspected of “drug-seeking” exacerbates the problem. Rates of opioid prescription have declined, while overdoses of illicitly manufactured fentanyl increased by 79% in 27 states from 2013 to 2014.20 In Massachusetts, only 8% of people who fatally overdosed had a prescription, while illicit fentanyl accounted for 54% of overdose deaths in 2015 and more than 74% in the third quarter of 2016.21 We need to screen for nonmedical use, drug misuse, and addiction before, during, and after we treat with this particular tool.
Unfortunately, the prevalence of pain and addiction are both increasing, especially for women and minorities—but there are safe, effective medications and non-drug approaches available to combat this.22-24 These problems will not go away on their own, and every health care professional must choose to be part of the solution rather than perpetuate the problem. A good place to start is to become familiar with the Surgeon General’s Report and the National Pain Strategy. Educate your patients, colleagues, and policy makers about the true nature of these problems. Take a public health approach to primary, secondary, and tertiary prevention by recognizing and treating these conditions in an expedient and effective matter. When problems persist, expand the treatment team to include specialists who can develop a patient-centered, multimodal treatment plan that treats co-occurring conditions. If we continue to ignore these problems, or focus on one at the expense of the other, both problems will worsen and our patients will suffer serious consequences.
Paul Arnstein, PhD, NP-C, FAAN, FNP-C
Boston, MA
Before pain was introduced as the “fifth vital sign” and the Joint Commission issued its standards, more than a decade’s worth of international research indicated that pain was largely ignored, untreated, or undertreated. The best tools available to treat pain (opioids) were reserved for patients on their deathbed. The horrific results of the SUPPORT study at the nation’s leading hospitals revealed that most patients had severe, uncontrolled pain up until their final days of life.1 Unfortunately, research suggests we are still reserving opioids for the last days or weeks of life.2
In 1992 and 1994, the Department of Health and Human Services issued clinical practice guidelines highlighting the huge gap between the availability of evidence-based pain control methods and the lack of pain assessment and treatment in practice.3 When these guidelines failed to change practice, the Joint Commission added “attending to pain” to its standards—the first effort to require that evidence-based practices be utilized. Twenty years later, the National Academy of Science issued a report stating that, despite transient improvements, the current state is inadequate since pain is the leading reason people seek health care. Patients with pain report an inability to get help, which is “viewed worldwide as poor medicine, unethical practice, and an abrogation of a fundamental human right.”4 Since I started working as an NP in 1983, I have never seen as many patients with pain stigmatized, ignored, labeled, and denied access to treatment as I have in the past year.
Pain afflicts more than 100 million Americans and is the leading cause of disability worldwide.5 Acute pain that is not effectively treated progresses to chronic pain in 51% of cases.6 An estimated 23 million Americans report frequent intense pain, 25 million endure daily chronic pain, and 40 million adults have high-impact, disabling, chronic pain that degrades health and requires health care intervention.6,7 The most notable damage is to the structure and function of the central nervous system.8 Brain remodeling and loss of gray matter occurs, producing changes in the brain similar to those observed with 10 to 20 years of aging; this explains why some of the learning, memory, and emotional difficulties endured by many with ongoing pain can be partially reversed with effective treatment.9 Left untreated, pain can result in significant biopsychosocial problems, frailty, financial ruin, and premature death.10-14
Prescription drug misuse and addiction also affect millions and have been a largely ignored public health problem for decades. Trying to fix the pain problem without attending equally to the problems of nonmedical drug use, addiction, and overdose deaths has contributed to the escalation of health problems to “epidemic” and “crisis” proportions. Although most patients who are prescribed medically indicated opioids for pain do not misuse their medications or become addicted, the failure to subsequently identify and properly treat an emergent substance use disorder is a problem in our current system.15 Unfortunately, making prescription opioids inaccessible to patients forces some to abuse alcohol or seek drugs from illicit sources, which only exacerbates the situation.16 A national study performed over a five-year period revealed that only 10% of patients admitted for prescription opioid treatment were referred from their health care providers.17 So, health care providers may have been part of the problem but have not been fully engaged in the solution.
Although opioids are neither the firstline, nor only, treatment option in our current evidence-based treatment toolbox, their prudent use does not cause addiction. Only 1% of patients who receive postoperative opioids go on to develop chronic opioid use, and adolescents treated with medically necessary opioids have no greater risk for future addiction than unexposed children. It is the nonmedical use of opioids, rather than proper medical use, that predisposes people to addiction.18,19 Discharging or not treating patients suspected of “drug-seeking” exacerbates the problem. Rates of opioid prescription have declined, while overdoses of illicitly manufactured fentanyl increased by 79% in 27 states from 2013 to 2014.20 In Massachusetts, only 8% of people who fatally overdosed had a prescription, while illicit fentanyl accounted for 54% of overdose deaths in 2015 and more than 74% in the third quarter of 2016.21 We need to screen for nonmedical use, drug misuse, and addiction before, during, and after we treat with this particular tool.
Unfortunately, the prevalence of pain and addiction are both increasing, especially for women and minorities—but there are safe, effective medications and non-drug approaches available to combat this.22-24 These problems will not go away on their own, and every health care professional must choose to be part of the solution rather than perpetuate the problem. A good place to start is to become familiar with the Surgeon General’s Report and the National Pain Strategy. Educate your patients, colleagues, and policy makers about the true nature of these problems. Take a public health approach to primary, secondary, and tertiary prevention by recognizing and treating these conditions in an expedient and effective matter. When problems persist, expand the treatment team to include specialists who can develop a patient-centered, multimodal treatment plan that treats co-occurring conditions. If we continue to ignore these problems, or focus on one at the expense of the other, both problems will worsen and our patients will suffer serious consequences.
Paul Arnstein, PhD, NP-C, FAAN, FNP-C
Boston, MA
1. Lynn J, Teno JM, Phillips RS, et al; SUPPORT Investigators. Perceptions by family members of the dying experience of older and seriously ill patients. Study to Understand Prognoses and Preferences for Outcomes and Risks of Treatments. Ann Intern Med. 1997;126(2):97-106.
2. Ziegler L, Mulvey M, Blenkinsopp A, et al. Opioid prescribing for patients with cancer in the last year of life: a longitudinal population cohort study. Pain. 2016;157(11):2445-2451.
3. Agency for Health Care Policy and Research [AHCPR]. Acute Pain Management: Operative or Medical Procedures and Trauma. Rockville, MD: US Department of Health and Human Services, Public Health Service; 1992.
4. Institute of Medicine (IOM). Relieving Pain in America: A Blueprint for Transforming Prevention, Care, Education, and Research. Washington DC: The National Academies Press; 2011.
5. GBD 2015 Disease and Injury Incidence and Prevalence Collaborators. Global, regional, and national incidence, prevalence, and years lived with disability for 310 diseases and injuries, 1990–2015: a systematic analysis for the Global Burden of Disease Study 2015. Lancet. 2016; 388(10053):1545-1602.
6. Macfarlane GJ. The epidemiology of chronic pain. Pain. 2016;157(10):2158-2159.
7. Nahin RL. Estimates of pain prevalence and severity in adults: United States, 2012. J Pain. 2015;16(8):769-780.
8. Pozek JP, Beausang D, Baratta JL, Viscusi ER. The acute to chronic pain transition: can chronic pain be prevented? Med Clin North Am. 2016;100(1):17-30.
9. Seminowicz DA, Wideman TH, Naso L, et al. Effective treatment of chronic low back pain in humans reverses abnormal brain anatomy and function. J Neurosci. 2011; 31(20):7540-7550.
10. Wade KF, Lee DM, McBeth J, et al. Chronic widespread pain is associated with worsening frailty in European men. Age Ageing. 2016;45(2):268-274.
11. Torrance N, Elliott A, Lee AJ, Smith BH. Severe chronic pain is associated with increased 10 year mortality. A cohort record linkage study. Eur J Pain. 2010;14(4):380-386.
12. Tang NK, Beckwith P, Ashworth P. Mental defeat is associated with suicide intent in patients with chronic pain. Clin J Pain. 2016;32(5):411-419.
13. Schaefer C, Sadosky A, Mann R, et al. Pain severity and the economic burden of neuropathic pain in the United States: BEAT Neuropathic Pain Observational Study. Clinicoecon Outcomes Res. 2014;6:483-496.
14. Schofield D, Kelly S, Shrestha R, et al. The impact of back problems on retirement wealth. Pain. 2012;153(1):203-210.
15. Chou R, Deyo R, Devine B, et al. The effectiveness and risks of long-term opioid treatment of chronic pain. AHRQ Report No. 218. Agency for Healthcare Research and Quality; September 2014. www.effectivehealthcare.ahrq.gov/ehc/products/557/1988/chronic-pain-opioid-treat ment-executive-141022.pdf. Accessed December 2, 2016.
16. Alford DP, German JS, Samet JH, et al. Primary care patients with drug use report chronic pain and self-medicate with alcohol and other drugs. J Gen Intern Med. 2016;31(5):486-491.
17. St. Marie BJ, Sahker E, Arndt S. Referrals and treatment completion for prescription opioid admissions: five years of national data. J Subst Abus Treat. 2015;59:109-114.
18. Sun EC, Darnall B, Baker LC, et al. Incidence of and risk factors for chronic opioid use among opioid-naive patients in the postoperative period. JAMA Intern Med. 2016; 176(9):1286-1293.
19. McCabe SE, Veliz P, Schulenberg JE. Adolescent context of exposure to prescription opioids and substance use disorder (SUD) symptoms at age 35: a national longitudinal study. Pain. 2016;157(10):2171-2178.
20. Gladden RM, Martinez P, Seth P. Fentanyl law enforcement submissions and increases in synthetic opioid-involved overdose deaths—27 states, 2013-2014. MMWR Morb Mortal Wkly Rep. 2016;65(33):837-843.
21. Massachusetts Department of Public Health. Data Brief: Opioid-related Overdose Deaths Among Massachusetts Residents. www.mass.gov/eohhs/docs/dph/quality/drugcontrol/county-level-pmp/data-brief-overdose-deaths-may-2016.pdf. Accessed December 2, 2016.
22. Barbour KE, Boring M, Helmick CG, et al. Prevalence of severe joint pain among adults with doctor-diagnosed arthritis—United States, 2002–2014. MMWR Morb Mortal Wkly Rep. 2016;65(39):1052-1056.
23. US Department of Health and Human Services (HHS), Office of the Surgeon General. Facing Addiction in America: The Surgeon General’s Report on Alcohol, Drugs, and Health, Executive Summary. Washington, DC: HHS; 2016. https://addiction.surgeongeneral.gov/executive-summary.pdf. Accessed December 2, 2016.
24. Herndon CM, Arnstein P, Darnall B, et al. Principles of Analgesic Use. 7th ed. Chicago, IL: American Pain Society Press; 2016.
1. Lynn J, Teno JM, Phillips RS, et al; SUPPORT Investigators. Perceptions by family members of the dying experience of older and seriously ill patients. Study to Understand Prognoses and Preferences for Outcomes and Risks of Treatments. Ann Intern Med. 1997;126(2):97-106.
2. Ziegler L, Mulvey M, Blenkinsopp A, et al. Opioid prescribing for patients with cancer in the last year of life: a longitudinal population cohort study. Pain. 2016;157(11):2445-2451.
3. Agency for Health Care Policy and Research [AHCPR]. Acute Pain Management: Operative or Medical Procedures and Trauma. Rockville, MD: US Department of Health and Human Services, Public Health Service; 1992.
4. Institute of Medicine (IOM). Relieving Pain in America: A Blueprint for Transforming Prevention, Care, Education, and Research. Washington DC: The National Academies Press; 2011.
5. GBD 2015 Disease and Injury Incidence and Prevalence Collaborators. Global, regional, and national incidence, prevalence, and years lived with disability for 310 diseases and injuries, 1990–2015: a systematic analysis for the Global Burden of Disease Study 2015. Lancet. 2016; 388(10053):1545-1602.
6. Macfarlane GJ. The epidemiology of chronic pain. Pain. 2016;157(10):2158-2159.
7. Nahin RL. Estimates of pain prevalence and severity in adults: United States, 2012. J Pain. 2015;16(8):769-780.
8. Pozek JP, Beausang D, Baratta JL, Viscusi ER. The acute to chronic pain transition: can chronic pain be prevented? Med Clin North Am. 2016;100(1):17-30.
9. Seminowicz DA, Wideman TH, Naso L, et al. Effective treatment of chronic low back pain in humans reverses abnormal brain anatomy and function. J Neurosci. 2011; 31(20):7540-7550.
10. Wade KF, Lee DM, McBeth J, et al. Chronic widespread pain is associated with worsening frailty in European men. Age Ageing. 2016;45(2):268-274.
11. Torrance N, Elliott A, Lee AJ, Smith BH. Severe chronic pain is associated with increased 10 year mortality. A cohort record linkage study. Eur J Pain. 2010;14(4):380-386.
12. Tang NK, Beckwith P, Ashworth P. Mental defeat is associated with suicide intent in patients with chronic pain. Clin J Pain. 2016;32(5):411-419.
13. Schaefer C, Sadosky A, Mann R, et al. Pain severity and the economic burden of neuropathic pain in the United States: BEAT Neuropathic Pain Observational Study. Clinicoecon Outcomes Res. 2014;6:483-496.
14. Schofield D, Kelly S, Shrestha R, et al. The impact of back problems on retirement wealth. Pain. 2012;153(1):203-210.
15. Chou R, Deyo R, Devine B, et al. The effectiveness and risks of long-term opioid treatment of chronic pain. AHRQ Report No. 218. Agency for Healthcare Research and Quality; September 2014. www.effectivehealthcare.ahrq.gov/ehc/products/557/1988/chronic-pain-opioid-treat ment-executive-141022.pdf. Accessed December 2, 2016.
16. Alford DP, German JS, Samet JH, et al. Primary care patients with drug use report chronic pain and self-medicate with alcohol and other drugs. J Gen Intern Med. 2016;31(5):486-491.
17. St. Marie BJ, Sahker E, Arndt S. Referrals and treatment completion for prescription opioid admissions: five years of national data. J Subst Abus Treat. 2015;59:109-114.
18. Sun EC, Darnall B, Baker LC, et al. Incidence of and risk factors for chronic opioid use among opioid-naive patients in the postoperative period. JAMA Intern Med. 2016; 176(9):1286-1293.
19. McCabe SE, Veliz P, Schulenberg JE. Adolescent context of exposure to prescription opioids and substance use disorder (SUD) symptoms at age 35: a national longitudinal study. Pain. 2016;157(10):2171-2178.
20. Gladden RM, Martinez P, Seth P. Fentanyl law enforcement submissions and increases in synthetic opioid-involved overdose deaths—27 states, 2013-2014. MMWR Morb Mortal Wkly Rep. 2016;65(33):837-843.
21. Massachusetts Department of Public Health. Data Brief: Opioid-related Overdose Deaths Among Massachusetts Residents. www.mass.gov/eohhs/docs/dph/quality/drugcontrol/county-level-pmp/data-brief-overdose-deaths-may-2016.pdf. Accessed December 2, 2016.
22. Barbour KE, Boring M, Helmick CG, et al. Prevalence of severe joint pain among adults with doctor-diagnosed arthritis—United States, 2002–2014. MMWR Morb Mortal Wkly Rep. 2016;65(39):1052-1056.
23. US Department of Health and Human Services (HHS), Office of the Surgeon General. Facing Addiction in America: The Surgeon General’s Report on Alcohol, Drugs, and Health, Executive Summary. Washington, DC: HHS; 2016. https://addiction.surgeongeneral.gov/executive-summary.pdf. Accessed December 2, 2016.
24. Herndon CM, Arnstein P, Darnall B, et al. Principles of Analgesic Use. 7th ed. Chicago, IL: American Pain Society Press; 2016.
Enterovirus D68 – An emerging threat to child health
In August 2014, we first heard of increased pediatric cases of severe respiratory tract disease, many requiring management in the ICU, and of acute flaccid myelitis/paralysis (AFM) of unknown etiology from many states across the United States. Concurrently with this outbreak in the United States, similar clinical cases were reported in Canada and Europe. Subsequently, enterovirus D68 was confirmed in some, but not all, of the paralyzed children. Although new to many of us, enterovirus D68 was already known as an atypical enterovirus sharing many of its structural and chemical properties with rhinovirus. For example, it most often was reported from respiratory samples and less common from stool samples. It also had been associated with clusters of respiratory disease since 2000 and a 2008 case of fatal AFM.
There were 120 cases of AFM, coinciding with the nationwide outbreak of enteroviral D68 disease, reported in 2014. The Centers for Disease Control and Prevention has evaluated the cerebrospinal fluid in many of these cases, and no pathogen has consistently been detected. The children were mostly school age, aged 7-11 years, presented with acute, febrile respiratory illness followed by acute onset of cranial nerve dysfunction or flaccid paralysis of one or more limbs. The CSF revealed mild pleocytosis, most often with mild elevation of protein and a normal glucose. However, the MRI was distinctly abnormal with focal lesion in the cranial nerve nuclei (in those with bulbar dysfunction) and/or in the anterior horn or spinal cord gray matter. Long-term prognosis is unknown, although most patients have persistent weakness, despite some improvement, to date.
In 2016, the CDC has reported an increase in cases after a decline in 2015 despite the absence of epidemic respiratory tract disease in the United States from enterovirus D68. In the Netherlands, an increase in respiratory disease from enterovirus D68 in children and adults also has been reported since June 2016. Respiratory disease has been observed in children as young as 3 months of age, and most of the children have underlying comorbidity, many with asthma or other pulmonary conditions. Thirteen of 17 (77%) cases in children have required ICU admission, while most of the adult cases were mild and influenzalike. One child developed bulbar dysfunction and limb weakness.
Enterovirus D68 infection should be suspected in children with moderate to severe respiratory tract infection or acute onset bulbar or flaccid paralysis of unknown etiology, especially in summer and fall. In such cases, respiratory specimens (nasopharyngeal or oral swabs or wash, tracheal secretions or bronchoalveolar lavage) should be obtained. Increasingly, hospitals and laboratories can perform multiplex polymerase chain reaction testing for enterovirus/rhinovirus. However, most do not determine the specific enterovirus. CDC and some state health departments use real-time reverse transcription polymerase chain reaction (rRT-PCR), which enables reporting of specific enterovirus species within days. CDC recommends that clinicians consider enterovirus D68 testing for children with unknown, severe respiratory illness or AFM. Details for sending specimens should be available from your state’s Department of Public Health website or the CDC.
Prevention strategies may be critical for limiting the spread of enterovirus D68 in the community. The CDC recommends:
- Wash your hands often with soap and water for 20 seconds.
- Avoid touching your eyes, nose and mouth with unwashed hands.
- Avoid close contact such as kissing, hugging, and sharing cups with people who are ill.
- Cover your coughs and sneezes with a tissue or shirt sleeve, not your hands.
- Clean and disinfect frequently touched surfaces, such as toys and doorknobs, especially if someone is sick.
- Stay home when you are ill.
In 2014, it was speculated that the epidemic might have been a one-time event. It now appears more likely that enterovirus D68 activity has been increasing since 2000, and that children and immunocompromised hosts will be at greatest risk because of a lack of neutralizing antibody. Ongoing enterovirus surveillance will be critical to understand the potential for severe respiratory disease as will the development of new and effective antivirals. A vaccine for enterovirus 71 recently demonstrated efficacy against hand, foot, and mouth disease in children and may provide insights into the development of vaccines against enterovirus D68.
References
Lancet Infect Dis. 2016 May;16(5):e64-75
Emerg Infect Dis. 2017 Jan;23(1):140-3.
J Med Virol. 2016 May;88(5):739-45
Dr. Pelton is chief of pediatric infectious disease and coordinator of the maternal-child HIV program at Boston Medical Center. Dr. Pelton said he had no relevant financial disclosures. Email him at [email protected].
In August 2014, we first heard of increased pediatric cases of severe respiratory tract disease, many requiring management in the ICU, and of acute flaccid myelitis/paralysis (AFM) of unknown etiology from many states across the United States. Concurrently with this outbreak in the United States, similar clinical cases were reported in Canada and Europe. Subsequently, enterovirus D68 was confirmed in some, but not all, of the paralyzed children. Although new to many of us, enterovirus D68 was already known as an atypical enterovirus sharing many of its structural and chemical properties with rhinovirus. For example, it most often was reported from respiratory samples and less common from stool samples. It also had been associated with clusters of respiratory disease since 2000 and a 2008 case of fatal AFM.
There were 120 cases of AFM, coinciding with the nationwide outbreak of enteroviral D68 disease, reported in 2014. The Centers for Disease Control and Prevention has evaluated the cerebrospinal fluid in many of these cases, and no pathogen has consistently been detected. The children were mostly school age, aged 7-11 years, presented with acute, febrile respiratory illness followed by acute onset of cranial nerve dysfunction or flaccid paralysis of one or more limbs. The CSF revealed mild pleocytosis, most often with mild elevation of protein and a normal glucose. However, the MRI was distinctly abnormal with focal lesion in the cranial nerve nuclei (in those with bulbar dysfunction) and/or in the anterior horn or spinal cord gray matter. Long-term prognosis is unknown, although most patients have persistent weakness, despite some improvement, to date.
In 2016, the CDC has reported an increase in cases after a decline in 2015 despite the absence of epidemic respiratory tract disease in the United States from enterovirus D68. In the Netherlands, an increase in respiratory disease from enterovirus D68 in children and adults also has been reported since June 2016. Respiratory disease has been observed in children as young as 3 months of age, and most of the children have underlying comorbidity, many with asthma or other pulmonary conditions. Thirteen of 17 (77%) cases in children have required ICU admission, while most of the adult cases were mild and influenzalike. One child developed bulbar dysfunction and limb weakness.
Enterovirus D68 infection should be suspected in children with moderate to severe respiratory tract infection or acute onset bulbar or flaccid paralysis of unknown etiology, especially in summer and fall. In such cases, respiratory specimens (nasopharyngeal or oral swabs or wash, tracheal secretions or bronchoalveolar lavage) should be obtained. Increasingly, hospitals and laboratories can perform multiplex polymerase chain reaction testing for enterovirus/rhinovirus. However, most do not determine the specific enterovirus. CDC and some state health departments use real-time reverse transcription polymerase chain reaction (rRT-PCR), which enables reporting of specific enterovirus species within days. CDC recommends that clinicians consider enterovirus D68 testing for children with unknown, severe respiratory illness or AFM. Details for sending specimens should be available from your state’s Department of Public Health website or the CDC.
Prevention strategies may be critical for limiting the spread of enterovirus D68 in the community. The CDC recommends:
- Wash your hands often with soap and water for 20 seconds.
- Avoid touching your eyes, nose and mouth with unwashed hands.
- Avoid close contact such as kissing, hugging, and sharing cups with people who are ill.
- Cover your coughs and sneezes with a tissue or shirt sleeve, not your hands.
- Clean and disinfect frequently touched surfaces, such as toys and doorknobs, especially if someone is sick.
- Stay home when you are ill.
In 2014, it was speculated that the epidemic might have been a one-time event. It now appears more likely that enterovirus D68 activity has been increasing since 2000, and that children and immunocompromised hosts will be at greatest risk because of a lack of neutralizing antibody. Ongoing enterovirus surveillance will be critical to understand the potential for severe respiratory disease as will the development of new and effective antivirals. A vaccine for enterovirus 71 recently demonstrated efficacy against hand, foot, and mouth disease in children and may provide insights into the development of vaccines against enterovirus D68.
References
Lancet Infect Dis. 2016 May;16(5):e64-75
Emerg Infect Dis. 2017 Jan;23(1):140-3.
J Med Virol. 2016 May;88(5):739-45
Dr. Pelton is chief of pediatric infectious disease and coordinator of the maternal-child HIV program at Boston Medical Center. Dr. Pelton said he had no relevant financial disclosures. Email him at [email protected].
In August 2014, we first heard of increased pediatric cases of severe respiratory tract disease, many requiring management in the ICU, and of acute flaccid myelitis/paralysis (AFM) of unknown etiology from many states across the United States. Concurrently with this outbreak in the United States, similar clinical cases were reported in Canada and Europe. Subsequently, enterovirus D68 was confirmed in some, but not all, of the paralyzed children. Although new to many of us, enterovirus D68 was already known as an atypical enterovirus sharing many of its structural and chemical properties with rhinovirus. For example, it most often was reported from respiratory samples and less common from stool samples. It also had been associated with clusters of respiratory disease since 2000 and a 2008 case of fatal AFM.
There were 120 cases of AFM, coinciding with the nationwide outbreak of enteroviral D68 disease, reported in 2014. The Centers for Disease Control and Prevention has evaluated the cerebrospinal fluid in many of these cases, and no pathogen has consistently been detected. The children were mostly school age, aged 7-11 years, presented with acute, febrile respiratory illness followed by acute onset of cranial nerve dysfunction or flaccid paralysis of one or more limbs. The CSF revealed mild pleocytosis, most often with mild elevation of protein and a normal glucose. However, the MRI was distinctly abnormal with focal lesion in the cranial nerve nuclei (in those with bulbar dysfunction) and/or in the anterior horn or spinal cord gray matter. Long-term prognosis is unknown, although most patients have persistent weakness, despite some improvement, to date.
In 2016, the CDC has reported an increase in cases after a decline in 2015 despite the absence of epidemic respiratory tract disease in the United States from enterovirus D68. In the Netherlands, an increase in respiratory disease from enterovirus D68 in children and adults also has been reported since June 2016. Respiratory disease has been observed in children as young as 3 months of age, and most of the children have underlying comorbidity, many with asthma or other pulmonary conditions. Thirteen of 17 (77%) cases in children have required ICU admission, while most of the adult cases were mild and influenzalike. One child developed bulbar dysfunction and limb weakness.
Enterovirus D68 infection should be suspected in children with moderate to severe respiratory tract infection or acute onset bulbar or flaccid paralysis of unknown etiology, especially in summer and fall. In such cases, respiratory specimens (nasopharyngeal or oral swabs or wash, tracheal secretions or bronchoalveolar lavage) should be obtained. Increasingly, hospitals and laboratories can perform multiplex polymerase chain reaction testing for enterovirus/rhinovirus. However, most do not determine the specific enterovirus. CDC and some state health departments use real-time reverse transcription polymerase chain reaction (rRT-PCR), which enables reporting of specific enterovirus species within days. CDC recommends that clinicians consider enterovirus D68 testing for children with unknown, severe respiratory illness or AFM. Details for sending specimens should be available from your state’s Department of Public Health website or the CDC.
Prevention strategies may be critical for limiting the spread of enterovirus D68 in the community. The CDC recommends:
- Wash your hands often with soap and water for 20 seconds.
- Avoid touching your eyes, nose and mouth with unwashed hands.
- Avoid close contact such as kissing, hugging, and sharing cups with people who are ill.
- Cover your coughs and sneezes with a tissue or shirt sleeve, not your hands.
- Clean and disinfect frequently touched surfaces, such as toys and doorknobs, especially if someone is sick.
- Stay home when you are ill.
In 2014, it was speculated that the epidemic might have been a one-time event. It now appears more likely that enterovirus D68 activity has been increasing since 2000, and that children and immunocompromised hosts will be at greatest risk because of a lack of neutralizing antibody. Ongoing enterovirus surveillance will be critical to understand the potential for severe respiratory disease as will the development of new and effective antivirals. A vaccine for enterovirus 71 recently demonstrated efficacy against hand, foot, and mouth disease in children and may provide insights into the development of vaccines against enterovirus D68.
References
Lancet Infect Dis. 2016 May;16(5):e64-75
Emerg Infect Dis. 2017 Jan;23(1):140-3.
J Med Virol. 2016 May;88(5):739-45
Dr. Pelton is chief of pediatric infectious disease and coordinator of the maternal-child HIV program at Boston Medical Center. Dr. Pelton said he had no relevant financial disclosures. Email him at [email protected].
COMMENTARY—EXPEDITION3: A Winding Path to Nowhere
This new phase III trial of solanezumab reveals that the drug is not effective for patients with mild Alzheimer’s disease, despite the hint that it was possibly effective based on post hoc analyses of earlier studies with this drug.
The findings expose the hazards of such post hoc analyses, typically done when the desired results are not observed, in the hope of squeezing lemonade from lemons. Although the subanalysis of patients with mild Alzheimer’s disease in the earlier studies suggested a 34% slowing of cognitive decline, as assessed by ADAS-Cog, an incremental slowing of 11% was seen in the new study that was not even statistically significant. While some secondary end points reached statistical significance, the slowing was so modest as to make no practical difference clinically.
I cannot emphasize enough that such equivocal results as seen in EXPEDITION3 do absolutely nothing to either confirm or deny the amyloid hypothesis. By now, there have been so many of these studies with antiamyloid agents, with little or no hint of efficacy, that we have long passed the definition of insanity: doing the same thing over and over in the hope of getting a different result.
The combination of all these clinical trial failures with the result of imaging studies that have shown amyloid deposition some 20 years before the expected onset of symptoms clearly tells us that antiamyloid agents should only be considered as potential prophylactics. By the time symptoms appear, disease progression is largely independent of amyloid and may be primarily tau-driven, spreading from neuron to neuron even when amyloid is effectively targeted by therapeutics. Even the A4 and DIAN studies are likely initiating treatment too late to make anything more than a modest effect with little practical value clinically. I am not suggesting that we drop amyloid as a target, only that we stop making these incremental changes in clinical trial design in the hope of getting a different result.
—Michael S. Wolfe, PhD
Mathias P. Mertes Professor of Medicinal Chemistry
University of Kansas, Lawrence
This new phase III trial of solanezumab reveals that the drug is not effective for patients with mild Alzheimer’s disease, despite the hint that it was possibly effective based on post hoc analyses of earlier studies with this drug.
The findings expose the hazards of such post hoc analyses, typically done when the desired results are not observed, in the hope of squeezing lemonade from lemons. Although the subanalysis of patients with mild Alzheimer’s disease in the earlier studies suggested a 34% slowing of cognitive decline, as assessed by ADAS-Cog, an incremental slowing of 11% was seen in the new study that was not even statistically significant. While some secondary end points reached statistical significance, the slowing was so modest as to make no practical difference clinically.
I cannot emphasize enough that such equivocal results as seen in EXPEDITION3 do absolutely nothing to either confirm or deny the amyloid hypothesis. By now, there have been so many of these studies with antiamyloid agents, with little or no hint of efficacy, that we have long passed the definition of insanity: doing the same thing over and over in the hope of getting a different result.
The combination of all these clinical trial failures with the result of imaging studies that have shown amyloid deposition some 20 years before the expected onset of symptoms clearly tells us that antiamyloid agents should only be considered as potential prophylactics. By the time symptoms appear, disease progression is largely independent of amyloid and may be primarily tau-driven, spreading from neuron to neuron even when amyloid is effectively targeted by therapeutics. Even the A4 and DIAN studies are likely initiating treatment too late to make anything more than a modest effect with little practical value clinically. I am not suggesting that we drop amyloid as a target, only that we stop making these incremental changes in clinical trial design in the hope of getting a different result.
—Michael S. Wolfe, PhD
Mathias P. Mertes Professor of Medicinal Chemistry
University of Kansas, Lawrence
This new phase III trial of solanezumab reveals that the drug is not effective for patients with mild Alzheimer’s disease, despite the hint that it was possibly effective based on post hoc analyses of earlier studies with this drug.
The findings expose the hazards of such post hoc analyses, typically done when the desired results are not observed, in the hope of squeezing lemonade from lemons. Although the subanalysis of patients with mild Alzheimer’s disease in the earlier studies suggested a 34% slowing of cognitive decline, as assessed by ADAS-Cog, an incremental slowing of 11% was seen in the new study that was not even statistically significant. While some secondary end points reached statistical significance, the slowing was so modest as to make no practical difference clinically.
I cannot emphasize enough that such equivocal results as seen in EXPEDITION3 do absolutely nothing to either confirm or deny the amyloid hypothesis. By now, there have been so many of these studies with antiamyloid agents, with little or no hint of efficacy, that we have long passed the definition of insanity: doing the same thing over and over in the hope of getting a different result.
The combination of all these clinical trial failures with the result of imaging studies that have shown amyloid deposition some 20 years before the expected onset of symptoms clearly tells us that antiamyloid agents should only be considered as potential prophylactics. By the time symptoms appear, disease progression is largely independent of amyloid and may be primarily tau-driven, spreading from neuron to neuron even when amyloid is effectively targeted by therapeutics. Even the A4 and DIAN studies are likely initiating treatment too late to make anything more than a modest effect with little practical value clinically. I am not suggesting that we drop amyloid as a target, only that we stop making these incremental changes in clinical trial design in the hope of getting a different result.
—Michael S. Wolfe, PhD
Mathias P. Mertes Professor of Medicinal Chemistry
University of Kansas, Lawrence
Preventing surgical site infections in hysterectomy
Surgical site infections are a major source of patient morbidity. They are also an important quality metric for surgeons and hospital systems, and are increasingly being linked to reimbursement.
They occur in approximately 2% of the 600,000 women undergoing hysterectomy in the United States each year. The U.S. Centers for Disease Control and Prevention defines surgical site infection (SSI) as an infection that occurs within 30 days of a procedure in the part of the body where the surgery took place. Most SSIs are superficial incisional, but they also include deep incisional or organ or space infections.
Classification
The incidence of SSI varies according to the classification of the wound, as defined by the National Academy of Sciences.1 Most hysterectomies are classified as clean-contaminated wounds because they involve entry into the mucosa of the genitourinary tract. However, hysterectomy with contamination of bowel flora, or in the setting of acute infection (such as suppurative pelvic inflammatory disease) are considered a contaminated wound class, and are associated with even higher rates of SSI.
Risk factors
The risk factors associated with SSI are both modifiable and unmodifiable. Broadly speaking, they include increased risk to endogenous flora (e.g., wound classification), increased exposure to exogenous flora (e.g., inadequate protection of a wound from external pathogens), and impairment of the body’s immune mechanisms to prevent and overcome infection (e.g., hypothermia and hypoglycemia).
Unmodifiable risk factors include increasing age, a history of radiation exposure, vascular disease, and a history of prior SSIs. Modifiable risk factors include obesity, tobacco use, immunosuppressive medications, hypoalbuminemia, route of hysterectomy, hair removal, preoperative infections (such as bacterial vaginosis), surgical scrub, skin and vaginal preparation, antimicrobial prophylaxis (inappropriate choice or timing, inadequate dosing or redosing), operative time, blood transfusion, surgical skill, and operating room characteristics (ventilation, increased OR traffic, and sterilization of surgical equipment).
Antimicrobial prophylaxis
The CDC and the American College of Obstetricians and Gynecologists (ACOG) have provided clear guidelines regarding methods to reduce SSI in hysterectomy.3,4 There is strong evidence for using antimicrobial prophylaxis for hysterectomy.
It is important that physicians confirm the validity of beta-lactam allergies with patients because there are higher rates of SSI with the use of non–beta-lactam regimens, even those endorsed by the CDC and ACOG.5
Antibiotics should be administered within 1 hour of skin incision, and ideally within 30 minutes. They should be discontinued within 24 hours. Dosing should be adjusted to weight, and antimicrobials should be redosed for long procedures (at intervals of two half-lives), and for increased blood loss.
Skin preparation
Hair removal should be avoided unless necessary for technical reasons. If it is required, it should be performed outside of the operative space using clippers, not razors. For patients colonized with methicillin-resistant S. aureus, there is supporting evidence for pretreatment with mupirocin ointment to the nares, and chlorhexidine showers for 5-10 days. Patients who have bacterial vaginosis should be treated before surgery to decrease the rate of vaginal cuff SSI.
If there is a planned or potential gastrointestinal procedure as part of the hysterectomy, the surgeon should consider using an impervious plastic wound protector in place of, or in addition to, other retractors. Preoperative oral antimicrobials with mechanical bowel preparation have been associated with decreased SSIs; however, this benefit is not observed with mechanical bowel preparation alone.
Wound closure
Surgical technique and wound closure techniques also impact SSI. Minimally invasive and vaginal hysterectomy routes are preferred, as these are associated with the lowest rates of SSI. Antimicrobial-impregnated suture materials appear to be unnecessary. Surgeons should ensure that there is delicate handling of tissues and closure of dead spaces. If the subcutaneous fat space depth measures more than 2.5 cm, it should be reapproximated with a rapidly-absorbing suture material.
Use of electrosurgery versus a scalpel when creating the incision does not appear to influence infection rates, nor does use of staples versus subcuticular suture during closure.7
Using a dilute iodine lavage in the subcutaneous space, opening a sterile closing tray, and having surgeons change gloves prior to skin closure should be considered. The CDC recommends keeping the skin dressing in place for 24 hours postoperatively.
Other strategies
Hyperglycemia is associated with impaired neutrophil response, and therefore blood glucose should be controlled before surgery (hemoglobin A1c levels of less than 7% preoperatively) and immediately postoperatively (less than 180 mg/dL within 18-24 hours after the end of anesthesia).
It is also important to minimize perioperative hypothermia (less than 35.5° F), as this also impairs the body’s immune response. Keeping operative room ambient temperatures higher, minimizing incision size, warming CO2 gas in minimally invasive procedures, warming fluids, and using extrinsic body warmers can help achieve this.
Excessive blood loss should be minimized because blood transfusion is associated with impaired macrophage function and increased risk for SSI.
In addition to teamwide (including nonsurgeon) strict adherence to hand hygiene, OR personnel should avoid unnecessary operating room traffic. Hospital officials should ensure that the facility’s ventilator systems are well maintained and that there is care and maintenance of air handlers.
Many strategies can be employed perioperatively to decrease SSI rates for hysterectomy. We advocate for a protocol-based approach (known as “bundling” strategies) to achieve consistency of practice and to maximize surgeon and institutional improvements in SSI rates. This is similar to the approach outlined in a recent consensus statement from the Council on Patient Safety in Women’s Health Care.8
A comprehensive multidisciplinary approach throughout the perioperative period is necessary. It is imperative that good communication exist with patients regarding SSIs after hysterectomy and how patients, surgeons, and hospitals can together minimize the risks of SSIs.
References
1. Altemeier WA. “Manual on Control of Infection in Surgical Patients” (Philadelphia: Lippincott Williams & Wilkins, 1984).
2. Rev Infect Dis. 1991 Sep-Oct;13(Suppl 10):S821-41.
3. Infect Control Hosp Epidemiol. 2014 Jun;35(6):605-27.
4. Obstet Gynecol. 2009 May;113(5):1180-9.
5. Obstet Gynecol. 2016 Feb;127(2):321-9.
6. Am J Obstet Gynecol. 2005 Feb;192(2):422-5.
7. J Gastrointest Surg. 2016 Dec;20(12):2083-92.
8. Obstet Gynecol. 2016 Dec 7. doi: 10.1097/AOG.0000000000001751.
Dr. Rossi is an assistant professor in the division of gynecologic oncology at the University of North Carolina at Chapel Hill. Dr. Jackson-Moore is an associate professor in gynecologic oncology at UNC. They reported having no relevant financial disclosures.
Surgical site infections are a major source of patient morbidity. They are also an important quality metric for surgeons and hospital systems, and are increasingly being linked to reimbursement.
They occur in approximately 2% of the 600,000 women undergoing hysterectomy in the United States each year. The U.S. Centers for Disease Control and Prevention defines surgical site infection (SSI) as an infection that occurs within 30 days of a procedure in the part of the body where the surgery took place. Most SSIs are superficial incisional, but they also include deep incisional or organ or space infections.
Classification
The incidence of SSI varies according to the classification of the wound, as defined by the National Academy of Sciences.1 Most hysterectomies are classified as clean-contaminated wounds because they involve entry into the mucosa of the genitourinary tract. However, hysterectomy with contamination of bowel flora, or in the setting of acute infection (such as suppurative pelvic inflammatory disease) are considered a contaminated wound class, and are associated with even higher rates of SSI.
Risk factors
The risk factors associated with SSI are both modifiable and unmodifiable. Broadly speaking, they include increased risk to endogenous flora (e.g., wound classification), increased exposure to exogenous flora (e.g., inadequate protection of a wound from external pathogens), and impairment of the body’s immune mechanisms to prevent and overcome infection (e.g., hypothermia and hypoglycemia).
Unmodifiable risk factors include increasing age, a history of radiation exposure, vascular disease, and a history of prior SSIs. Modifiable risk factors include obesity, tobacco use, immunosuppressive medications, hypoalbuminemia, route of hysterectomy, hair removal, preoperative infections (such as bacterial vaginosis), surgical scrub, skin and vaginal preparation, antimicrobial prophylaxis (inappropriate choice or timing, inadequate dosing or redosing), operative time, blood transfusion, surgical skill, and operating room characteristics (ventilation, increased OR traffic, and sterilization of surgical equipment).
Antimicrobial prophylaxis
The CDC and the American College of Obstetricians and Gynecologists (ACOG) have provided clear guidelines regarding methods to reduce SSI in hysterectomy.3,4 There is strong evidence for using antimicrobial prophylaxis for hysterectomy.
It is important that physicians confirm the validity of beta-lactam allergies with patients because there are higher rates of SSI with the use of non–beta-lactam regimens, even those endorsed by the CDC and ACOG.5
Antibiotics should be administered within 1 hour of skin incision, and ideally within 30 minutes. They should be discontinued within 24 hours. Dosing should be adjusted to weight, and antimicrobials should be redosed for long procedures (at intervals of two half-lives), and for increased blood loss.
Skin preparation
Hair removal should be avoided unless necessary for technical reasons. If it is required, it should be performed outside of the operative space using clippers, not razors. For patients colonized with methicillin-resistant S. aureus, there is supporting evidence for pretreatment with mupirocin ointment to the nares, and chlorhexidine showers for 5-10 days. Patients who have bacterial vaginosis should be treated before surgery to decrease the rate of vaginal cuff SSI.
If there is a planned or potential gastrointestinal procedure as part of the hysterectomy, the surgeon should consider using an impervious plastic wound protector in place of, or in addition to, other retractors. Preoperative oral antimicrobials with mechanical bowel preparation have been associated with decreased SSIs; however, this benefit is not observed with mechanical bowel preparation alone.
Wound closure
Surgical technique and wound closure techniques also impact SSI. Minimally invasive and vaginal hysterectomy routes are preferred, as these are associated with the lowest rates of SSI. Antimicrobial-impregnated suture materials appear to be unnecessary. Surgeons should ensure that there is delicate handling of tissues and closure of dead spaces. If the subcutaneous fat space depth measures more than 2.5 cm, it should be reapproximated with a rapidly-absorbing suture material.
Use of electrosurgery versus a scalpel when creating the incision does not appear to influence infection rates, nor does use of staples versus subcuticular suture during closure.7
Using a dilute iodine lavage in the subcutaneous space, opening a sterile closing tray, and having surgeons change gloves prior to skin closure should be considered. The CDC recommends keeping the skin dressing in place for 24 hours postoperatively.
Other strategies
Hyperglycemia is associated with impaired neutrophil response, and therefore blood glucose should be controlled before surgery (hemoglobin A1c levels of less than 7% preoperatively) and immediately postoperatively (less than 180 mg/dL within 18-24 hours after the end of anesthesia).
It is also important to minimize perioperative hypothermia (less than 35.5° F), as this also impairs the body’s immune response. Keeping operative room ambient temperatures higher, minimizing incision size, warming CO2 gas in minimally invasive procedures, warming fluids, and using extrinsic body warmers can help achieve this.
Excessive blood loss should be minimized because blood transfusion is associated with impaired macrophage function and increased risk for SSI.
In addition to teamwide (including nonsurgeon) strict adherence to hand hygiene, OR personnel should avoid unnecessary operating room traffic. Hospital officials should ensure that the facility’s ventilator systems are well maintained and that there is care and maintenance of air handlers.
Many strategies can be employed perioperatively to decrease SSI rates for hysterectomy. We advocate for a protocol-based approach (known as “bundling” strategies) to achieve consistency of practice and to maximize surgeon and institutional improvements in SSI rates. This is similar to the approach outlined in a recent consensus statement from the Council on Patient Safety in Women’s Health Care.8
A comprehensive multidisciplinary approach throughout the perioperative period is necessary. It is imperative that good communication exist with patients regarding SSIs after hysterectomy and how patients, surgeons, and hospitals can together minimize the risks of SSIs.
References
1. Altemeier WA. “Manual on Control of Infection in Surgical Patients” (Philadelphia: Lippincott Williams & Wilkins, 1984).
2. Rev Infect Dis. 1991 Sep-Oct;13(Suppl 10):S821-41.
3. Infect Control Hosp Epidemiol. 2014 Jun;35(6):605-27.
4. Obstet Gynecol. 2009 May;113(5):1180-9.
5. Obstet Gynecol. 2016 Feb;127(2):321-9.
6. Am J Obstet Gynecol. 2005 Feb;192(2):422-5.
7. J Gastrointest Surg. 2016 Dec;20(12):2083-92.
8. Obstet Gynecol. 2016 Dec 7. doi: 10.1097/AOG.0000000000001751.
Dr. Rossi is an assistant professor in the division of gynecologic oncology at the University of North Carolina at Chapel Hill. Dr. Jackson-Moore is an associate professor in gynecologic oncology at UNC. They reported having no relevant financial disclosures.
Surgical site infections are a major source of patient morbidity. They are also an important quality metric for surgeons and hospital systems, and are increasingly being linked to reimbursement.
They occur in approximately 2% of the 600,000 women undergoing hysterectomy in the United States each year. The U.S. Centers for Disease Control and Prevention defines surgical site infection (SSI) as an infection that occurs within 30 days of a procedure in the part of the body where the surgery took place. Most SSIs are superficial incisional, but they also include deep incisional or organ or space infections.
Classification
The incidence of SSI varies according to the classification of the wound, as defined by the National Academy of Sciences.1 Most hysterectomies are classified as clean-contaminated wounds because they involve entry into the mucosa of the genitourinary tract. However, hysterectomy with contamination of bowel flora, or in the setting of acute infection (such as suppurative pelvic inflammatory disease) are considered a contaminated wound class, and are associated with even higher rates of SSI.
Risk factors
The risk factors associated with SSI are both modifiable and unmodifiable. Broadly speaking, they include increased risk to endogenous flora (e.g., wound classification), increased exposure to exogenous flora (e.g., inadequate protection of a wound from external pathogens), and impairment of the body’s immune mechanisms to prevent and overcome infection (e.g., hypothermia and hypoglycemia).
Unmodifiable risk factors include increasing age, a history of radiation exposure, vascular disease, and a history of prior SSIs. Modifiable risk factors include obesity, tobacco use, immunosuppressive medications, hypoalbuminemia, route of hysterectomy, hair removal, preoperative infections (such as bacterial vaginosis), surgical scrub, skin and vaginal preparation, antimicrobial prophylaxis (inappropriate choice or timing, inadequate dosing or redosing), operative time, blood transfusion, surgical skill, and operating room characteristics (ventilation, increased OR traffic, and sterilization of surgical equipment).
Antimicrobial prophylaxis
The CDC and the American College of Obstetricians and Gynecologists (ACOG) have provided clear guidelines regarding methods to reduce SSI in hysterectomy.3,4 There is strong evidence for using antimicrobial prophylaxis for hysterectomy.
It is important that physicians confirm the validity of beta-lactam allergies with patients because there are higher rates of SSI with the use of non–beta-lactam regimens, even those endorsed by the CDC and ACOG.5
Antibiotics should be administered within 1 hour of skin incision, and ideally within 30 minutes. They should be discontinued within 24 hours. Dosing should be adjusted to weight, and antimicrobials should be redosed for long procedures (at intervals of two half-lives), and for increased blood loss.
Skin preparation
Hair removal should be avoided unless necessary for technical reasons. If it is required, it should be performed outside of the operative space using clippers, not razors. For patients colonized with methicillin-resistant S. aureus, there is supporting evidence for pretreatment with mupirocin ointment to the nares, and chlorhexidine showers for 5-10 days. Patients who have bacterial vaginosis should be treated before surgery to decrease the rate of vaginal cuff SSI.
If there is a planned or potential gastrointestinal procedure as part of the hysterectomy, the surgeon should consider using an impervious plastic wound protector in place of, or in addition to, other retractors. Preoperative oral antimicrobials with mechanical bowel preparation have been associated with decreased SSIs; however, this benefit is not observed with mechanical bowel preparation alone.
Wound closure
Surgical technique and wound closure techniques also impact SSI. Minimally invasive and vaginal hysterectomy routes are preferred, as these are associated with the lowest rates of SSI. Antimicrobial-impregnated suture materials appear to be unnecessary. Surgeons should ensure that there is delicate handling of tissues and closure of dead spaces. If the subcutaneous fat space depth measures more than 2.5 cm, it should be reapproximated with a rapidly-absorbing suture material.
Use of electrosurgery versus a scalpel when creating the incision does not appear to influence infection rates, nor does use of staples versus subcuticular suture during closure.7
Using a dilute iodine lavage in the subcutaneous space, opening a sterile closing tray, and having surgeons change gloves prior to skin closure should be considered. The CDC recommends keeping the skin dressing in place for 24 hours postoperatively.
Other strategies
Hyperglycemia is associated with impaired neutrophil response, and therefore blood glucose should be controlled before surgery (hemoglobin A1c levels of less than 7% preoperatively) and immediately postoperatively (less than 180 mg/dL within 18-24 hours after the end of anesthesia).
It is also important to minimize perioperative hypothermia (less than 35.5° F), as this also impairs the body’s immune response. Keeping operative room ambient temperatures higher, minimizing incision size, warming CO2 gas in minimally invasive procedures, warming fluids, and using extrinsic body warmers can help achieve this.
Excessive blood loss should be minimized because blood transfusion is associated with impaired macrophage function and increased risk for SSI.
In addition to teamwide (including nonsurgeon) strict adherence to hand hygiene, OR personnel should avoid unnecessary operating room traffic. Hospital officials should ensure that the facility’s ventilator systems are well maintained and that there is care and maintenance of air handlers.
Many strategies can be employed perioperatively to decrease SSI rates for hysterectomy. We advocate for a protocol-based approach (known as “bundling” strategies) to achieve consistency of practice and to maximize surgeon and institutional improvements in SSI rates. This is similar to the approach outlined in a recent consensus statement from the Council on Patient Safety in Women’s Health Care.8
A comprehensive multidisciplinary approach throughout the perioperative period is necessary. It is imperative that good communication exist with patients regarding SSIs after hysterectomy and how patients, surgeons, and hospitals can together minimize the risks of SSIs.
References
1. Altemeier WA. “Manual on Control of Infection in Surgical Patients” (Philadelphia: Lippincott Williams & Wilkins, 1984).
2. Rev Infect Dis. 1991 Sep-Oct;13(Suppl 10):S821-41.
3. Infect Control Hosp Epidemiol. 2014 Jun;35(6):605-27.
4. Obstet Gynecol. 2009 May;113(5):1180-9.
5. Obstet Gynecol. 2016 Feb;127(2):321-9.
6. Am J Obstet Gynecol. 2005 Feb;192(2):422-5.
7. J Gastrointest Surg. 2016 Dec;20(12):2083-92.
8. Obstet Gynecol. 2016 Dec 7. doi: 10.1097/AOG.0000000000001751.
Dr. Rossi is an assistant professor in the division of gynecologic oncology at the University of North Carolina at Chapel Hill. Dr. Jackson-Moore is an associate professor in gynecologic oncology at UNC. They reported having no relevant financial disclosures.
Letters to the Editor: Benefit of self-administered vaginal lidocaine gel in IUD placement
“BENEFIT OF SELF-ADMINISTERED VAGINAL LIDOCAINE GEL IN IUD PLACEMENT"
ANDREW M. KAUNITZ, MD (COMMENTARY; DECEMBER 2016)
Use anesthesia for in-office GYN procedures
The recent article by Dr. Kaunitz on the use of self-administered lidocaine gel prior to intrauterine device (IUD) placement was excellent. Having been known as the “lidocaine queen” in the Department of ObGyn at the Mayo Clinic, I feel strongly that gynecologic office procedures should always involve some form of anesthesia, whether with topical lidocaine, intracervical lidocaine, or paracervical block. Such anesthesia often makes the procedure a “nonevent” for the patient. While Dr. Kaunitz describes the use of a fine-toothed tenaculum, I have found that after administration of lidocaine gel, an Allis clamp applied superficially to the cervix provides sufficient traction, is often not detected by the patient, and does not leave any holes. It is unusual for it to slip off.
It is important to teach residents that it is not necessary for women to “tolerate” pain to have good health. I use the above techniques for endometrial biopsy and cervical biopsy as well—there is never a reason for a woman’s biopsy to be done without anesthesia.
Ingrid Carlson, MD
Ponte Vedra, Florida
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.
“BENEFIT OF SELF-ADMINISTERED VAGINAL LIDOCAINE GEL IN IUD PLACEMENT"
ANDREW M. KAUNITZ, MD (COMMENTARY; DECEMBER 2016)
Use anesthesia for in-office GYN procedures
The recent article by Dr. Kaunitz on the use of self-administered lidocaine gel prior to intrauterine device (IUD) placement was excellent. Having been known as the “lidocaine queen” in the Department of ObGyn at the Mayo Clinic, I feel strongly that gynecologic office procedures should always involve some form of anesthesia, whether with topical lidocaine, intracervical lidocaine, or paracervical block. Such anesthesia often makes the procedure a “nonevent” for the patient. While Dr. Kaunitz describes the use of a fine-toothed tenaculum, I have found that after administration of lidocaine gel, an Allis clamp applied superficially to the cervix provides sufficient traction, is often not detected by the patient, and does not leave any holes. It is unusual for it to slip off.
It is important to teach residents that it is not necessary for women to “tolerate” pain to have good health. I use the above techniques for endometrial biopsy and cervical biopsy as well—there is never a reason for a woman’s biopsy to be done without anesthesia.
Ingrid Carlson, MD
Ponte Vedra, Florida
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.
“BENEFIT OF SELF-ADMINISTERED VAGINAL LIDOCAINE GEL IN IUD PLACEMENT"
ANDREW M. KAUNITZ, MD (COMMENTARY; DECEMBER 2016)
Use anesthesia for in-office GYN procedures
The recent article by Dr. Kaunitz on the use of self-administered lidocaine gel prior to intrauterine device (IUD) placement was excellent. Having been known as the “lidocaine queen” in the Department of ObGyn at the Mayo Clinic, I feel strongly that gynecologic office procedures should always involve some form of anesthesia, whether with topical lidocaine, intracervical lidocaine, or paracervical block. Such anesthesia often makes the procedure a “nonevent” for the patient. While Dr. Kaunitz describes the use of a fine-toothed tenaculum, I have found that after administration of lidocaine gel, an Allis clamp applied superficially to the cervix provides sufficient traction, is often not detected by the patient, and does not leave any holes. It is unusual for it to slip off.
It is important to teach residents that it is not necessary for women to “tolerate” pain to have good health. I use the above techniques for endometrial biopsy and cervical biopsy as well—there is never a reason for a woman’s biopsy to be done without anesthesia.
Ingrid Carlson, MD
Ponte Vedra, Florida
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.
Letters to the Editor: Avoid uterine vessels when injecting vasopressin
“DO YOU UTILIZE VASOPRESSIN IN YOUR DIFFICULT CESAREAN DELIVERY SURGERIES?”
ROBERT L. BARBIERI, MD (EDITORIAL; NOVEMBER 2016)
Avoid uterine vessels when injecting vasopressin
Thank you for your recent editorial discussing using vasopressin in difficult cesarean deliveries. I am very interested in using vasopressin for our placenta previa cases.
I reviewed the Kato et al article that Dr. Barbieri referenced, and the authors note a risk of injecting vasopressin into a vessel.1 If you are injecting into the placental bed, how can you confirm you are not in a vessel? (When you withdraw, you will get some blood regardless.)
Sara Garmel, MD
Dearborn, Michigan
REFERENCE
- Kato S, Tanabe A, Kanki K, et al. Local injection of vasopressin reduces the blood loss during cesarean section in placenta previa. J Obstet Gynaecol Res. 2014;40(5):1249–1256.
Dr. Barbieri responds
I agree with Dr. Garmel that we should avoid the intravascular injection of vasopressin. As I noted in the editorial, “I prefer to inject vasopressin in the subserosa of the uterus rather than inject it in a highly vascular area such as the subendometrium or near the uterine artery and vein.” Subserosal injection creates a depot bleb of vasopressin that is absorbed over a few minutes. You can visualize the reduced blood flow to the uterus following vasopressin injection because the uterus blanches and the diameter of the uterine vessels decreases significantly.
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.
“DO YOU UTILIZE VASOPRESSIN IN YOUR DIFFICULT CESAREAN DELIVERY SURGERIES?”
ROBERT L. BARBIERI, MD (EDITORIAL; NOVEMBER 2016)
Avoid uterine vessels when injecting vasopressin
Thank you for your recent editorial discussing using vasopressin in difficult cesarean deliveries. I am very interested in using vasopressin for our placenta previa cases.
I reviewed the Kato et al article that Dr. Barbieri referenced, and the authors note a risk of injecting vasopressin into a vessel.1 If you are injecting into the placental bed, how can you confirm you are not in a vessel? (When you withdraw, you will get some blood regardless.)
Sara Garmel, MD
Dearborn, Michigan
REFERENCE
- Kato S, Tanabe A, Kanki K, et al. Local injection of vasopressin reduces the blood loss during cesarean section in placenta previa. J Obstet Gynaecol Res. 2014;40(5):1249–1256.
Dr. Barbieri responds
I agree with Dr. Garmel that we should avoid the intravascular injection of vasopressin. As I noted in the editorial, “I prefer to inject vasopressin in the subserosa of the uterus rather than inject it in a highly vascular area such as the subendometrium or near the uterine artery and vein.” Subserosal injection creates a depot bleb of vasopressin that is absorbed over a few minutes. You can visualize the reduced blood flow to the uterus following vasopressin injection because the uterus blanches and the diameter of the uterine vessels decreases significantly.
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.
“DO YOU UTILIZE VASOPRESSIN IN YOUR DIFFICULT CESAREAN DELIVERY SURGERIES?”
ROBERT L. BARBIERI, MD (EDITORIAL; NOVEMBER 2016)
Avoid uterine vessels when injecting vasopressin
Thank you for your recent editorial discussing using vasopressin in difficult cesarean deliveries. I am very interested in using vasopressin for our placenta previa cases.
I reviewed the Kato et al article that Dr. Barbieri referenced, and the authors note a risk of injecting vasopressin into a vessel.1 If you are injecting into the placental bed, how can you confirm you are not in a vessel? (When you withdraw, you will get some blood regardless.)
Sara Garmel, MD
Dearborn, Michigan
REFERENCE
- Kato S, Tanabe A, Kanki K, et al. Local injection of vasopressin reduces the blood loss during cesarean section in placenta previa. J Obstet Gynaecol Res. 2014;40(5):1249–1256.
Dr. Barbieri responds
I agree with Dr. Garmel that we should avoid the intravascular injection of vasopressin. As I noted in the editorial, “I prefer to inject vasopressin in the subserosa of the uterus rather than inject it in a highly vascular area such as the subendometrium or near the uterine artery and vein.” Subserosal injection creates a depot bleb of vasopressin that is absorbed over a few minutes. You can visualize the reduced blood flow to the uterus following vasopressin injection because the uterus blanches and the diameter of the uterine vessels decreases significantly.
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.
Letters to the Editor: Patient with a breast mass: Why did she pursue litigation?
“PATIENT WITH A BREAST MASS: WHY DID SHE PURSUE LITIGATION?”
JOSEPH S. SANFILIPPO, MD, MBA, AND STEVEN R. SMITH, JD (WHAT'S THE VERDICT?; DECEMBER 2016)
Clear communication is often key to avoiding litigation
Thank you for the article concerning the patient who commenced action for delay in diagnosis of her breast lesion. In my opinion the gynecologist lost control of the situation because of inadequate communication with the patient either on his or her part and/or on the part of the staff.
J. S. Calabrese, MD, JD
Buffalo, New York
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.
“PATIENT WITH A BREAST MASS: WHY DID SHE PURSUE LITIGATION?”
JOSEPH S. SANFILIPPO, MD, MBA, AND STEVEN R. SMITH, JD (WHAT'S THE VERDICT?; DECEMBER 2016)
Clear communication is often key to avoiding litigation
Thank you for the article concerning the patient who commenced action for delay in diagnosis of her breast lesion. In my opinion the gynecologist lost control of the situation because of inadequate communication with the patient either on his or her part and/or on the part of the staff.
J. S. Calabrese, MD, JD
Buffalo, New York
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.
“PATIENT WITH A BREAST MASS: WHY DID SHE PURSUE LITIGATION?”
JOSEPH S. SANFILIPPO, MD, MBA, AND STEVEN R. SMITH, JD (WHAT'S THE VERDICT?; DECEMBER 2016)
Clear communication is often key to avoiding litigation
Thank you for the article concerning the patient who commenced action for delay in diagnosis of her breast lesion. In my opinion the gynecologist lost control of the situation because of inadequate communication with the patient either on his or her part and/or on the part of the staff.
J. S. Calabrese, MD, JD
Buffalo, New York
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.
Point/Counterpoint: Is limb salvage always best in diabetes?
Salvage limbs at all costs
Aggressive limb salvage in people with diabetes leads to an overall reduction in cost not only economically, but also from the patient’s perspective. The vast majority of diabetic patients with critical ischemia are actually good candidates for limb salvage. Tragically, many of these patients are never referred for evaluation for limb salvage because of misconceptions about the pathophysiology of the disease.
An argument against limb salvage is that primary amputation prevents or shortens the course of wound care and enables patients to become ambulatory, albeit with a prosthesis, faster. However, in the modern era of vascular surgery, revascularization can be performed successfully with minimal mortality and excellent rates of limb salvage, especially when it’s done within a team-based approach.
The mortality in primary amputation is shockingly high, anywhere from 5% to 23% higher than revascularization alone, and the major complication rate of amputation associated with diabetes is also unacceptably high – up to 37%. This is in contrast to a 17% rate in major nonamputation vascular surgery and 1%-5% in endovascular procedures (BMC Nephrol. 2005;6:3).
We can’t ignore the economic burden this places on the country. In 2014, primary amputations cost the health care system $11 billion annually, and that is expected to grow to more than $25 billion in the next several years, according to the SAGE Group. It’s important to keep in mind that Medicare covers over 80% of this cost.
A number of studies have shown that conservative management with wound care and amputation is more cost effective than primary amputation in ambulatory, independent adults. Data can be difficult to interpret because of different recording strategies for all the costs associated with amputation, but a single-institution study concluded that revascularization costs almost $5,280 more than expectant management, but $33,900 less than primary amputation alone (Cardiovasc Surg. 1999;7;62-9).
We must also consider the costs of revision after primary amputation; above-the-knee amputation has a 12% in-hospital revision rate, and below-the-knee amputation about 20%. Endovascular interventions, on the other hand, have a 1%-9% in-hospital revision rate, and only 2%-4% of these patients will go on to require an amputation during the same admission (Eur J Vasc Endovasc Surg. 2006;32:484-90; Arch Phys Med Rehabil. 2005;86:480-6).This does not include the costs of those complications as well as other indirect costs of amputation, such as nursing home care and living situation modification (Int J Behav Med. 2016;23:714-21; Pak J Med Sci. 2014; 30:1044-9). They quickly add up to that $25 billion.
The proponents of primary amputation tell us that it leads to quicker recovery time and an earlier time to ambulation. However, only 47% of patients will actually ambulate after amputation, in contrast to 97% who will ambulate after limb salvage as a primary procedure. In a nonambulatory cohort, 21% of those patients go on to regain functional status that was lost prior to surgery (J Vasc Surg. 1997;25;287-95).
Many question if our success with vascular surgery over the past few decades can translate to helping the most difficult subset of patients. An Italian study reported on a cohort of diabetic vs. nondiabetic patients and determined both groups have similar amputation-free rates after infrainguinal arterial reconstruction for critical limb ischemia, with excellent primary and secondary patency rates and a limb salvage rate of 88% at 5 years (J Vasc Surg. 2014;59:708-19). This tells us that we do have the skill set necessary to save these limbs.
A multidisciplinary limb preservation team is paramount to the success of any limb salvage program. A revascularization team should be in place which uses early intervention to achieve the highest limb salvage rates possible. Wound care needs to be an integrated part of it. Advanced podiatric reconstructive surgery also is key because this can provide complex foot reconstructions and help ambulatory patients return home.
Dr. Trissa A. Babrowski is an assistant professor of surgery, specializing in vascular surgery and endovascular therapy, at the University of Chicago Heart and Vascular Center. She had no financial relationships to disclose.
Primary amputation can be OK
I am not an amputationalist. I do practice limb salvage. In fact I’m probably the most aggressive limb salvage surgeon in my hospital. But primary amputation is a completely acceptable option for a selected group of patients with diabetes. We should not try to do limb salvage “at all costs.”
I do not find this to be a contradictory position. In fact, I think it adds credence to my support of limb salvage that I think primary amputation can be OK. In all honesty, there are very few things in life that should be done at all costs.
A study out of Loma Linda University involving patients with CLI compared primary amputation vs. revascularization; 43% of patients had a primary amputation (Ann Vasc Surg. 2007;21:458-63). A multivariate analysis showed that patients with major tissue loss, end-stage renal disease (ESRD), diabetes and nonambulatory status were more likely to undergo primary amputation rather than revascularization.
While major tissue loss (Rutherford category 6) is certainly an indication for primary amputation, ambulatory status can represent a gray area in determining the best course. ESRD and diabetes are much more nonspecific factors; probably more than 10% of the patients that we see with CLI have ESRD. Also, 50%-70% of these patients with CLI, and in some series even higher percentages, have diabetes. Thus, these factors by themselves do not assist us in determining which patients potentially should be offered primary amputation vs. revascularization.
In general, we know that we can get good results in limb bypass or revascularization in patients with CLI: The PREVENT III multicenter trial, with the use of the vein as the conduit, showed 1-year limb salvage rates of 88% in these high-risk patients (J Vasc Surg. 2006;43:742-51). However, one of the major risk factors that adversely affected outcome was ESRD.
We know that ESRD is a significant predictor of lowering our chances of saving a limb successfully. Knowing the cost of multiple continued episodes of revascularization in these patients prior to proceeding with an amputation, it’s intuitive that these patients would benefit from a more precise process in their treatment from the beginning. A number of papers have concluded that a primary amputation may be the preferred approach in patients with ESRD.
Can we preoperatively predict which patients with CLI will fail operative revascularization? Data from the New England Vascular Quality Initiative identified eight variables associated with failure of revascularization, among them age younger than 59, ESRD, diabetes, CLI, conduit requiring venovenostomy, tarsal target, and nursing home residence (Ann Vasc Surg. 2010;24:57-68). The presence of three or more risk factors has a 27.7% risk of limb loss and/or graft thrombosis within 1 year.
Postponing amputation is a major cost issue. Direct costs of bypass for critical limb ischemia were $3.6 billion in 2004 (J Vasc Surg. 2011;54:1021-31), and we know that a functional outcome can be problematic in this patient group. Factors associated with a poor functional outcome include dementia, dependent-living situation preoperatively and nonambulatory status.
Unfortunately, there are not a lot of data that deal with quality of life outcomes for patients with CLI who have undergone bypass. Using a point system comprised of dialysis (4 points), tissue loss (3 points), age above 75 (2 points), hematocrit less than or equal to 30 (2 points), and coronary artery disease (1 point), a follow-up study of patients in the PREVENT III trial found that a high-risk group (greater than or equal to 8 points) had an amputation-free survival of only 45% (J Vasc Surg. 2009;50:769-75). Again, these results do not justify the effort and costs of limb salvage in this high-risk patient group.
We should consider the following options carefully in selecting a cost-effective patient-focused approach in patients with CLI: wound care, primary amputation, bypass revascularization, or endovascular revascularization. I would argue that the vascular surgeon who is qualified as an expert in all of the above is best positioned to select an appropriate plan of treatment based upon the patient’s risk factors, wound factors, ambulatory ability, pattern of disease, severity of ischemia, and living status.
Thus, upon presentation, a patient with CLI should undergo confirmatory tests and optimize his or her risk factors. The vascular surgeon then has the option, in discussion with the patient and family, to pursue an appropriate treatment plan inclusive of primary amputation – not one of limb salvage “at all costs.”
Primary amputation should be used in situations where there is dementia and nonambulatory status, and in patients who are poor candidates for revascularization because of high risk of failure and limited life expectancy. The recently developed WIfI (wound, ischemia, and foot infection) classification can also be utilized, as stage 4 WIfI classification is associated with high risk of limb loss – 38%-40% at 1 year.
Primary amputation is an option that can result in better care overall, and it is a cost-effective approach for a selected group of patients. We should not try to do limb salvage at all cost. Primary amputation, in selected patients, is OK.
Dr. Timothy J. Nypaver is head of vascular surgery at Henry Ford Hospital, Detroit. He had no financial relationships to disclose.
Salvage limbs at all costs
Aggressive limb salvage in people with diabetes leads to an overall reduction in cost not only economically, but also from the patient’s perspective. The vast majority of diabetic patients with critical ischemia are actually good candidates for limb salvage. Tragically, many of these patients are never referred for evaluation for limb salvage because of misconceptions about the pathophysiology of the disease.
An argument against limb salvage is that primary amputation prevents or shortens the course of wound care and enables patients to become ambulatory, albeit with a prosthesis, faster. However, in the modern era of vascular surgery, revascularization can be performed successfully with minimal mortality and excellent rates of limb salvage, especially when it’s done within a team-based approach.
The mortality in primary amputation is shockingly high, anywhere from 5% to 23% higher than revascularization alone, and the major complication rate of amputation associated with diabetes is also unacceptably high – up to 37%. This is in contrast to a 17% rate in major nonamputation vascular surgery and 1%-5% in endovascular procedures (BMC Nephrol. 2005;6:3).
We can’t ignore the economic burden this places on the country. In 2014, primary amputations cost the health care system $11 billion annually, and that is expected to grow to more than $25 billion in the next several years, according to the SAGE Group. It’s important to keep in mind that Medicare covers over 80% of this cost.
A number of studies have shown that conservative management with wound care and amputation is more cost effective than primary amputation in ambulatory, independent adults. Data can be difficult to interpret because of different recording strategies for all the costs associated with amputation, but a single-institution study concluded that revascularization costs almost $5,280 more than expectant management, but $33,900 less than primary amputation alone (Cardiovasc Surg. 1999;7;62-9).
We must also consider the costs of revision after primary amputation; above-the-knee amputation has a 12% in-hospital revision rate, and below-the-knee amputation about 20%. Endovascular interventions, on the other hand, have a 1%-9% in-hospital revision rate, and only 2%-4% of these patients will go on to require an amputation during the same admission (Eur J Vasc Endovasc Surg. 2006;32:484-90; Arch Phys Med Rehabil. 2005;86:480-6).This does not include the costs of those complications as well as other indirect costs of amputation, such as nursing home care and living situation modification (Int J Behav Med. 2016;23:714-21; Pak J Med Sci. 2014; 30:1044-9). They quickly add up to that $25 billion.
The proponents of primary amputation tell us that it leads to quicker recovery time and an earlier time to ambulation. However, only 47% of patients will actually ambulate after amputation, in contrast to 97% who will ambulate after limb salvage as a primary procedure. In a nonambulatory cohort, 21% of those patients go on to regain functional status that was lost prior to surgery (J Vasc Surg. 1997;25;287-95).
Many question if our success with vascular surgery over the past few decades can translate to helping the most difficult subset of patients. An Italian study reported on a cohort of diabetic vs. nondiabetic patients and determined both groups have similar amputation-free rates after infrainguinal arterial reconstruction for critical limb ischemia, with excellent primary and secondary patency rates and a limb salvage rate of 88% at 5 years (J Vasc Surg. 2014;59:708-19). This tells us that we do have the skill set necessary to save these limbs.
A multidisciplinary limb preservation team is paramount to the success of any limb salvage program. A revascularization team should be in place which uses early intervention to achieve the highest limb salvage rates possible. Wound care needs to be an integrated part of it. Advanced podiatric reconstructive surgery also is key because this can provide complex foot reconstructions and help ambulatory patients return home.
Dr. Trissa A. Babrowski is an assistant professor of surgery, specializing in vascular surgery and endovascular therapy, at the University of Chicago Heart and Vascular Center. She had no financial relationships to disclose.
Primary amputation can be OK
I am not an amputationalist. I do practice limb salvage. In fact I’m probably the most aggressive limb salvage surgeon in my hospital. But primary amputation is a completely acceptable option for a selected group of patients with diabetes. We should not try to do limb salvage “at all costs.”
I do not find this to be a contradictory position. In fact, I think it adds credence to my support of limb salvage that I think primary amputation can be OK. In all honesty, there are very few things in life that should be done at all costs.
A study out of Loma Linda University involving patients with CLI compared primary amputation vs. revascularization; 43% of patients had a primary amputation (Ann Vasc Surg. 2007;21:458-63). A multivariate analysis showed that patients with major tissue loss, end-stage renal disease (ESRD), diabetes and nonambulatory status were more likely to undergo primary amputation rather than revascularization.
While major tissue loss (Rutherford category 6) is certainly an indication for primary amputation, ambulatory status can represent a gray area in determining the best course. ESRD and diabetes are much more nonspecific factors; probably more than 10% of the patients that we see with CLI have ESRD. Also, 50%-70% of these patients with CLI, and in some series even higher percentages, have diabetes. Thus, these factors by themselves do not assist us in determining which patients potentially should be offered primary amputation vs. revascularization.
In general, we know that we can get good results in limb bypass or revascularization in patients with CLI: The PREVENT III multicenter trial, with the use of the vein as the conduit, showed 1-year limb salvage rates of 88% in these high-risk patients (J Vasc Surg. 2006;43:742-51). However, one of the major risk factors that adversely affected outcome was ESRD.
We know that ESRD is a significant predictor of lowering our chances of saving a limb successfully. Knowing the cost of multiple continued episodes of revascularization in these patients prior to proceeding with an amputation, it’s intuitive that these patients would benefit from a more precise process in their treatment from the beginning. A number of papers have concluded that a primary amputation may be the preferred approach in patients with ESRD.
Can we preoperatively predict which patients with CLI will fail operative revascularization? Data from the New England Vascular Quality Initiative identified eight variables associated with failure of revascularization, among them age younger than 59, ESRD, diabetes, CLI, conduit requiring venovenostomy, tarsal target, and nursing home residence (Ann Vasc Surg. 2010;24:57-68). The presence of three or more risk factors has a 27.7% risk of limb loss and/or graft thrombosis within 1 year.
Postponing amputation is a major cost issue. Direct costs of bypass for critical limb ischemia were $3.6 billion in 2004 (J Vasc Surg. 2011;54:1021-31), and we know that a functional outcome can be problematic in this patient group. Factors associated with a poor functional outcome include dementia, dependent-living situation preoperatively and nonambulatory status.
Unfortunately, there are not a lot of data that deal with quality of life outcomes for patients with CLI who have undergone bypass. Using a point system comprised of dialysis (4 points), tissue loss (3 points), age above 75 (2 points), hematocrit less than or equal to 30 (2 points), and coronary artery disease (1 point), a follow-up study of patients in the PREVENT III trial found that a high-risk group (greater than or equal to 8 points) had an amputation-free survival of only 45% (J Vasc Surg. 2009;50:769-75). Again, these results do not justify the effort and costs of limb salvage in this high-risk patient group.
We should consider the following options carefully in selecting a cost-effective patient-focused approach in patients with CLI: wound care, primary amputation, bypass revascularization, or endovascular revascularization. I would argue that the vascular surgeon who is qualified as an expert in all of the above is best positioned to select an appropriate plan of treatment based upon the patient’s risk factors, wound factors, ambulatory ability, pattern of disease, severity of ischemia, and living status.
Thus, upon presentation, a patient with CLI should undergo confirmatory tests and optimize his or her risk factors. The vascular surgeon then has the option, in discussion with the patient and family, to pursue an appropriate treatment plan inclusive of primary amputation – not one of limb salvage “at all costs.”
Primary amputation should be used in situations where there is dementia and nonambulatory status, and in patients who are poor candidates for revascularization because of high risk of failure and limited life expectancy. The recently developed WIfI (wound, ischemia, and foot infection) classification can also be utilized, as stage 4 WIfI classification is associated with high risk of limb loss – 38%-40% at 1 year.
Primary amputation is an option that can result in better care overall, and it is a cost-effective approach for a selected group of patients. We should not try to do limb salvage at all cost. Primary amputation, in selected patients, is OK.
Dr. Timothy J. Nypaver is head of vascular surgery at Henry Ford Hospital, Detroit. He had no financial relationships to disclose.
Salvage limbs at all costs
Aggressive limb salvage in people with diabetes leads to an overall reduction in cost not only economically, but also from the patient’s perspective. The vast majority of diabetic patients with critical ischemia are actually good candidates for limb salvage. Tragically, many of these patients are never referred for evaluation for limb salvage because of misconceptions about the pathophysiology of the disease.
An argument against limb salvage is that primary amputation prevents or shortens the course of wound care and enables patients to become ambulatory, albeit with a prosthesis, faster. However, in the modern era of vascular surgery, revascularization can be performed successfully with minimal mortality and excellent rates of limb salvage, especially when it’s done within a team-based approach.
The mortality in primary amputation is shockingly high, anywhere from 5% to 23% higher than revascularization alone, and the major complication rate of amputation associated with diabetes is also unacceptably high – up to 37%. This is in contrast to a 17% rate in major nonamputation vascular surgery and 1%-5% in endovascular procedures (BMC Nephrol. 2005;6:3).
We can’t ignore the economic burden this places on the country. In 2014, primary amputations cost the health care system $11 billion annually, and that is expected to grow to more than $25 billion in the next several years, according to the SAGE Group. It’s important to keep in mind that Medicare covers over 80% of this cost.
A number of studies have shown that conservative management with wound care and amputation is more cost effective than primary amputation in ambulatory, independent adults. Data can be difficult to interpret because of different recording strategies for all the costs associated with amputation, but a single-institution study concluded that revascularization costs almost $5,280 more than expectant management, but $33,900 less than primary amputation alone (Cardiovasc Surg. 1999;7;62-9).
We must also consider the costs of revision after primary amputation; above-the-knee amputation has a 12% in-hospital revision rate, and below-the-knee amputation about 20%. Endovascular interventions, on the other hand, have a 1%-9% in-hospital revision rate, and only 2%-4% of these patients will go on to require an amputation during the same admission (Eur J Vasc Endovasc Surg. 2006;32:484-90; Arch Phys Med Rehabil. 2005;86:480-6).This does not include the costs of those complications as well as other indirect costs of amputation, such as nursing home care and living situation modification (Int J Behav Med. 2016;23:714-21; Pak J Med Sci. 2014; 30:1044-9). They quickly add up to that $25 billion.
The proponents of primary amputation tell us that it leads to quicker recovery time and an earlier time to ambulation. However, only 47% of patients will actually ambulate after amputation, in contrast to 97% who will ambulate after limb salvage as a primary procedure. In a nonambulatory cohort, 21% of those patients go on to regain functional status that was lost prior to surgery (J Vasc Surg. 1997;25;287-95).
Many question if our success with vascular surgery over the past few decades can translate to helping the most difficult subset of patients. An Italian study reported on a cohort of diabetic vs. nondiabetic patients and determined both groups have similar amputation-free rates after infrainguinal arterial reconstruction for critical limb ischemia, with excellent primary and secondary patency rates and a limb salvage rate of 88% at 5 years (J Vasc Surg. 2014;59:708-19). This tells us that we do have the skill set necessary to save these limbs.
A multidisciplinary limb preservation team is paramount to the success of any limb salvage program. A revascularization team should be in place which uses early intervention to achieve the highest limb salvage rates possible. Wound care needs to be an integrated part of it. Advanced podiatric reconstructive surgery also is key because this can provide complex foot reconstructions and help ambulatory patients return home.
Dr. Trissa A. Babrowski is an assistant professor of surgery, specializing in vascular surgery and endovascular therapy, at the University of Chicago Heart and Vascular Center. She had no financial relationships to disclose.
Primary amputation can be OK
I am not an amputationalist. I do practice limb salvage. In fact I’m probably the most aggressive limb salvage surgeon in my hospital. But primary amputation is a completely acceptable option for a selected group of patients with diabetes. We should not try to do limb salvage “at all costs.”
I do not find this to be a contradictory position. In fact, I think it adds credence to my support of limb salvage that I think primary amputation can be OK. In all honesty, there are very few things in life that should be done at all costs.
A study out of Loma Linda University involving patients with CLI compared primary amputation vs. revascularization; 43% of patients had a primary amputation (Ann Vasc Surg. 2007;21:458-63). A multivariate analysis showed that patients with major tissue loss, end-stage renal disease (ESRD), diabetes and nonambulatory status were more likely to undergo primary amputation rather than revascularization.
While major tissue loss (Rutherford category 6) is certainly an indication for primary amputation, ambulatory status can represent a gray area in determining the best course. ESRD and diabetes are much more nonspecific factors; probably more than 10% of the patients that we see with CLI have ESRD. Also, 50%-70% of these patients with CLI, and in some series even higher percentages, have diabetes. Thus, these factors by themselves do not assist us in determining which patients potentially should be offered primary amputation vs. revascularization.
In general, we know that we can get good results in limb bypass or revascularization in patients with CLI: The PREVENT III multicenter trial, with the use of the vein as the conduit, showed 1-year limb salvage rates of 88% in these high-risk patients (J Vasc Surg. 2006;43:742-51). However, one of the major risk factors that adversely affected outcome was ESRD.
We know that ESRD is a significant predictor of lowering our chances of saving a limb successfully. Knowing the cost of multiple continued episodes of revascularization in these patients prior to proceeding with an amputation, it’s intuitive that these patients would benefit from a more precise process in their treatment from the beginning. A number of papers have concluded that a primary amputation may be the preferred approach in patients with ESRD.
Can we preoperatively predict which patients with CLI will fail operative revascularization? Data from the New England Vascular Quality Initiative identified eight variables associated with failure of revascularization, among them age younger than 59, ESRD, diabetes, CLI, conduit requiring venovenostomy, tarsal target, and nursing home residence (Ann Vasc Surg. 2010;24:57-68). The presence of three or more risk factors has a 27.7% risk of limb loss and/or graft thrombosis within 1 year.
Postponing amputation is a major cost issue. Direct costs of bypass for critical limb ischemia were $3.6 billion in 2004 (J Vasc Surg. 2011;54:1021-31), and we know that a functional outcome can be problematic in this patient group. Factors associated with a poor functional outcome include dementia, dependent-living situation preoperatively and nonambulatory status.
Unfortunately, there are not a lot of data that deal with quality of life outcomes for patients with CLI who have undergone bypass. Using a point system comprised of dialysis (4 points), tissue loss (3 points), age above 75 (2 points), hematocrit less than or equal to 30 (2 points), and coronary artery disease (1 point), a follow-up study of patients in the PREVENT III trial found that a high-risk group (greater than or equal to 8 points) had an amputation-free survival of only 45% (J Vasc Surg. 2009;50:769-75). Again, these results do not justify the effort and costs of limb salvage in this high-risk patient group.
We should consider the following options carefully in selecting a cost-effective patient-focused approach in patients with CLI: wound care, primary amputation, bypass revascularization, or endovascular revascularization. I would argue that the vascular surgeon who is qualified as an expert in all of the above is best positioned to select an appropriate plan of treatment based upon the patient’s risk factors, wound factors, ambulatory ability, pattern of disease, severity of ischemia, and living status.
Thus, upon presentation, a patient with CLI should undergo confirmatory tests and optimize his or her risk factors. The vascular surgeon then has the option, in discussion with the patient and family, to pursue an appropriate treatment plan inclusive of primary amputation – not one of limb salvage “at all costs.”
Primary amputation should be used in situations where there is dementia and nonambulatory status, and in patients who are poor candidates for revascularization because of high risk of failure and limited life expectancy. The recently developed WIfI (wound, ischemia, and foot infection) classification can also be utilized, as stage 4 WIfI classification is associated with high risk of limb loss – 38%-40% at 1 year.
Primary amputation is an option that can result in better care overall, and it is a cost-effective approach for a selected group of patients. We should not try to do limb salvage at all cost. Primary amputation, in selected patients, is OK.
Dr. Timothy J. Nypaver is head of vascular surgery at Henry Ford Hospital, Detroit. He had no financial relationships to disclose.