Commentary

In an increasingly sleepless society inundated with caffeine drinks and social media, it is not surprising that 15%-30% of teens present with complaints of fatigue.¹ As fatigue can be a symptom of many disorders, a careful work-up is important.

Fewer than 8 hours’ sleep, large intake of caffeine, and several hours on social media each day are linked with fatigue. Poor eating habits are more likely than not; nearly 21% of teens are overweight.² Video games have also contributed to symptoms of fatigue by encouraging a sedentary life style.

The work-up for teens with fatigue requires a detailed history of present symptoms and a careful review of systems, which should specifically address weight gain or loss, menstrual change, palpitations, and respiratory changes. It is important to screen for signs of stress and depression.

The physical exam should identify systems that need further work-up, and a standard serum screen would include a complete blood cell count (CBC), complete metabolic panel (CMP), and a thyroid panel.

As many experienced physicians can attest, more often than not, this work-up results in normal findings. Suggesting that the basis for fatigue may be a psychiatric cause is usually not well received.

Another consideration is a diagnosis of chronic fatigue syndrome (CFS), a well-documented disorder with defined diagnostic criteria since 1994. Although CFS is more common in adults, research now reveals an annual incidence of 0.5% and a prevalence of 0.19%-1.29% in teens.³ The characteristics are severe and disabling new-onset fatigue lasting greater than 6 months and four of the following symptoms: impaired memory, sore throat, tender cervical and axillary lymph nodes, muscle pain, headaches, unrefreshing sleep, generalized malaise. Orthostatic intolerance has also been identified as a symptom.⁴

The cause of CFS is unknown, although its onset usually follows an illness.¹ The diagnosis is challenging, as there is no definitive test. If the criteria are met, however, a diagnosis of CFS should be given. This allows the patient to feel validated and can foster a better physician-patient relationship.

Treatment for CFS is symptomatic. The first step is good “sleep hygiene.” Reducing or eliminating caffeine and promoting exercise and a healthy diet all contribute to better sleep. Also, the blue light emitted by electronic devices suppresses melatonin and makes it more difficult to fall asleep.⁵

Resuming normal activity and improving school attendance is the goal achieved through graded exercises, behavioral therapy, and management of pain with acetaminophen and NSAIDs. Tricyclic antidepressants have been studied in CFS but their effectiveness has not been proven.¹ Significant improvements are seen in 50% of teens who are appropriately diagnosed and adhere to treatments.¹

CFS is a debilitating disorder that can be frustrating to treat. Acknowledging CFS as a legitimate syndrome can aid in treatment by fostering a good physician-patient relationship.

References

1. Findlay, SM. “The Tired Teen: A Review of the Assessment and Management of the Adolescent with Sleepiness and Fatigue” Paediatr Child Health. 2008 Jan;13(1):37-42. Print.

2. Prevalence of Childhood Obesity in the United States, 2011-2012, CDC.

3. Nijhof SL, et al. “Adolescent Chronic Fatigue Syndrome: Prevalence, Incidence, and Morbidity” Pediatrics. 2011 May;127(5):e1169-e1175.

4. Orthostatic intolerance in adolescent chronic fatigue syndrome. Stewart JM, et al. Pediatrics. 1999 Jan;103(1):116-21.

5. “The impact of light from computer monitors on melatonin levels in college students” Figueiro MG, et al. Neuro Endocrinol Lett. 2011;32(2):158-163.

In an increasingly sleepless society inundated with caffeine drinks and social media, it is not surprising that 15%-30% of teens present with complaints of fatigue.¹ As fatigue can be a symptom of many disorders, a careful work-up is important.

Fewer than 8 hours’ sleep, large intake of caffeine, and several hours on social media each day are linked with fatigue. Poor eating habits are more likely than not; nearly 21% of teens are overweight.² Video games have also contributed to symptoms of fatigue by encouraging a sedentary life style.

The work-up for teens with fatigue requires a detailed history of present symptoms and a careful review of systems, which should specifically address weight gain or loss, menstrual change, palpitations, and respiratory changes. It is important to screen for signs of stress and depression.

The physical exam should identify systems that need further work-up, and a standard serum screen would include a complete blood cell count (CBC), complete metabolic panel (CMP), and a thyroid panel.

As many experienced physicians can attest, more often than not, this work-up results in normal findings. Suggesting that the basis for fatigue may be a psychiatric cause is usually not well received.

Another consideration is a diagnosis of chronic fatigue syndrome (CFS), a well-documented disorder with defined diagnostic criteria since 1994. Although CFS is more common in adults, research now reveals an annual incidence of 0.5% and a prevalence of 0.19%-1.29% in teens.³ The characteristics are severe and disabling new-onset fatigue lasting greater than 6 months and four of the following symptoms: impaired memory, sore throat, tender cervical and axillary lymph nodes, muscle pain, headaches, unrefreshing sleep, generalized malaise. Orthostatic intolerance has also been identified as a symptom.⁴

The cause of CFS is unknown, although its onset usually follows an illness.¹ The diagnosis is challenging, as there is no definitive test. If the criteria are met, however, a diagnosis of CFS should be given. This allows the patient to feel validated and can foster a better physician-patient relationship.

Treatment for CFS is symptomatic. The first step is good “sleep hygiene.” Reducing or eliminating caffeine and promoting exercise and a healthy diet all contribute to better sleep. Also, the blue light emitted by electronic devices suppresses melatonin and makes it more difficult to fall asleep.⁵

Resuming normal activity and improving school attendance is the goal achieved through graded exercises, behavioral therapy, and management of pain with acetaminophen and NSAIDs. Tricyclic antidepressants have been studied in CFS but their effectiveness has not been proven.¹ Significant improvements are seen in 50% of teens who are appropriately diagnosed and adhere to treatments.¹

CFS is a debilitating disorder that can be frustrating to treat. Acknowledging CFS as a legitimate syndrome can aid in treatment by fostering a good physician-patient relationship.

References

1. Findlay, SM. “The Tired Teen: A Review of the Assessment and Management of the Adolescent with Sleepiness and Fatigue” Paediatr Child Health. 2008 Jan;13(1):37-42. Print.

2. Prevalence of Childhood Obesity in the United States, 2011-2012, CDC.

3. Nijhof SL, et al. “Adolescent Chronic Fatigue Syndrome: Prevalence, Incidence, and Morbidity” Pediatrics. 2011 May;127(5):e1169-e1175.

4. Orthostatic intolerance in adolescent chronic fatigue syndrome. Stewart JM, et al. Pediatrics. 1999 Jan;103(1):116-21.

5. “The impact of light from computer monitors on melatonin levels in college students” Figueiro MG, et al. Neuro Endocrinol Lett. 2011;32(2):158-163.

In an increasingly sleepless society inundated with caffeine drinks and social media, it is not surprising that 15%-30% of teens present with complaints of fatigue.¹ As fatigue can be a symptom of many disorders, a careful work-up is important.

Fewer than 8 hours’ sleep, large intake of caffeine, and several hours on social media each day are linked with fatigue. Poor eating habits are more likely than not; nearly 21% of teens are overweight.² Video games have also contributed to symptoms of fatigue by encouraging a sedentary life style.

The work-up for teens with fatigue requires a detailed history of present symptoms and a careful review of systems, which should specifically address weight gain or loss, menstrual change, palpitations, and respiratory changes. It is important to screen for signs of stress and depression.

The physical exam should identify systems that need further work-up, and a standard serum screen would include a complete blood cell count (CBC), complete metabolic panel (CMP), and a thyroid panel.

As many experienced physicians can attest, more often than not, this work-up results in normal findings. Suggesting that the basis for fatigue may be a psychiatric cause is usually not well received.

Another consideration is a diagnosis of chronic fatigue syndrome (CFS), a well-documented disorder with defined diagnostic criteria since 1994. Although CFS is more common in adults, research now reveals an annual incidence of 0.5% and a prevalence of 0.19%-1.29% in teens.³ The characteristics are severe and disabling new-onset fatigue lasting greater than 6 months and four of the following symptoms: impaired memory, sore throat, tender cervical and axillary lymph nodes, muscle pain, headaches, unrefreshing sleep, generalized malaise. Orthostatic intolerance has also been identified as a symptom.⁴

The cause of CFS is unknown, although its onset usually follows an illness.¹ The diagnosis is challenging, as there is no definitive test. If the criteria are met, however, a diagnosis of CFS should be given. This allows the patient to feel validated and can foster a better physician-patient relationship.

Treatment for CFS is symptomatic. The first step is good “sleep hygiene.” Reducing or eliminating caffeine and promoting exercise and a healthy diet all contribute to better sleep. Also, the blue light emitted by electronic devices suppresses melatonin and makes it more difficult to fall asleep.⁵

Resuming normal activity and improving school attendance is the goal achieved through graded exercises, behavioral therapy, and management of pain with acetaminophen and NSAIDs. Tricyclic antidepressants have been studied in CFS but their effectiveness has not been proven.¹ Significant improvements are seen in 50% of teens who are appropriately diagnosed and adhere to treatments.¹

CFS is a debilitating disorder that can be frustrating to treat. Acknowledging CFS as a legitimate syndrome can aid in treatment by fostering a good physician-patient relationship.

References

1. Findlay, SM. “The Tired Teen: A Review of the Assessment and Management of the Adolescent with Sleepiness and Fatigue” Paediatr Child Health. 2008 Jan;13(1):37-42. Print.

2. Prevalence of Childhood Obesity in the United States, 2011-2012, CDC.

3. Nijhof SL, et al. “Adolescent Chronic Fatigue Syndrome: Prevalence, Incidence, and Morbidity” Pediatrics. 2011 May;127(5):e1169-e1175.

4. Orthostatic intolerance in adolescent chronic fatigue syndrome. Stewart JM, et al. Pediatrics. 1999 Jan;103(1):116-21.

5. “The impact of light from computer monitors on melatonin levels in college students” Figueiro MG, et al. Neuro Endocrinol Lett. 2011;32(2):158-163.

“STOP USING RECTAL MISOPROSTOL FOR THE TREATMENT OF POSTPARTUM HEMORRHAGE CAUSED BY UTERINE ATONY”Robert L. Barbieri, MD (Editorial; July 2016)

The BEPCOP strategy for uterine atony

I appreciated Dr. Barbieri’s editorial about oxytocics for postpartum uterine atony and have personally noted the poor effectiveness of rectal misoprostol. I was reminded of his previous editorial that recommended administering intravenous (IV) oxytocin to postcesarean delivery patients for about 6 to 8 hours to reduce the risk of postoperative hemorrhage.

At my current hospital we usually use postpartum oxytocin, 30 units in 500 mL of 5% dextrose in water (D5W) for vaginal deliveries, and that infusion typically is administered for only 1 to 2 hours. Cesarean delivery patients receive oxytocin, 20 units in 1,000 mL of Ringer’s lactate, over the first 1 to 2 hours postoperatively. As an OB hospitalist I have been summoned occasionally to the bedside of patients who have uterine atony and hemorrhage, which usually occurs several hours after their oxytocin infusion has finished.

With this in mind I developed a proactive protocol that I call BEPCOP, an acronym for “Barnes’ Excellent Post Cesarean Oxytocin Protocol.” This involves simply running a 500-mL bag of oxytocin (30 units in 500 mL of D5W) at a constant rate of 50 mL/hour, which provides 50 mU/min oxytocin over the first 10 hours postdelivery.

I recommend BEPCOP for every cesarean delivery patient, as well as for any vaginally delivered patients who are at increased risk for atony, such as those with prolonged labor, large babies, polyhydramnios, multifetal gestation, chorioamnio‑nitis, and history of hemorrhage after a previous delivery, and for patients who are Jehovah’s Witnesses. It is important to reduce the rate of the mainline IV bag while the oxytocin is infusing to reduce the risk of fluid overload.

Since starting this routine I have seen a noticeable decrease in postpartum and postcesarean uterine atony.

E. Darryl Barnes, MD
Mechanicsville, Virginia
 

Nondissolving misoprostol is ineffective

There is something about misoprostol that is not mentioned in Dr. Barbieri’s editorial. There are 2 types of misoprostol: the proprietary formulation (Cytotec, Pfizer) and the generic form (probably the one used in most hospitals, and possibly also the one used in the randomized studies alluded to).

The generic form, manufactured overseas, is literally insoluble. In my experience, these undissolved tabletsare expelled intact from the rectum5 hours after insertion and they therefore do nothing. The proprietary brand of misoprostol dissolves instantly in the rectum, and the results are dramatic to say the least.

Helio Zapata, MD
Skokie, Illinois

Bundles of care protocols useful in critical events

We often assume the etiology of the postpartum hemorrhage (PPH) is purely and exclusively uterine atony. A frequent clinical scenario is as follows: A hospital birth is conducted by a trained attendant, in a US learning hospital, on a parturient assessed as being at low risk; the single circulating nurse is busy at the keyboard complying with the data entry requirements; the just-delivered patient is enjoying skin-to-skin contact as recommended; and the new father is obtaining all the appropriate pictorial material when a massive vaginal bleed ensues, diagnosed as due to uterine atony. There is little time to remember the results of the randomized controlled trials condemning the use of misoprostol, or the effectiveness of the individual components of the AMTSL (active management of the third stage of labor). The IV oxytocin at the prescribed dose is running wide open, extra personnel are summoned to help, the first doses of methylergonovine are given, and the misoprostol tablets are stored in the nearby drawer as prescribed by the institution’s protocol.

Currently, a multi-state, multi-institutional initiative spearheaded by the American College of Obstetricians and Gynecologists and known as AIM (Alliance for Innovation in Maternity Care) supports the use of “bundles of care” to standardize obstetric care as recommended by the Joint Commission and the Society for Maternal-Fetal Medicine. One of the “bundles” addresses PPH. It is understood that each institution may adjust the steps in accord with its individual capabilities. Included in the algorithm is the use of rectal misoprostol 800 to 1,000 μg.¹⁻⁵

The International Federation of Gynecology and Obstetrics, in referencing the Blum trial,⁶ states that the results indicated misoprostol was noninferior to oxytocin at controlling bleeding (90% vs 89%) and preventing additional blood loss (31% vs 34%).⁷ Misoprostol’s contraindications and side effects are recognized by all investigators. In the field of obstetrics, changes are slow in permeating into daily practice.⁸ Dr. Barbieri’s recommendation, originating from an influential academic institution, opens the door to continue the dialog on a critical clinical event.

Federico G. Mariona, MD
Dearborn, Michigan

References

1. Shields LE, Wiesner S, Fulton J, Pelletreau B. Comprehensive maternal hemorrhage protocols reduce the use of blood products and improve patient safety. Am J Obstet Gynecol. 2015;212(3):272–280.
2. Obstetric hemorrhage checklist. Beaumont Health, Michigan. October 2015.
3. California Maternal Quality Care Collaborative, California Department of Public Health. OB hemorrhage toolkit, Version 2.0. https://www.cmqcc.org/resources-tool-kits/toolkits/ob-hemorrhage-toolkit. Published March 24, 2015. Accessed August 24, 2015.
4. Main EK, Goffman D, Scavone BM, et al; National Partnership for Maternal Safety Council on Patient Safety in Women’s Health Care. Consensus bundle on obstetric hemorrhage. Obstet Gynecol. 2015;126(1):155–162.
5. American College of Obstetricians and Gynecologists. ACOG Practice Bulletin No. 76: postpartum hemorrhage. Obstet Gynecol. 2006;108(4):1039–1047.
6. Blum J, Winikoff B, Raghavan S, et al. Treatment of post-partum haemorrhage with sublingual misoprostol versus oxytocin in women receiving prophylactic oxytocin: a double blind randomised, non-inferiority trial. Lancet. 2010;375(9710):217–223.
7. International Federation of Gynecology and Obstetrics. Treatment of post-partum haemorrhage with misoprostol. FIGO guideline, annotated version. http://www.figo.org/sites/default/files/uploads/project-publications/Miso/PPH%20treatment/Annotated%20versions/Treatment%20of%20PPH%20with%20Misoprostol_Annotated_2012_English.pdf. Published May 2012. Accessed August 24, 2015.
8. Mariona FG, Roura LC. The role of placental alpha macroglobulin-1 amnisure in determining the status of the fetal membranes; its associations with preterm birth. Traditions, traditions. J Matern Fetal Neonatal Med. 2016;29(6):1016–1020.

Rectal misoprostol has merit

It is well established in medicine that IV medications have a rapid onset of action. Therefore, IV uterotonics would be the first choice to control PPH. Most likely they will control the majority of uterine atony.

However, the causes of uterine atony are numerous, and they most commonly include prolonged labor and/or infection. Like any fatigued muscle, there is rebound relaxation. Intravenous uterotonics have a very short half-life and have a maximum total dose. Repeating oxytocin 40 U in a 1,000-mL infusion over 15 minutes carries the risk of water intoxication due to the antidiuretic effect.

Misoprostol 800 to 1,000 mg when used rectally will have a longer effect—up to 4 hours—and fewer side effects. It should be used in combination with other parenteral uterotonics to act in synergistic way. This way the more serious cases of PPH can be reduced or even prevented.

Raymond Michael, MD
Marshall, Minnesota

Dr. Barbieri responds

I deeply appreciate the perspectives provided by Drs. Barnes, Zapata, Mariona, and Michael. The obstetricians and gynecologists who read OBG Management have vast clinical experience, expertise, and exceptional insights. By sharing our knowledge with each other we best advance the care provided to women and their families.

As a hospitalist, Dr. Barnes is privileged to care for women at the highest-risk time of their pregnancy. I think his BEPCOP proactive protocol to reduce the rate of PPH is superb and urge him to publish his experience. I appreciate Dr. Zapata’s insight that misoprostol tablets from different manufacturers have markedly different rates of dissolution. I agree with him that I have seen entire, undissolved misoprostol tablets expelled from the rectum many hours after they were administered for the treatment of PPH. If the tablet does not dissolve, it certainly cannot work. Dr. Mariona’s guidance to adhere to protocol bundles and continuously improve and update the bundles is absolutely critical to advancing health care for pregnant women. Dr. Michael rightly points out that one advantage of misoprostol is that it has a longer half-life than many parenteral uterotonics. However, in my practice I prefer Dr. Barnes’ BEPCOP protocol involving the multi-hour administration of oxytocin to prevent and treat a PPH.

“STOP USING RECTAL MISOPROSTOL FOR THE TREATMENT OF POSTPARTUM HEMORRHAGE CAUSED BY UTERINE ATONY”Robert L. Barbieri, MD (Editorial; July 2016)

The BEPCOP strategy for uterine atony

I appreciated Dr. Barbieri’s editorial about oxytocics for postpartum uterine atony and have personally noted the poor effectiveness of rectal misoprostol. I was reminded of his previous editorial that recommended administering intravenous (IV) oxytocin to postcesarean delivery patients for about 6 to 8 hours to reduce the risk of postoperative hemorrhage.

At my current hospital we usually use postpartum oxytocin, 30 units in 500 mL of 5% dextrose in water (D5W) for vaginal deliveries, and that infusion typically is administered for only 1 to 2 hours. Cesarean delivery patients receive oxytocin, 20 units in 1,000 mL of Ringer’s lactate, over the first 1 to 2 hours postoperatively. As an OB hospitalist I have been summoned occasionally to the bedside of patients who have uterine atony and hemorrhage, which usually occurs several hours after their oxytocin infusion has finished.

With this in mind I developed a proactive protocol that I call BEPCOP, an acronym for “Barnes’ Excellent Post Cesarean Oxytocin Protocol.” This involves simply running a 500-mL bag of oxytocin (30 units in 500 mL of D5W) at a constant rate of 50 mL/hour, which provides 50 mU/min oxytocin over the first 10 hours postdelivery.

I recommend BEPCOP for every cesarean delivery patient, as well as for any vaginally delivered patients who are at increased risk for atony, such as those with prolonged labor, large babies, polyhydramnios, multifetal gestation, chorioamnio‑nitis, and history of hemorrhage after a previous delivery, and for patients who are Jehovah’s Witnesses. It is important to reduce the rate of the mainline IV bag while the oxytocin is infusing to reduce the risk of fluid overload.

Since starting this routine I have seen a noticeable decrease in postpartum and postcesarean uterine atony.

E. Darryl Barnes, MD
Mechanicsville, Virginia
 

Nondissolving misoprostol is ineffective

There is something about misoprostol that is not mentioned in Dr. Barbieri’s editorial. There are 2 types of misoprostol: the proprietary formulation (Cytotec, Pfizer) and the generic form (probably the one used in most hospitals, and possibly also the one used in the randomized studies alluded to).

The generic form, manufactured overseas, is literally insoluble. In my experience, these undissolved tabletsare expelled intact from the rectum5 hours after insertion and they therefore do nothing. The proprietary brand of misoprostol dissolves instantly in the rectum, and the results are dramatic to say the least.

Helio Zapata, MD
Skokie, Illinois

Bundles of care protocols useful in critical events

We often assume the etiology of the postpartum hemorrhage (PPH) is purely and exclusively uterine atony. A frequent clinical scenario is as follows: A hospital birth is conducted by a trained attendant, in a US learning hospital, on a parturient assessed as being at low risk; the single circulating nurse is busy at the keyboard complying with the data entry requirements; the just-delivered patient is enjoying skin-to-skin contact as recommended; and the new father is obtaining all the appropriate pictorial material when a massive vaginal bleed ensues, diagnosed as due to uterine atony. There is little time to remember the results of the randomized controlled trials condemning the use of misoprostol, or the effectiveness of the individual components of the AMTSL (active management of the third stage of labor). The IV oxytocin at the prescribed dose is running wide open, extra personnel are summoned to help, the first doses of methylergonovine are given, and the misoprostol tablets are stored in the nearby drawer as prescribed by the institution’s protocol.

Currently, a multi-state, multi-institutional initiative spearheaded by the American College of Obstetricians and Gynecologists and known as AIM (Alliance for Innovation in Maternity Care) supports the use of “bundles of care” to standardize obstetric care as recommended by the Joint Commission and the Society for Maternal-Fetal Medicine. One of the “bundles” addresses PPH. It is understood that each institution may adjust the steps in accord with its individual capabilities. Included in the algorithm is the use of rectal misoprostol 800 to 1,000 μg.¹⁻⁵

The International Federation of Gynecology and Obstetrics, in referencing the Blum trial,⁶ states that the results indicated misoprostol was noninferior to oxytocin at controlling bleeding (90% vs 89%) and preventing additional blood loss (31% vs 34%).⁷ Misoprostol’s contraindications and side effects are recognized by all investigators. In the field of obstetrics, changes are slow in permeating into daily practice.⁸ Dr. Barbieri’s recommendation, originating from an influential academic institution, opens the door to continue the dialog on a critical clinical event.

Federico G. Mariona, MD
Dearborn, Michigan

References

1. Shields LE, Wiesner S, Fulton J, Pelletreau B. Comprehensive maternal hemorrhage protocols reduce the use of blood products and improve patient safety. Am J Obstet Gynecol. 2015;212(3):272–280.
2. Obstetric hemorrhage checklist. Beaumont Health, Michigan. October 2015.
3. California Maternal Quality Care Collaborative, California Department of Public Health. OB hemorrhage toolkit, Version 2.0. https://www.cmqcc.org/resources-tool-kits/toolkits/ob-hemorrhage-toolkit. Published March 24, 2015. Accessed August 24, 2015.
4. Main EK, Goffman D, Scavone BM, et al; National Partnership for Maternal Safety Council on Patient Safety in Women’s Health Care. Consensus bundle on obstetric hemorrhage. Obstet Gynecol. 2015;126(1):155–162.
5. American College of Obstetricians and Gynecologists. ACOG Practice Bulletin No. 76: postpartum hemorrhage. Obstet Gynecol. 2006;108(4):1039–1047.
6. Blum J, Winikoff B, Raghavan S, et al. Treatment of post-partum haemorrhage with sublingual misoprostol versus oxytocin in women receiving prophylactic oxytocin: a double blind randomised, non-inferiority trial. Lancet. 2010;375(9710):217–223.
7. International Federation of Gynecology and Obstetrics. Treatment of post-partum haemorrhage with misoprostol. FIGO guideline, annotated version. http://www.figo.org/sites/default/files/uploads/project-publications/Miso/PPH%20treatment/Annotated%20versions/Treatment%20of%20PPH%20with%20Misoprostol_Annotated_2012_English.pdf. Published May 2012. Accessed August 24, 2015.
8. Mariona FG, Roura LC. The role of placental alpha macroglobulin-1 amnisure in determining the status of the fetal membranes; its associations with preterm birth. Traditions, traditions. J Matern Fetal Neonatal Med. 2016;29(6):1016–1020.

Rectal misoprostol has merit

It is well established in medicine that IV medications have a rapid onset of action. Therefore, IV uterotonics would be the first choice to control PPH. Most likely they will control the majority of uterine atony.

However, the causes of uterine atony are numerous, and they most commonly include prolonged labor and/or infection. Like any fatigued muscle, there is rebound relaxation. Intravenous uterotonics have a very short half-life and have a maximum total dose. Repeating oxytocin 40 U in a 1,000-mL infusion over 15 minutes carries the risk of water intoxication due to the antidiuretic effect.

Misoprostol 800 to 1,000 mg when used rectally will have a longer effect—up to 4 hours—and fewer side effects. It should be used in combination with other parenteral uterotonics to act in synergistic way. This way the more serious cases of PPH can be reduced or even prevented.

Raymond Michael, MD
Marshall, Minnesota

Dr. Barbieri responds

I deeply appreciate the perspectives provided by Drs. Barnes, Zapata, Mariona, and Michael. The obstetricians and gynecologists who read OBG Management have vast clinical experience, expertise, and exceptional insights. By sharing our knowledge with each other we best advance the care provided to women and their families.

As a hospitalist, Dr. Barnes is privileged to care for women at the highest-risk time of their pregnancy. I think his BEPCOP proactive protocol to reduce the rate of PPH is superb and urge him to publish his experience. I appreciate Dr. Zapata’s insight that misoprostol tablets from different manufacturers have markedly different rates of dissolution. I agree with him that I have seen entire, undissolved misoprostol tablets expelled from the rectum many hours after they were administered for the treatment of PPH. If the tablet does not dissolve, it certainly cannot work. Dr. Mariona’s guidance to adhere to protocol bundles and continuously improve and update the bundles is absolutely critical to advancing health care for pregnant women. Dr. Michael rightly points out that one advantage of misoprostol is that it has a longer half-life than many parenteral uterotonics. However, in my practice I prefer Dr. Barnes’ BEPCOP protocol involving the multi-hour administration of oxytocin to prevent and treat a PPH.

“STOP USING RECTAL MISOPROSTOL FOR THE TREATMENT OF POSTPARTUM HEMORRHAGE CAUSED BY UTERINE ATONY”Robert L. Barbieri, MD (Editorial; July 2016)

The BEPCOP strategy for uterine atony

I appreciated Dr. Barbieri’s editorial about oxytocics for postpartum uterine atony and have personally noted the poor effectiveness of rectal misoprostol. I was reminded of his previous editorial that recommended administering intravenous (IV) oxytocin to postcesarean delivery patients for about 6 to 8 hours to reduce the risk of postoperative hemorrhage.

At my current hospital we usually use postpartum oxytocin, 30 units in 500 mL of 5% dextrose in water (D5W) for vaginal deliveries, and that infusion typically is administered for only 1 to 2 hours. Cesarean delivery patients receive oxytocin, 20 units in 1,000 mL of Ringer’s lactate, over the first 1 to 2 hours postoperatively. As an OB hospitalist I have been summoned occasionally to the bedside of patients who have uterine atony and hemorrhage, which usually occurs several hours after their oxytocin infusion has finished.

With this in mind I developed a proactive protocol that I call BEPCOP, an acronym for “Barnes’ Excellent Post Cesarean Oxytocin Protocol.” This involves simply running a 500-mL bag of oxytocin (30 units in 500 mL of D5W) at a constant rate of 50 mL/hour, which provides 50 mU/min oxytocin over the first 10 hours postdelivery.

I recommend BEPCOP for every cesarean delivery patient, as well as for any vaginally delivered patients who are at increased risk for atony, such as those with prolonged labor, large babies, polyhydramnios, multifetal gestation, chorioamnio‑nitis, and history of hemorrhage after a previous delivery, and for patients who are Jehovah’s Witnesses. It is important to reduce the rate of the mainline IV bag while the oxytocin is infusing to reduce the risk of fluid overload.

Since starting this routine I have seen a noticeable decrease in postpartum and postcesarean uterine atony.

E. Darryl Barnes, MD
Mechanicsville, Virginia
 

Nondissolving misoprostol is ineffective

There is something about misoprostol that is not mentioned in Dr. Barbieri’s editorial. There are 2 types of misoprostol: the proprietary formulation (Cytotec, Pfizer) and the generic form (probably the one used in most hospitals, and possibly also the one used in the randomized studies alluded to).

The generic form, manufactured overseas, is literally insoluble. In my experience, these undissolved tabletsare expelled intact from the rectum5 hours after insertion and they therefore do nothing. The proprietary brand of misoprostol dissolves instantly in the rectum, and the results are dramatic to say the least.

Helio Zapata, MD
Skokie, Illinois

Bundles of care protocols useful in critical events

We often assume the etiology of the postpartum hemorrhage (PPH) is purely and exclusively uterine atony. A frequent clinical scenario is as follows: A hospital birth is conducted by a trained attendant, in a US learning hospital, on a parturient assessed as being at low risk; the single circulating nurse is busy at the keyboard complying with the data entry requirements; the just-delivered patient is enjoying skin-to-skin contact as recommended; and the new father is obtaining all the appropriate pictorial material when a massive vaginal bleed ensues, diagnosed as due to uterine atony. There is little time to remember the results of the randomized controlled trials condemning the use of misoprostol, or the effectiveness of the individual components of the AMTSL (active management of the third stage of labor). The IV oxytocin at the prescribed dose is running wide open, extra personnel are summoned to help, the first doses of methylergonovine are given, and the misoprostol tablets are stored in the nearby drawer as prescribed by the institution’s protocol.

Currently, a multi-state, multi-institutional initiative spearheaded by the American College of Obstetricians and Gynecologists and known as AIM (Alliance for Innovation in Maternity Care) supports the use of “bundles of care” to standardize obstetric care as recommended by the Joint Commission and the Society for Maternal-Fetal Medicine. One of the “bundles” addresses PPH. It is understood that each institution may adjust the steps in accord with its individual capabilities. Included in the algorithm is the use of rectal misoprostol 800 to 1,000 μg.¹⁻⁵

The International Federation of Gynecology and Obstetrics, in referencing the Blum trial,⁶ states that the results indicated misoprostol was noninferior to oxytocin at controlling bleeding (90% vs 89%) and preventing additional blood loss (31% vs 34%).⁷ Misoprostol’s contraindications and side effects are recognized by all investigators. In the field of obstetrics, changes are slow in permeating into daily practice.⁸ Dr. Barbieri’s recommendation, originating from an influential academic institution, opens the door to continue the dialog on a critical clinical event.

Federico G. Mariona, MD
Dearborn, Michigan

References

1. Shields LE, Wiesner S, Fulton J, Pelletreau B. Comprehensive maternal hemorrhage protocols reduce the use of blood products and improve patient safety. Am J Obstet Gynecol. 2015;212(3):272–280.
2. Obstetric hemorrhage checklist. Beaumont Health, Michigan. October 2015.
3. California Maternal Quality Care Collaborative, California Department of Public Health. OB hemorrhage toolkit, Version 2.0. https://www.cmqcc.org/resources-tool-kits/toolkits/ob-hemorrhage-toolkit. Published March 24, 2015. Accessed August 24, 2015.
4. Main EK, Goffman D, Scavone BM, et al; National Partnership for Maternal Safety Council on Patient Safety in Women’s Health Care. Consensus bundle on obstetric hemorrhage. Obstet Gynecol. 2015;126(1):155–162.
5. American College of Obstetricians and Gynecologists. ACOG Practice Bulletin No. 76: postpartum hemorrhage. Obstet Gynecol. 2006;108(4):1039–1047.
6. Blum J, Winikoff B, Raghavan S, et al. Treatment of post-partum haemorrhage with sublingual misoprostol versus oxytocin in women receiving prophylactic oxytocin: a double blind randomised, non-inferiority trial. Lancet. 2010;375(9710):217–223.
7. International Federation of Gynecology and Obstetrics. Treatment of post-partum haemorrhage with misoprostol. FIGO guideline, annotated version. http://www.figo.org/sites/default/files/uploads/project-publications/Miso/PPH%20treatment/Annotated%20versions/Treatment%20of%20PPH%20with%20Misoprostol_Annotated_2012_English.pdf. Published May 2012. Accessed August 24, 2015.
8. Mariona FG, Roura LC. The role of placental alpha macroglobulin-1 amnisure in determining the status of the fetal membranes; its associations with preterm birth. Traditions, traditions. J Matern Fetal Neonatal Med. 2016;29(6):1016–1020.

Rectal misoprostol has merit

It is well established in medicine that IV medications have a rapid onset of action. Therefore, IV uterotonics would be the first choice to control PPH. Most likely they will control the majority of uterine atony.

However, the causes of uterine atony are numerous, and they most commonly include prolonged labor and/or infection. Like any fatigued muscle, there is rebound relaxation. Intravenous uterotonics have a very short half-life and have a maximum total dose. Repeating oxytocin 40 U in a 1,000-mL infusion over 15 minutes carries the risk of water intoxication due to the antidiuretic effect.

Misoprostol 800 to 1,000 mg when used rectally will have a longer effect—up to 4 hours—and fewer side effects. It should be used in combination with other parenteral uterotonics to act in synergistic way. This way the more serious cases of PPH can be reduced or even prevented.

Raymond Michael, MD
Marshall, Minnesota

Dr. Barbieri responds

I deeply appreciate the perspectives provided by Drs. Barnes, Zapata, Mariona, and Michael. The obstetricians and gynecologists who read OBG Management have vast clinical experience, expertise, and exceptional insights. By sharing our knowledge with each other we best advance the care provided to women and their families.

As a hospitalist, Dr. Barnes is privileged to care for women at the highest-risk time of their pregnancy. I think his BEPCOP proactive protocol to reduce the rate of PPH is superb and urge him to publish his experience. I appreciate Dr. Zapata’s insight that misoprostol tablets from different manufacturers have markedly different rates of dissolution. I agree with him that I have seen entire, undissolved misoprostol tablets expelled from the rectum many hours after they were administered for the treatment of PPH. If the tablet does not dissolve, it certainly cannot work. Dr. Mariona’s guidance to adhere to protocol bundles and continuously improve and update the bundles is absolutely critical to advancing health care for pregnant women. Dr. Michael rightly points out that one advantage of misoprostol is that it has a longer half-life than many parenteral uterotonics. However, in my practice I prefer Dr. Barnes’ BEPCOP protocol involving the multi-hour administration of oxytocin to prevent and treat a PPH.

Walking around the Cardiac Intensive Care Unit (CICU) with one of my heart failure colleagues, I was struck by the relative absence of patients with acute myocardial infarctions. Over the past 50 years, they have been replaced by patients with advanced heart failure, many of whom had been implanted with left ventricular assist devices or connected to a variety of extracorporeal support devices.

Although some of the patients were new New York Heart Association class IV patients, many had been treated for years with beta-blockers and renal ACE inhibitors or aldosterone antagonists. Their disease had now recurred and progressed despite what I had presumed to be curative drug therapy. They were experiencing the relentless progression of heart failure despite treatment that was developed almost 20 years ago and which has not advanced much since then. Many cardiologists of my generation presumed that heart failure was no longer a problem even though we knew that annual mortality rates of heart failure remained in the 10% range and that its incidence was increasing.

It has become clear to many of us that there has been little advance in the treatment of heart failure since the introduction of those 20th century drugs, notwithstanding the importance of the development of end stage cardiac support devices.

It seems our success in treating patients with ischemic heart disease had only delayed the expression and progression of cardiac dysfunction. Even with our success in treating patients with nonischemic heart failure, whatever that is, after reaching a brief plateau with drug therapy, they often experienced recurrence. It is true that many patients had improved as a result of drug therapy and that progression had been arrested and in some patients heart failure had actually been reversed. But many, like the patients I saw in our CICU, had progressed to advanced heart failure with little to be offered other than end-stage device therapy or heart transplantation. Both of these outcomes, although lifesaving, represent therapeutic failures.

It is time that we refocus our efforts on the treatment and eradication of heart failure. Although a number of contemporary treatment strategies have been developed, for the most part they have only resulted in modest additive benefit. We need to reconsider the protection of the heart during and after an ischemic event and prevent the insidious progression of ischemia in those patients with chronic coronary heart disease. In addition we need to direct our research to understand the pathophysiology of the “heart” in heart failure and to unlock the mysticism associated with the many etiologies of idiopathic nonischemic heart failure. Our knowledge in this disease or diseases is embarrassingly poor.

It is time to move on from the 20th century drug foundation of therapy based on neurohumoral control, to a 21st century understanding of the cellular and molecular targets affecting cardiac function. Recent investigations of collagen synthesis and degradation, cardiac energetics, and mitochondrial function have provided provocative information but represent only forays into the vast unknown mechanism of heart failure. The solution to worldwide heart failure is not in device therapy for everyone but in a deeper understanding of the mechanisms of heart failure and its application to therapy.

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

Walking around the Cardiac Intensive Care Unit (CICU) with one of my heart failure colleagues, I was struck by the relative absence of patients with acute myocardial infarctions. Over the past 50 years, they have been replaced by patients with advanced heart failure, many of whom had been implanted with left ventricular assist devices or connected to a variety of extracorporeal support devices.

Although some of the patients were new New York Heart Association class IV patients, many had been treated for years with beta-blockers and renal ACE inhibitors or aldosterone antagonists. Their disease had now recurred and progressed despite what I had presumed to be curative drug therapy. They were experiencing the relentless progression of heart failure despite treatment that was developed almost 20 years ago and which has not advanced much since then. Many cardiologists of my generation presumed that heart failure was no longer a problem even though we knew that annual mortality rates of heart failure remained in the 10% range and that its incidence was increasing.

It has become clear to many of us that there has been little advance in the treatment of heart failure since the introduction of those 20th century drugs, notwithstanding the importance of the development of end stage cardiac support devices.

It seems our success in treating patients with ischemic heart disease had only delayed the expression and progression of cardiac dysfunction. Even with our success in treating patients with nonischemic heart failure, whatever that is, after reaching a brief plateau with drug therapy, they often experienced recurrence. It is true that many patients had improved as a result of drug therapy and that progression had been arrested and in some patients heart failure had actually been reversed. But many, like the patients I saw in our CICU, had progressed to advanced heart failure with little to be offered other than end-stage device therapy or heart transplantation. Both of these outcomes, although lifesaving, represent therapeutic failures.

It is time that we refocus our efforts on the treatment and eradication of heart failure. Although a number of contemporary treatment strategies have been developed, for the most part they have only resulted in modest additive benefit. We need to reconsider the protection of the heart during and after an ischemic event and prevent the insidious progression of ischemia in those patients with chronic coronary heart disease. In addition we need to direct our research to understand the pathophysiology of the “heart” in heart failure and to unlock the mysticism associated with the many etiologies of idiopathic nonischemic heart failure. Our knowledge in this disease or diseases is embarrassingly poor.

It is time to move on from the 20th century drug foundation of therapy based on neurohumoral control, to a 21st century understanding of the cellular and molecular targets affecting cardiac function. Recent investigations of collagen synthesis and degradation, cardiac energetics, and mitochondrial function have provided provocative information but represent only forays into the vast unknown mechanism of heart failure. The solution to worldwide heart failure is not in device therapy for everyone but in a deeper understanding of the mechanisms of heart failure and its application to therapy.

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

Walking around the Cardiac Intensive Care Unit (CICU) with one of my heart failure colleagues, I was struck by the relative absence of patients with acute myocardial infarctions. Over the past 50 years, they have been replaced by patients with advanced heart failure, many of whom had been implanted with left ventricular assist devices or connected to a variety of extracorporeal support devices.

Although some of the patients were new New York Heart Association class IV patients, many had been treated for years with beta-blockers and renal ACE inhibitors or aldosterone antagonists. Their disease had now recurred and progressed despite what I had presumed to be curative drug therapy. They were experiencing the relentless progression of heart failure despite treatment that was developed almost 20 years ago and which has not advanced much since then. Many cardiologists of my generation presumed that heart failure was no longer a problem even though we knew that annual mortality rates of heart failure remained in the 10% range and that its incidence was increasing.

It has become clear to many of us that there has been little advance in the treatment of heart failure since the introduction of those 20th century drugs, notwithstanding the importance of the development of end stage cardiac support devices.

It seems our success in treating patients with ischemic heart disease had only delayed the expression and progression of cardiac dysfunction. Even with our success in treating patients with nonischemic heart failure, whatever that is, after reaching a brief plateau with drug therapy, they often experienced recurrence. It is true that many patients had improved as a result of drug therapy and that progression had been arrested and in some patients heart failure had actually been reversed. But many, like the patients I saw in our CICU, had progressed to advanced heart failure with little to be offered other than end-stage device therapy or heart transplantation. Both of these outcomes, although lifesaving, represent therapeutic failures.

It is time that we refocus our efforts on the treatment and eradication of heart failure. Although a number of contemporary treatment strategies have been developed, for the most part they have only resulted in modest additive benefit. We need to reconsider the protection of the heart during and after an ischemic event and prevent the insidious progression of ischemia in those patients with chronic coronary heart disease. In addition we need to direct our research to understand the pathophysiology of the “heart” in heart failure and to unlock the mysticism associated with the many etiologies of idiopathic nonischemic heart failure. Our knowledge in this disease or diseases is embarrassingly poor.

It is time to move on from the 20th century drug foundation of therapy based on neurohumoral control, to a 21st century understanding of the cellular and molecular targets affecting cardiac function. Recent investigations of collagen synthesis and degradation, cardiac energetics, and mitochondrial function have provided provocative information but represent only forays into the vast unknown mechanism of heart failure. The solution to worldwide heart failure is not in device therapy for everyone but in a deeper understanding of the mechanisms of heart failure and its application to therapy.

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

I refuse to do retreads.

This has nothing to do with my car. If a retread tire gives me the same performance and safety at a lower price, I’m all for it.

Sometimes patients fire me. This is often acrimonious, with them sending me a letter complaining about my competence, bedside manner, personal appearance, staff, office decor, phone system ... whatever. For some reason they weren’t happy with me and instead of just sending a release of records, they decided to let me know in no uncertain terms that they aren’t coming back. We all get these notes.

When I was younger this would really upset me. I took a lot of things personally when I first started out. Now, after almost 20 years on the neurology front lines, it’s just another day. I learned a long time ago that you can’t please everyone or be the doctor they all love. So I fax their chart to wherever they want and move on.

Surprisingly, a few times a year patients will try to come back. Maybe they didn’t like the new doc, or are sorry about their outburst, or can’t find someone else nearby who takes their insurance. So they call and try to make a follow-up. Not surprisingly, they never mention their previous letter. When it’s brought up, they typically claim we misinterpreted it, that they didn’t mean it, or that they’ve decided to forgive me.

This is what I call a retread. A patient who wants to come back after leaving under unpleasant circumstances. I don’t allow it.

To me the doctor-patient relationship is based on trust and objectivity. Once a patient sends an acrimonious letter, it’s very difficult to return to an impartial condition. The fact that they did it once means they may do it again, or think they can get their way with threatening or insulting behavior. These are not things that are good for the connection between us.

So I turn them away. Some just hang up. Others yell, and a few threaten me with legal action. But I don’t back down. Do you want to care for someone who’s done the same to you?

This is a high-stress field. I don’t need the additional distraction of dealing with a toxic medical relationship. If you don’t like me, I have no issue with that. Not everyone does. But once you’ve made that decision, you’re stuck with it.

Dr. Block has a solo neurology practice in Scottsdale, Ariz.

I refuse to do retreads.

This has nothing to do with my car. If a retread tire gives me the same performance and safety at a lower price, I’m all for it.

Sometimes patients fire me. This is often acrimonious, with them sending me a letter complaining about my competence, bedside manner, personal appearance, staff, office decor, phone system ... whatever. For some reason they weren’t happy with me and instead of just sending a release of records, they decided to let me know in no uncertain terms that they aren’t coming back. We all get these notes.

When I was younger this would really upset me. I took a lot of things personally when I first started out. Now, after almost 20 years on the neurology front lines, it’s just another day. I learned a long time ago that you can’t please everyone or be the doctor they all love. So I fax their chart to wherever they want and move on.

Surprisingly, a few times a year patients will try to come back. Maybe they didn’t like the new doc, or are sorry about their outburst, or can’t find someone else nearby who takes their insurance. So they call and try to make a follow-up. Not surprisingly, they never mention their previous letter. When it’s brought up, they typically claim we misinterpreted it, that they didn’t mean it, or that they’ve decided to forgive me.

This is what I call a retread. A patient who wants to come back after leaving under unpleasant circumstances. I don’t allow it.

To me the doctor-patient relationship is based on trust and objectivity. Once a patient sends an acrimonious letter, it’s very difficult to return to an impartial condition. The fact that they did it once means they may do it again, or think they can get their way with threatening or insulting behavior. These are not things that are good for the connection between us.

So I turn them away. Some just hang up. Others yell, and a few threaten me with legal action. But I don’t back down. Do you want to care for someone who’s done the same to you?

This is a high-stress field. I don’t need the additional distraction of dealing with a toxic medical relationship. If you don’t like me, I have no issue with that. Not everyone does. But once you’ve made that decision, you’re stuck with it.

Dr. Block has a solo neurology practice in Scottsdale, Ariz.

I refuse to do retreads.

This has nothing to do with my car. If a retread tire gives me the same performance and safety at a lower price, I’m all for it.

Sometimes patients fire me. This is often acrimonious, with them sending me a letter complaining about my competence, bedside manner, personal appearance, staff, office decor, phone system ... whatever. For some reason they weren’t happy with me and instead of just sending a release of records, they decided to let me know in no uncertain terms that they aren’t coming back. We all get these notes.

When I was younger this would really upset me. I took a lot of things personally when I first started out. Now, after almost 20 years on the neurology front lines, it’s just another day. I learned a long time ago that you can’t please everyone or be the doctor they all love. So I fax their chart to wherever they want and move on.

Surprisingly, a few times a year patients will try to come back. Maybe they didn’t like the new doc, or are sorry about their outburst, or can’t find someone else nearby who takes their insurance. So they call and try to make a follow-up. Not surprisingly, they never mention their previous letter. When it’s brought up, they typically claim we misinterpreted it, that they didn’t mean it, or that they’ve decided to forgive me.

This is what I call a retread. A patient who wants to come back after leaving under unpleasant circumstances. I don’t allow it.

To me the doctor-patient relationship is based on trust and objectivity. Once a patient sends an acrimonious letter, it’s very difficult to return to an impartial condition. The fact that they did it once means they may do it again, or think they can get their way with threatening or insulting behavior. These are not things that are good for the connection between us.

So I turn them away. Some just hang up. Others yell, and a few threaten me with legal action. But I don’t back down. Do you want to care for someone who’s done the same to you?

This is a high-stress field. I don’t need the additional distraction of dealing with a toxic medical relationship. If you don’t like me, I have no issue with that. Not everyone does. But once you’ve made that decision, you’re stuck with it.

Dr. Block has a solo neurology practice in Scottsdale, Ariz.

Two children presented with influenza, and both recovered without the need for hospitalization. This scenario would fail to pique the interest of any pediatrician in January. But what about when it happens in July?

In early August, public health authorities in Ohio announced that two children had tested positive for the variant swine influenza virus H3N2v. Both children had direct contact with pigs at the Clark County Fair in late July. Along with a handful of cases diagnosed in Michigan, these represent the first H₃N_2v cases in the United States in 2016.

Influenza viruses that normally circulate in swine are designated as “variant” when they infect humans. According to the Centers for Disease Control and Prevention (CDC), human infections with H₁N_1v, H₁N_2v, and H₃N_2v have been identified in the United States. Influenza A H3N2v viruses carrying the matrix gene from the 2009 H₁N₁ pandemic virus were first detected in pigs in 2010, and in people in the summer of 2011. Since that time, 357 human cases have been reported from 14 states, with nearly 75% occurring in Indiana and Ohio. Most infections occurred after prolonged exposure to pigs at agricultural fairs.

Fortunately, most H₃N_2v infections have been mild: Since July 2012, only 21 individuals have required hospitalization and a single case resulted in death. Notably, though, many of the hospitalizations involved children.

On Aug. 15, the Centers for Disease Control and Prevention released Interim Guidance for Clinicians on Human Infections with Variant Influenza Viruses.

Because variant virus infection is indistinguishable from seasonal influenza or any other virus that cause influenzalike illness (think fever, cough, sore throat), physicians and other frontline providers need to maintain an index of suspicion. The key is eliciting a history of swine exposure in the week before illness onset. Practically, this means asking about direct contact with pigs, indirect contact with pigs, or close contact with an ill person who has had contact with pigs. Kudos to the astute clinicians in Ohio who thought to send the appropriate influenza testing in July.

When variant influenza virus is suspected, a nasopharyngeal swab or aspirate should be obtained for testing at a state public health lab or the CDC. Rapid antigen tests for influenza may be falsely negative in the setting of H₃N_2v infection, just as they may be with seasonal influenza infection. Molecular tests such as reverse transcription polymerase chain reaction (RT-PCR) are likely more sensitive, but cannot distinguish variant influenza A viruses from seasonal influenza A viruses.

The Kentucky State Fair opened on Aug. 18, making the CDC guidance especially timely for health care providers in my area. I called a friend who is a pediatric emergency medicine physician to ask if she and her colleagues were routinely screening patients for encounters of the porcine kind.

“For example, are you asking, ‘Have you been showing, raising or feeding swine? Have you been to the pig barn at the fair?’ ”

When my friend quit laughing, I confessed to her that I had not been doing that routinely either. The exposure history is often the most interesting part of the infectious disease evaluation and in the last month, I’ve asked about exposure to sheep (a risk factor for Q fever), exposure to chickens (a risk factor for Salmonella infections), and exposure to beaver dams (a risk factor for blastomycosis). But I’ve not asked about exposure to pigs.

“The emergency medicine approach is to avoid a lot of viral diagnostic testing unless it is going to impact management,” she said. “Tell me how this changes management of my patient.”

From the patient perspective, making a presumptive diagnosis of H₃N_2v infection would open the door to empiric treatment with antivirals, at least for individuals who are hospitalized, have severe or progressive disease, or who at high risk for complications of influenza. Neuraminidase inhibitors, including oral oseltamivir, inhaled zanamivir, and intravenous peramivir, can be used for treatment of H₃N_2v infections.

From a societal perspective, making the diagnosis gives public health experts the opportunity to investigate and potentially prevent further infections by isolating sick pigs. Human to human transmission of H₃N_2v is rare, but has occasionally occurred in households and in one instance, a child care setting. Careful surveillance of each swine flu case in a human is important to exclude the possibility that the virus has developed the ability to spread efficiently from person to person, creating the risk for an epidemic.

Seasonal influenza vaccine does not prevent infection with variant viruses, so avoidance is key. Those at high risk for complications from influenza infection, including children younger than 5 years of age and those with asthma, diabetes, heart disease, immunocompromised conditions, and neurologic or neurodevelopmental disorders, are urged to avoid pigs and swine barns when visiting fairs where the animals are present. Everyone else needs to follow common sense measures to prevent the spread of infection.

• Don’t take food or drink into pig areas; don’t eat, drink or put anything in your mouth in pig areas.

• Don’t take toys, pacifiers, cups, baby bottles, strollers, or similar items into pig areas.

• Wash your hands often with soap and running water before and after exposure to pigs. If soap and water are not available, use an alcohol-based hand rub.

• Avoid close contact with pigs that look or act ill.

• Take protective measures if you must come in contact with pigs that are known or suspected to be sick. This includes wearing personal protective equipment like protective clothing, gloves, and masks that cover your mouth and nose when contact is required.

• To further reduce the risk of infection, minimize contact with pigs in the pig barn and arenas.

It shouldn’t be surprising that flu viruses spread from pigs to people in the same way that regular seasonal influenza spread from person to person. An infected pig coughs or sneezes influenza-containing droplets, and these droplets are inhaled or swallowed by a susceptible human. That makes avoiding contact with pigs that look or act ill especially important. For the record, a pig with flu might have fever, depression, cough, nasal or eye discharge, eye redness, or a poor appetite.

On the bright side, you can’t get H₃N_2v or any other variant virus from eating properly prepared pork meat. Fairgoers can feel free to indulge in a deep-fried pork chop or one of this year’s featured food items: a basket of French fries topped with smoked pork, cheddar cheese sauce, red onions, jalapeño peppers and barbecue sauce.

Or maybe not. The CDC has a web page devoted to food safety at fairs and festivals. It notes that cases of foodborne illness increase during summer months, and usual safety controls “like monitoring of food temperatures, refrigeration, workers trained in food safety and washing facilities, may not be available when cooking and dining at fairs and festivals.”

The public is urged to seek out “healthy options” from fair vendors first. If healthy options aren’t available, we’re advised to consider bringing food from home to save money and calories.

Sigh. I remember when summer used to be more fun.

Dr. Bryant is a pediatrician specializing in infectious diseases at the University of Louisville, Ky. and Kosair Children’s Hospital, also in Louisville.

Two children presented with influenza, and both recovered without the need for hospitalization. This scenario would fail to pique the interest of any pediatrician in January. But what about when it happens in July?

In early August, public health authorities in Ohio announced that two children had tested positive for the variant swine influenza virus H3N2v. Both children had direct contact with pigs at the Clark County Fair in late July. Along with a handful of cases diagnosed in Michigan, these represent the first H₃N_2v cases in the United States in 2016.

Influenza viruses that normally circulate in swine are designated as “variant” when they infect humans. According to the Centers for Disease Control and Prevention (CDC), human infections with H₁N_1v, H₁N_2v, and H₃N_2v have been identified in the United States. Influenza A H3N2v viruses carrying the matrix gene from the 2009 H₁N₁ pandemic virus were first detected in pigs in 2010, and in people in the summer of 2011. Since that time, 357 human cases have been reported from 14 states, with nearly 75% occurring in Indiana and Ohio. Most infections occurred after prolonged exposure to pigs at agricultural fairs.

Fortunately, most H₃N_2v infections have been mild: Since July 2012, only 21 individuals have required hospitalization and a single case resulted in death. Notably, though, many of the hospitalizations involved children.

On Aug. 15, the Centers for Disease Control and Prevention released Interim Guidance for Clinicians on Human Infections with Variant Influenza Viruses.

Because variant virus infection is indistinguishable from seasonal influenza or any other virus that cause influenzalike illness (think fever, cough, sore throat), physicians and other frontline providers need to maintain an index of suspicion. The key is eliciting a history of swine exposure in the week before illness onset. Practically, this means asking about direct contact with pigs, indirect contact with pigs, or close contact with an ill person who has had contact with pigs. Kudos to the astute clinicians in Ohio who thought to send the appropriate influenza testing in July.

When variant influenza virus is suspected, a nasopharyngeal swab or aspirate should be obtained for testing at a state public health lab or the CDC. Rapid antigen tests for influenza may be falsely negative in the setting of H₃N_2v infection, just as they may be with seasonal influenza infection. Molecular tests such as reverse transcription polymerase chain reaction (RT-PCR) are likely more sensitive, but cannot distinguish variant influenza A viruses from seasonal influenza A viruses.

The Kentucky State Fair opened on Aug. 18, making the CDC guidance especially timely for health care providers in my area. I called a friend who is a pediatric emergency medicine physician to ask if she and her colleagues were routinely screening patients for encounters of the porcine kind.

“For example, are you asking, ‘Have you been showing, raising or feeding swine? Have you been to the pig barn at the fair?’ ”

When my friend quit laughing, I confessed to her that I had not been doing that routinely either. The exposure history is often the most interesting part of the infectious disease evaluation and in the last month, I’ve asked about exposure to sheep (a risk factor for Q fever), exposure to chickens (a risk factor for Salmonella infections), and exposure to beaver dams (a risk factor for blastomycosis). But I’ve not asked about exposure to pigs.

“The emergency medicine approach is to avoid a lot of viral diagnostic testing unless it is going to impact management,” she said. “Tell me how this changes management of my patient.”

From the patient perspective, making a presumptive diagnosis of H₃N_2v infection would open the door to empiric treatment with antivirals, at least for individuals who are hospitalized, have severe or progressive disease, or who at high risk for complications of influenza. Neuraminidase inhibitors, including oral oseltamivir, inhaled zanamivir, and intravenous peramivir, can be used for treatment of H₃N_2v infections.

From a societal perspective, making the diagnosis gives public health experts the opportunity to investigate and potentially prevent further infections by isolating sick pigs. Human to human transmission of H₃N_2v is rare, but has occasionally occurred in households and in one instance, a child care setting. Careful surveillance of each swine flu case in a human is important to exclude the possibility that the virus has developed the ability to spread efficiently from person to person, creating the risk for an epidemic.

Seasonal influenza vaccine does not prevent infection with variant viruses, so avoidance is key. Those at high risk for complications from influenza infection, including children younger than 5 years of age and those with asthma, diabetes, heart disease, immunocompromised conditions, and neurologic or neurodevelopmental disorders, are urged to avoid pigs and swine barns when visiting fairs where the animals are present. Everyone else needs to follow common sense measures to prevent the spread of infection.

• Don’t take food or drink into pig areas; don’t eat, drink or put anything in your mouth in pig areas.

• Don’t take toys, pacifiers, cups, baby bottles, strollers, or similar items into pig areas.

• Wash your hands often with soap and running water before and after exposure to pigs. If soap and water are not available, use an alcohol-based hand rub.

• Avoid close contact with pigs that look or act ill.

• Take protective measures if you must come in contact with pigs that are known or suspected to be sick. This includes wearing personal protective equipment like protective clothing, gloves, and masks that cover your mouth and nose when contact is required.

• To further reduce the risk of infection, minimize contact with pigs in the pig barn and arenas.

It shouldn’t be surprising that flu viruses spread from pigs to people in the same way that regular seasonal influenza spread from person to person. An infected pig coughs or sneezes influenza-containing droplets, and these droplets are inhaled or swallowed by a susceptible human. That makes avoiding contact with pigs that look or act ill especially important. For the record, a pig with flu might have fever, depression, cough, nasal or eye discharge, eye redness, or a poor appetite.

On the bright side, you can’t get H₃N_2v or any other variant virus from eating properly prepared pork meat. Fairgoers can feel free to indulge in a deep-fried pork chop or one of this year’s featured food items: a basket of French fries topped with smoked pork, cheddar cheese sauce, red onions, jalapeño peppers and barbecue sauce.

Or maybe not. The CDC has a web page devoted to food safety at fairs and festivals. It notes that cases of foodborne illness increase during summer months, and usual safety controls “like monitoring of food temperatures, refrigeration, workers trained in food safety and washing facilities, may not be available when cooking and dining at fairs and festivals.”

The public is urged to seek out “healthy options” from fair vendors first. If healthy options aren’t available, we’re advised to consider bringing food from home to save money and calories.

Sigh. I remember when summer used to be more fun.

Dr. Bryant is a pediatrician specializing in infectious diseases at the University of Louisville, Ky. and Kosair Children’s Hospital, also in Louisville.

Two children presented with influenza, and both recovered without the need for hospitalization. This scenario would fail to pique the interest of any pediatrician in January. But what about when it happens in July?

In early August, public health authorities in Ohio announced that two children had tested positive for the variant swine influenza virus H3N2v. Both children had direct contact with pigs at the Clark County Fair in late July. Along with a handful of cases diagnosed in Michigan, these represent the first H₃N_2v cases in the United States in 2016.

Influenza viruses that normally circulate in swine are designated as “variant” when they infect humans. According to the Centers for Disease Control and Prevention (CDC), human infections with H₁N_1v, H₁N_2v, and H₃N_2v have been identified in the United States. Influenza A H3N2v viruses carrying the matrix gene from the 2009 H₁N₁ pandemic virus were first detected in pigs in 2010, and in people in the summer of 2011. Since that time, 357 human cases have been reported from 14 states, with nearly 75% occurring in Indiana and Ohio. Most infections occurred after prolonged exposure to pigs at agricultural fairs.

Fortunately, most H₃N_2v infections have been mild: Since July 2012, only 21 individuals have required hospitalization and a single case resulted in death. Notably, though, many of the hospitalizations involved children.

On Aug. 15, the Centers for Disease Control and Prevention released Interim Guidance for Clinicians on Human Infections with Variant Influenza Viruses.

Because variant virus infection is indistinguishable from seasonal influenza or any other virus that cause influenzalike illness (think fever, cough, sore throat), physicians and other frontline providers need to maintain an index of suspicion. The key is eliciting a history of swine exposure in the week before illness onset. Practically, this means asking about direct contact with pigs, indirect contact with pigs, or close contact with an ill person who has had contact with pigs. Kudos to the astute clinicians in Ohio who thought to send the appropriate influenza testing in July.

When variant influenza virus is suspected, a nasopharyngeal swab or aspirate should be obtained for testing at a state public health lab or the CDC. Rapid antigen tests for influenza may be falsely negative in the setting of H₃N_2v infection, just as they may be with seasonal influenza infection. Molecular tests such as reverse transcription polymerase chain reaction (RT-PCR) are likely more sensitive, but cannot distinguish variant influenza A viruses from seasonal influenza A viruses.

The Kentucky State Fair opened on Aug. 18, making the CDC guidance especially timely for health care providers in my area. I called a friend who is a pediatric emergency medicine physician to ask if she and her colleagues were routinely screening patients for encounters of the porcine kind.

“For example, are you asking, ‘Have you been showing, raising or feeding swine? Have you been to the pig barn at the fair?’ ”

When my friend quit laughing, I confessed to her that I had not been doing that routinely either. The exposure history is often the most interesting part of the infectious disease evaluation and in the last month, I’ve asked about exposure to sheep (a risk factor for Q fever), exposure to chickens (a risk factor for Salmonella infections), and exposure to beaver dams (a risk factor for blastomycosis). But I’ve not asked about exposure to pigs.

“The emergency medicine approach is to avoid a lot of viral diagnostic testing unless it is going to impact management,” she said. “Tell me how this changes management of my patient.”

From the patient perspective, making a presumptive diagnosis of H₃N_2v infection would open the door to empiric treatment with antivirals, at least for individuals who are hospitalized, have severe or progressive disease, or who at high risk for complications of influenza. Neuraminidase inhibitors, including oral oseltamivir, inhaled zanamivir, and intravenous peramivir, can be used for treatment of H₃N_2v infections.

From a societal perspective, making the diagnosis gives public health experts the opportunity to investigate and potentially prevent further infections by isolating sick pigs. Human to human transmission of H₃N_2v is rare, but has occasionally occurred in households and in one instance, a child care setting. Careful surveillance of each swine flu case in a human is important to exclude the possibility that the virus has developed the ability to spread efficiently from person to person, creating the risk for an epidemic.

Seasonal influenza vaccine does not prevent infection with variant viruses, so avoidance is key. Those at high risk for complications from influenza infection, including children younger than 5 years of age and those with asthma, diabetes, heart disease, immunocompromised conditions, and neurologic or neurodevelopmental disorders, are urged to avoid pigs and swine barns when visiting fairs where the animals are present. Everyone else needs to follow common sense measures to prevent the spread of infection.

• Don’t take food or drink into pig areas; don’t eat, drink or put anything in your mouth in pig areas.

• Don’t take toys, pacifiers, cups, baby bottles, strollers, or similar items into pig areas.

• Wash your hands often with soap and running water before and after exposure to pigs. If soap and water are not available, use an alcohol-based hand rub.

• Avoid close contact with pigs that look or act ill.

• Take protective measures if you must come in contact with pigs that are known or suspected to be sick. This includes wearing personal protective equipment like protective clothing, gloves, and masks that cover your mouth and nose when contact is required.

• To further reduce the risk of infection, minimize contact with pigs in the pig barn and arenas.

It shouldn’t be surprising that flu viruses spread from pigs to people in the same way that regular seasonal influenza spread from person to person. An infected pig coughs or sneezes influenza-containing droplets, and these droplets are inhaled or swallowed by a susceptible human. That makes avoiding contact with pigs that look or act ill especially important. For the record, a pig with flu might have fever, depression, cough, nasal or eye discharge, eye redness, or a poor appetite.

On the bright side, you can’t get H₃N_2v or any other variant virus from eating properly prepared pork meat. Fairgoers can feel free to indulge in a deep-fried pork chop or one of this year’s featured food items: a basket of French fries topped with smoked pork, cheddar cheese sauce, red onions, jalapeño peppers and barbecue sauce.

Or maybe not. The CDC has a web page devoted to food safety at fairs and festivals. It notes that cases of foodborne illness increase during summer months, and usual safety controls “like monitoring of food temperatures, refrigeration, workers trained in food safety and washing facilities, may not be available when cooking and dining at fairs and festivals.”

The public is urged to seek out “healthy options” from fair vendors first. If healthy options aren’t available, we’re advised to consider bringing food from home to save money and calories.

Sigh. I remember when summer used to be more fun.

Dr. Bryant is a pediatrician specializing in infectious diseases at the University of Louisville, Ky. and Kosair Children’s Hospital, also in Louisville.

When it comes to political candidates and psychiatric disorders, the idea of diagnosing from afar is not new. In 1964, Fact magazine published an article called “The Unconscious of a Conservative: A Special Issue on the Mind of Barry Goldwater.” For the article, more than 2,400 psychiatrists responded to a survey, and many described the presidential candidate using a host of diagnostic and symptomatic terms. Mr. Goldwater lost the election in a landslide and successfully sued the magazine for $75,000.

In 1973, nearly a decade later, the American Psychiatric Association specifically noted in its code of ethics that psychiatrists should not offer diagnostic opinions on anyone who has not been personally examined and has not signed the proper authorization for this information to be released. The edict has been informally called The Goldwater Rule.

In the current election cycle, it has been a challenge for some psychiatrists to refrain from making public statements about our presidential candidates. Some have said the Goldwater Rule amounts to a gag order, and that the specifics of this election are different from other elections, and might warrant allowing psychiatrists to issue their professional opinions. The APA has reminded psychiatrists that to do so is unethical, and on Aug. 15, The New York Times ran an article by Benedict Carey titled: “The Psychiatric Question: Is it Fair to Analyze Donald Trump from Afar?”

I want to look at the question from a different stance. In assessing our political candidates, I’d like you to consider this: What difference does it make? Psychiatric diagnostic criteria are determined by consensus opinions of APA workgroup members. They aren’t perfect; they aren’t always accurate even when a patient is evaluated in person and seen over time; they are influenced by culture; and they aren’t always prognostic. One person’s experience of bipolar disorder is not another person’s experience of bipolar disorder, and personality disorders – such as narcissism or antisocial personality disorder – don’t have uniform presentations or outcomes. Some people with these difficulties head corporations and nations, while others wilt in prisons.

Half of the population will suffer from an episode of psychiatric illness at some point in their lives, and one in five people is affected in any given year. While we might all agree that many psychiatric symptoms are not compatible with being president, should the fact that a candidate has had a distant episode of mental illness, either fully resolved or controlled with treatment, disqualify him or her from holding office?

In an article published in the January 2006 issue of the Journal of Nervous and Mental Disease, Jonathan R. Davidson, MD; Kathryn M. Connor, MD; and Marvin Swartz, MD, looked at the biographical data on U.S. presidents from 1776 to 1974 and concluded that 49% met criteria for an Axis I psychiatric disorder. During those cycles, 27% had psychiatric difficulties while in office. Our presidents have suffered from depression and bipolar disorder, anxiety and alcoholism (J Nerv Ment Dis. 2006 Jan;194[1]47-51). No one has publicly attempted to tally personality disorders or use of other addictive substances. It may be safe to say that if the existence of psychiatric pathology had always been a disqualifier for public office, we’d live in a very different country.

Hopefully, when we approach our patients, we do so with warmth, kindness, and a genuine desire to help them heal. Psychiatry, at its best, is about intimacy and trust, and it is in that venue that people share their inner worlds and allow themselves to be vulnerable. Compassion is part of the deal; no one wants to have a mental illness. To refer to an unknown celebrity as “schizophrenic,” “psychotic,” or “having a godlike self-image” – or calling him “a dangerous lunatic,” as Sen. Goldwater was called – is not about careful diagnosis and compassion; it’s simply about name calling. To say that a politician or celebrity’s undesirable behavior is the result of a psychiatric illness based on cavalier observation is an insult to our patients, and it perpetuates stigma.

Psychiatric diagnoses are made by observing a constellation of symptoms that occur together. Mr. Trump has given the whole world years of data – he’s lived his life in a very public way. As a real estate developer, he has had countless employees who all know how they’ve been treated. We’ve seen him through three marriages and watched how he interacts with his children. We’ve seen him take out full-page ads calling for the death penalty for a group of young men who were wrongly convicted in the rape and assault of the Central Park jogger in 1988. If that’s not enough, he has hosted his own reality television show, and we’ve now seen him countless times in debates and rallies. We know how he treats his running mates, journalist Megyn Kelly, a news reporter with a disability, and the parents of a fallen soldier. We’ve watched him assure the nation during a primary debate that his genitals are big enough. Every individual is free to decide if Mr. Trump’s widely viewed patterns of behavior represent much-needed spunk and change with political beliefs that align with their own, or if his words and behaviors represent cruelty, impulsivity, poor judgment, and a pattern of actions that some might not feel is dignified enough for our country’s leader. No degree is required to observe and draw conclusions.

And please, let me be the first to admit that my perspective is biased: I’ve pointed out some of Mr. Trump’s more troubling behaviors and said nothing of the many wonderful things he may have done as both an entrepreneur and as a human being. Those don’t make the headlines or Twitter, and so I’m left with my own observations and those of a liberal press (Of course, there’s a right-wing press, too, but that’s a topic for another time). For voters who align their beliefs with the National Rifle Association, and feel that illegal immigrants are a drain on our country and that people of certain faiths represent a terror threat to Americans, Mr. Trump apparently remains a reasonable candidate.

Is there a role here for living room consults from psychiatrists? Is there something for us as professionals to add to the prediction of Mr. Trump’s behavior if he becomes president? I don’t think so. Every American has ample data, and for those who are curious about Mr. Trump’s psychiatric status, they are free to Google the criteria for psychiatric disorders and see if they believe he meets them. The input of psychiatrists would neither change the election outcome nor accurately predict his behavior if elected. But it might make us look a bit grandiose.

Finally, I’ve focused here on Mr. Trump, while saying nothing about Secretary Hillary Clinton and her psychiatric status. She, too, has lived a public life, and while many of her activities have attracted media attention and scrutiny, I’ve seen nothing that has suggested she suffers from a psychiatric condition. There was, however, an op-ed piece in The New York Times on Aug. 23, 2016, by Frank Bruni, suggesting that Mrs. Clinton may have an 11th toe.

If nothing else, it’s time for this election to be over.

Dr. Miller is coauthor of “Committed: The Battle Over Involuntary Psychiatric Care,” forthcoming from Johns Hopkins University Press in fall 2016.

When it comes to political candidates and psychiatric disorders, the idea of diagnosing from afar is not new. In 1964, Fact magazine published an article called “The Unconscious of a Conservative: A Special Issue on the Mind of Barry Goldwater.” For the article, more than 2,400 psychiatrists responded to a survey, and many described the presidential candidate using a host of diagnostic and symptomatic terms. Mr. Goldwater lost the election in a landslide and successfully sued the magazine for $75,000.

In 1973, nearly a decade later, the American Psychiatric Association specifically noted in its code of ethics that psychiatrists should not offer diagnostic opinions on anyone who has not been personally examined and has not signed the proper authorization for this information to be released. The edict has been informally called The Goldwater Rule.

In the current election cycle, it has been a challenge for some psychiatrists to refrain from making public statements about our presidential candidates. Some have said the Goldwater Rule amounts to a gag order, and that the specifics of this election are different from other elections, and might warrant allowing psychiatrists to issue their professional opinions. The APA has reminded psychiatrists that to do so is unethical, and on Aug. 15, The New York Times ran an article by Benedict Carey titled: “The Psychiatric Question: Is it Fair to Analyze Donald Trump from Afar?”

I want to look at the question from a different stance. In assessing our political candidates, I’d like you to consider this: What difference does it make? Psychiatric diagnostic criteria are determined by consensus opinions of APA workgroup members. They aren’t perfect; they aren’t always accurate even when a patient is evaluated in person and seen over time; they are influenced by culture; and they aren’t always prognostic. One person’s experience of bipolar disorder is not another person’s experience of bipolar disorder, and personality disorders – such as narcissism or antisocial personality disorder – don’t have uniform presentations or outcomes. Some people with these difficulties head corporations and nations, while others wilt in prisons.

Half of the population will suffer from an episode of psychiatric illness at some point in their lives, and one in five people is affected in any given year. While we might all agree that many psychiatric symptoms are not compatible with being president, should the fact that a candidate has had a distant episode of mental illness, either fully resolved or controlled with treatment, disqualify him or her from holding office?

In an article published in the January 2006 issue of the Journal of Nervous and Mental Disease, Jonathan R. Davidson, MD; Kathryn M. Connor, MD; and Marvin Swartz, MD, looked at the biographical data on U.S. presidents from 1776 to 1974 and concluded that 49% met criteria for an Axis I psychiatric disorder. During those cycles, 27% had psychiatric difficulties while in office. Our presidents have suffered from depression and bipolar disorder, anxiety and alcoholism (J Nerv Ment Dis. 2006 Jan;194[1]47-51). No one has publicly attempted to tally personality disorders or use of other addictive substances. It may be safe to say that if the existence of psychiatric pathology had always been a disqualifier for public office, we’d live in a very different country.

Hopefully, when we approach our patients, we do so with warmth, kindness, and a genuine desire to help them heal. Psychiatry, at its best, is about intimacy and trust, and it is in that venue that people share their inner worlds and allow themselves to be vulnerable. Compassion is part of the deal; no one wants to have a mental illness. To refer to an unknown celebrity as “schizophrenic,” “psychotic,” or “having a godlike self-image” – or calling him “a dangerous lunatic,” as Sen. Goldwater was called – is not about careful diagnosis and compassion; it’s simply about name calling. To say that a politician or celebrity’s undesirable behavior is the result of a psychiatric illness based on cavalier observation is an insult to our patients, and it perpetuates stigma.

Psychiatric diagnoses are made by observing a constellation of symptoms that occur together. Mr. Trump has given the whole world years of data – he’s lived his life in a very public way. As a real estate developer, he has had countless employees who all know how they’ve been treated. We’ve seen him through three marriages and watched how he interacts with his children. We’ve seen him take out full-page ads calling for the death penalty for a group of young men who were wrongly convicted in the rape and assault of the Central Park jogger in 1988. If that’s not enough, he has hosted his own reality television show, and we’ve now seen him countless times in debates and rallies. We know how he treats his running mates, journalist Megyn Kelly, a news reporter with a disability, and the parents of a fallen soldier. We’ve watched him assure the nation during a primary debate that his genitals are big enough. Every individual is free to decide if Mr. Trump’s widely viewed patterns of behavior represent much-needed spunk and change with political beliefs that align with their own, or if his words and behaviors represent cruelty, impulsivity, poor judgment, and a pattern of actions that some might not feel is dignified enough for our country’s leader. No degree is required to observe and draw conclusions.

And please, let me be the first to admit that my perspective is biased: I’ve pointed out some of Mr. Trump’s more troubling behaviors and said nothing of the many wonderful things he may have done as both an entrepreneur and as a human being. Those don’t make the headlines or Twitter, and so I’m left with my own observations and those of a liberal press (Of course, there’s a right-wing press, too, but that’s a topic for another time). For voters who align their beliefs with the National Rifle Association, and feel that illegal immigrants are a drain on our country and that people of certain faiths represent a terror threat to Americans, Mr. Trump apparently remains a reasonable candidate.

Is there a role here for living room consults from psychiatrists? Is there something for us as professionals to add to the prediction of Mr. Trump’s behavior if he becomes president? I don’t think so. Every American has ample data, and for those who are curious about Mr. Trump’s psychiatric status, they are free to Google the criteria for psychiatric disorders and see if they believe he meets them. The input of psychiatrists would neither change the election outcome nor accurately predict his behavior if elected. But it might make us look a bit grandiose.

Finally, I’ve focused here on Mr. Trump, while saying nothing about Secretary Hillary Clinton and her psychiatric status. She, too, has lived a public life, and while many of her activities have attracted media attention and scrutiny, I’ve seen nothing that has suggested she suffers from a psychiatric condition. There was, however, an op-ed piece in The New York Times on Aug. 23, 2016, by Frank Bruni, suggesting that Mrs. Clinton may have an 11th toe.

If nothing else, it’s time for this election to be over.

Dr. Miller is coauthor of “Committed: The Battle Over Involuntary Psychiatric Care,” forthcoming from Johns Hopkins University Press in fall 2016.

When it comes to political candidates and psychiatric disorders, the idea of diagnosing from afar is not new. In 1964, Fact magazine published an article called “The Unconscious of a Conservative: A Special Issue on the Mind of Barry Goldwater.” For the article, more than 2,400 psychiatrists responded to a survey, and many described the presidential candidate using a host of diagnostic and symptomatic terms. Mr. Goldwater lost the election in a landslide and successfully sued the magazine for $75,000.

In 1973, nearly a decade later, the American Psychiatric Association specifically noted in its code of ethics that psychiatrists should not offer diagnostic opinions on anyone who has not been personally examined and has not signed the proper authorization for this information to be released. The edict has been informally called The Goldwater Rule.

In the current election cycle, it has been a challenge for some psychiatrists to refrain from making public statements about our presidential candidates. Some have said the Goldwater Rule amounts to a gag order, and that the specifics of this election are different from other elections, and might warrant allowing psychiatrists to issue their professional opinions. The APA has reminded psychiatrists that to do so is unethical, and on Aug. 15, The New York Times ran an article by Benedict Carey titled: “The Psychiatric Question: Is it Fair to Analyze Donald Trump from Afar?”

I want to look at the question from a different stance. In assessing our political candidates, I’d like you to consider this: What difference does it make? Psychiatric diagnostic criteria are determined by consensus opinions of APA workgroup members. They aren’t perfect; they aren’t always accurate even when a patient is evaluated in person and seen over time; they are influenced by culture; and they aren’t always prognostic. One person’s experience of bipolar disorder is not another person’s experience of bipolar disorder, and personality disorders – such as narcissism or antisocial personality disorder – don’t have uniform presentations or outcomes. Some people with these difficulties head corporations and nations, while others wilt in prisons.

Half of the population will suffer from an episode of psychiatric illness at some point in their lives, and one in five people is affected in any given year. While we might all agree that many psychiatric symptoms are not compatible with being president, should the fact that a candidate has had a distant episode of mental illness, either fully resolved or controlled with treatment, disqualify him or her from holding office?

In an article published in the January 2006 issue of the Journal of Nervous and Mental Disease, Jonathan R. Davidson, MD; Kathryn M. Connor, MD; and Marvin Swartz, MD, looked at the biographical data on U.S. presidents from 1776 to 1974 and concluded that 49% met criteria for an Axis I psychiatric disorder. During those cycles, 27% had psychiatric difficulties while in office. Our presidents have suffered from depression and bipolar disorder, anxiety and alcoholism (J Nerv Ment Dis. 2006 Jan;194[1]47-51). No one has publicly attempted to tally personality disorders or use of other addictive substances. It may be safe to say that if the existence of psychiatric pathology had always been a disqualifier for public office, we’d live in a very different country.

Hopefully, when we approach our patients, we do so with warmth, kindness, and a genuine desire to help them heal. Psychiatry, at its best, is about intimacy and trust, and it is in that venue that people share their inner worlds and allow themselves to be vulnerable. Compassion is part of the deal; no one wants to have a mental illness. To refer to an unknown celebrity as “schizophrenic,” “psychotic,” or “having a godlike self-image” – or calling him “a dangerous lunatic,” as Sen. Goldwater was called – is not about careful diagnosis and compassion; it’s simply about name calling. To say that a politician or celebrity’s undesirable behavior is the result of a psychiatric illness based on cavalier observation is an insult to our patients, and it perpetuates stigma.

Psychiatric diagnoses are made by observing a constellation of symptoms that occur together. Mr. Trump has given the whole world years of data – he’s lived his life in a very public way. As a real estate developer, he has had countless employees who all know how they’ve been treated. We’ve seen him through three marriages and watched how he interacts with his children. We’ve seen him take out full-page ads calling for the death penalty for a group of young men who were wrongly convicted in the rape and assault of the Central Park jogger in 1988. If that’s not enough, he has hosted his own reality television show, and we’ve now seen him countless times in debates and rallies. We know how he treats his running mates, journalist Megyn Kelly, a news reporter with a disability, and the parents of a fallen soldier. We’ve watched him assure the nation during a primary debate that his genitals are big enough. Every individual is free to decide if Mr. Trump’s widely viewed patterns of behavior represent much-needed spunk and change with political beliefs that align with their own, or if his words and behaviors represent cruelty, impulsivity, poor judgment, and a pattern of actions that some might not feel is dignified enough for our country’s leader. No degree is required to observe and draw conclusions.

And please, let me be the first to admit that my perspective is biased: I’ve pointed out some of Mr. Trump’s more troubling behaviors and said nothing of the many wonderful things he may have done as both an entrepreneur and as a human being. Those don’t make the headlines or Twitter, and so I’m left with my own observations and those of a liberal press (Of course, there’s a right-wing press, too, but that’s a topic for another time). For voters who align their beliefs with the National Rifle Association, and feel that illegal immigrants are a drain on our country and that people of certain faiths represent a terror threat to Americans, Mr. Trump apparently remains a reasonable candidate.

Is there a role here for living room consults from psychiatrists? Is there something for us as professionals to add to the prediction of Mr. Trump’s behavior if he becomes president? I don’t think so. Every American has ample data, and for those who are curious about Mr. Trump’s psychiatric status, they are free to Google the criteria for psychiatric disorders and see if they believe he meets them. The input of psychiatrists would neither change the election outcome nor accurately predict his behavior if elected. But it might make us look a bit grandiose.

Finally, I’ve focused here on Mr. Trump, while saying nothing about Secretary Hillary Clinton and her psychiatric status. She, too, has lived a public life, and while many of her activities have attracted media attention and scrutiny, I’ve seen nothing that has suggested she suffers from a psychiatric condition. There was, however, an op-ed piece in The New York Times on Aug. 23, 2016, by Frank Bruni, suggesting that Mrs. Clinton may have an 11th toe.

If nothing else, it’s time for this election to be over.

Dr. Miller is coauthor of “Committed: The Battle Over Involuntary Psychiatric Care,” forthcoming from Johns Hopkins University Press in fall 2016.

As summer winds down, it is routine for children and adolescents to feel a little melancholy or even worried about the approaching start of school. But for some students, anxiety about school is more than routine; it is insurmountable. School refusal is a serious behavioral problem: without assertive management, it can become a pattern which is very difficult to alter. Whether a child is complaining of vague somatic concerns or is explicitly refusing to go to school, the pediatrician’s office is often the first place a parent will turn to for help. If you can recognize the true nature of the problem, help to determine its cause, and facilitate the needed management, you will have effectively treated what can become a disabling problem for vulnerable young people.

School refusal is happening when a child has major difficulty attending school, associated with intense emotional distress. It can be a refusal to attend school or difficulty remaining in school for an entire day. It is distinct (but not mutually exclusive) from truancy, which is a failure to attend school associated with antisocial behavior or other conduct problems. In the pediatrician’s office, school refusal sounds like, “He was moaning about a stomachache yesterday, I kept him home, but he had no fever and ate okay. Then it all repeated again this morning.” Or you might hear, “She was whining about a headache, but when I said she had to go to school, she started crying and couldn’t stop. She was hysterical!” In teenagers, there may be somatic complaints or just a sleepy, sulky refusal to get out of bed. Children with truancy might fake illness (as compared with feeling sick), or simply leave school. Truant children often want to be out of school doing other things, and may keep their whereabouts a secret from their parents. While it might seem like just one tough morning that can be shrugged off, true school refusal will continue or escalate unless it is properly managed.

School refusal affects approximately 5% of all children annually, affecting girls and boys in equal numbers and with peaks in incidence at the ages of 5 to 6 years and again at 10 to 11 years. Approximately half of children and teenagers with school refusal have a treatable psychiatric illness. In the Great Smoky Mountain Study of 2003, where more than 1,400 children were observed, they categorized children as being anxious school refusers, truant, or “mixed school refusers,” with features of both truancy and anxiety. In children with truancy or anxious school refusal, 25% had a psychiatric illness. In the mixed school refusers, they found 88% had at least one psychiatric diagnosis and 42% had somatic complaints. While pure truancy will require different management strategies from school and parents, those young people who display features of both anxiety and truancy around school attendance are most likely to be suffering from a psychiatric illness. Those illnesses most commonly associated with difficulty attending school include anxiety disorders (separation anxiety, social phobia, generalized anxiety disorder) and depression.

While psychiatric illness is a common factor, there is also always a behavioral component to school refusal. This simply means that children are either avoiding unpleasant feelings associated with school, such as anxiety, or escaping uncomfortable situations, such as bullying or the stress of performance. On the positive side, children may be refusing school because they are pursuing the attention of important people (parents, peers) or pursuing pleasurable activities (playing video games, surfing the web or hanging out in town). Beyond an internal anxiety disorder, some children may be facing bullying or threats at school or may have to walk through a dangerous neighborhood to get to school. Some children may be missing school because of significant stress or transitions at home, such as financial difficulties or divorce. Other children may be staying home to take care of younger siblings because of a parent’s medical illness or substance abuse problem. Children who are being abused may be kept home to prevent suspicion about bruises. Lastly, some children feel they have to stay home to be with a lonely or depressed parent. Gently asking about these very real concerns will help determine the necessary course of action.

Pediatricians can play a central role in the management of school refusal. Often, the most important step is helping parents to understand that there is not an insidious medical problem driving the morning stomachaches and headaches. It is critical to clarify that (usually) their child is not feigning illness, but that there is significant distress around school that has led to this behavioral problem. Even children who have a genuine medical problem also can have school refusal. Once parents understand that without proper management, this behavior will continue or worsen, they usually are ready to collaborate on effective management. Their child may need a thorough psychiatric evaluation to rule out a treatable underlying psychiatric diagnosis, particularly if they have both anxious and truant behaviors. Most of the psychiatric problems associated with school refusal will require therapy and some may require medications for effective treatment.

Successfully getting children back to school will require a behavior plan that is agreed upon by the parents and the school, and then used consistently. This plan will simply detail strategies to “demagnetize” the home and “remagnetize” the school. Such strategies might include ensuring that children are not allowed “screen time” when home from school, and that their homework expectations continue. It should support healthy routines, including a regular sleep schedule and exercise. It should facilitate their being able to gradually manage any anxiety associated with school (shorter days initially, the option to have time-outs in a favorite part of the school or with a favorite teacher). A behavior plan should detail strategies for the child to manage stress (relaxation strategies, connecting with supportive individuals, even singing a favorite song). This plan can detail reasonable accommodations for a medical or psychiatric condition and appropriate rewards for regular attendance, such as being able to go on a class trip.

Through all of this, the pediatrician is in a uniquely authoritative position to provide support and reassurance to parents of a school refusing child. The pediatrician has a unique ability to clarify for parents the seriousness of the behavioral problem, even if there is no medical problem. Compassionately acknowledging how much a child is suffering (and the parents, as well) is powerful. Remind parents that accommodating anxiety only shows a child you don’t think they can master it, and often keeps them from trying. Express confidence that this is a relatively common and treatable phenomenon. If a pediatrician’s and parents’ efforts do not work quickly, in a matter of a few days, urgent referral to a mental health consultant is indicated, as falling behind in school and any acceptance of staying home makes return to school more difficult every day.

Dr. Swick is an attending psychiatrist in the division of child psychiatry at Massachusetts General Hospital, Boston, and director of the Parenting at a Challenging Time (PACT) Program at the Vernon Cancer Center at Newton Wellesley Hospital, also in Boston. Dr. Jellinek is professor emeritus of psychiatry and pediatrics, Harvard Medical School, Boston.

As summer winds down, it is routine for children and adolescents to feel a little melancholy or even worried about the approaching start of school. But for some students, anxiety about school is more than routine; it is insurmountable. School refusal is a serious behavioral problem: without assertive management, it can become a pattern which is very difficult to alter. Whether a child is complaining of vague somatic concerns or is explicitly refusing to go to school, the pediatrician’s office is often the first place a parent will turn to for help. If you can recognize the true nature of the problem, help to determine its cause, and facilitate the needed management, you will have effectively treated what can become a disabling problem for vulnerable young people.

School refusal is happening when a child has major difficulty attending school, associated with intense emotional distress. It can be a refusal to attend school or difficulty remaining in school for an entire day. It is distinct (but not mutually exclusive) from truancy, which is a failure to attend school associated with antisocial behavior or other conduct problems. In the pediatrician’s office, school refusal sounds like, “He was moaning about a stomachache yesterday, I kept him home, but he had no fever and ate okay. Then it all repeated again this morning.” Or you might hear, “She was whining about a headache, but when I said she had to go to school, she started crying and couldn’t stop. She was hysterical!” In teenagers, there may be somatic complaints or just a sleepy, sulky refusal to get out of bed. Children with truancy might fake illness (as compared with feeling sick), or simply leave school. Truant children often want to be out of school doing other things, and may keep their whereabouts a secret from their parents. While it might seem like just one tough morning that can be shrugged off, true school refusal will continue or escalate unless it is properly managed.

School refusal affects approximately 5% of all children annually, affecting girls and boys in equal numbers and with peaks in incidence at the ages of 5 to 6 years and again at 10 to 11 years. Approximately half of children and teenagers with school refusal have a treatable psychiatric illness. In the Great Smoky Mountain Study of 2003, where more than 1,400 children were observed, they categorized children as being anxious school refusers, truant, or “mixed school refusers,” with features of both truancy and anxiety. In children with truancy or anxious school refusal, 25% had a psychiatric illness. In the mixed school refusers, they found 88% had at least one psychiatric diagnosis and 42% had somatic complaints. While pure truancy will require different management strategies from school and parents, those young people who display features of both anxiety and truancy around school attendance are most likely to be suffering from a psychiatric illness. Those illnesses most commonly associated with difficulty attending school include anxiety disorders (separation anxiety, social phobia, generalized anxiety disorder) and depression.

While psychiatric illness is a common factor, there is also always a behavioral component to school refusal. This simply means that children are either avoiding unpleasant feelings associated with school, such as anxiety, or escaping uncomfortable situations, such as bullying or the stress of performance. On the positive side, children may be refusing school because they are pursuing the attention of important people (parents, peers) or pursuing pleasurable activities (playing video games, surfing the web or hanging out in town). Beyond an internal anxiety disorder, some children may be facing bullying or threats at school or may have to walk through a dangerous neighborhood to get to school. Some children may be missing school because of significant stress or transitions at home, such as financial difficulties or divorce. Other children may be staying home to take care of younger siblings because of a parent’s medical illness or substance abuse problem. Children who are being abused may be kept home to prevent suspicion about bruises. Lastly, some children feel they have to stay home to be with a lonely or depressed parent. Gently asking about these very real concerns will help determine the necessary course of action.

Pediatricians can play a central role in the management of school refusal. Often, the most important step is helping parents to understand that there is not an insidious medical problem driving the morning stomachaches and headaches. It is critical to clarify that (usually) their child is not feigning illness, but that there is significant distress around school that has led to this behavioral problem. Even children who have a genuine medical problem also can have school refusal. Once parents understand that without proper management, this behavior will continue or worsen, they usually are ready to collaborate on effective management. Their child may need a thorough psychiatric evaluation to rule out a treatable underlying psychiatric diagnosis, particularly if they have both anxious and truant behaviors. Most of the psychiatric problems associated with school refusal will require therapy and some may require medications for effective treatment.

Successfully getting children back to school will require a behavior plan that is agreed upon by the parents and the school, and then used consistently. This plan will simply detail strategies to “demagnetize” the home and “remagnetize” the school. Such strategies might include ensuring that children are not allowed “screen time” when home from school, and that their homework expectations continue. It should support healthy routines, including a regular sleep schedule and exercise. It should facilitate their being able to gradually manage any anxiety associated with school (shorter days initially, the option to have time-outs in a favorite part of the school or with a favorite teacher). A behavior plan should detail strategies for the child to manage stress (relaxation strategies, connecting with supportive individuals, even singing a favorite song). This plan can detail reasonable accommodations for a medical or psychiatric condition and appropriate rewards for regular attendance, such as being able to go on a class trip.

Through all of this, the pediatrician is in a uniquely authoritative position to provide support and reassurance to parents of a school refusing child. The pediatrician has a unique ability to clarify for parents the seriousness of the behavioral problem, even if there is no medical problem. Compassionately acknowledging how much a child is suffering (and the parents, as well) is powerful. Remind parents that accommodating anxiety only shows a child you don’t think they can master it, and often keeps them from trying. Express confidence that this is a relatively common and treatable phenomenon. If a pediatrician’s and parents’ efforts do not work quickly, in a matter of a few days, urgent referral to a mental health consultant is indicated, as falling behind in school and any acceptance of staying home makes return to school more difficult every day.

Dr. Swick is an attending psychiatrist in the division of child psychiatry at Massachusetts General Hospital, Boston, and director of the Parenting at a Challenging Time (PACT) Program at the Vernon Cancer Center at Newton Wellesley Hospital, also in Boston. Dr. Jellinek is professor emeritus of psychiatry and pediatrics, Harvard Medical School, Boston.

As summer winds down, it is routine for children and adolescents to feel a little melancholy or even worried about the approaching start of school. But for some students, anxiety about school is more than routine; it is insurmountable. School refusal is a serious behavioral problem: without assertive management, it can become a pattern which is very difficult to alter. Whether a child is complaining of vague somatic concerns or is explicitly refusing to go to school, the pediatrician’s office is often the first place a parent will turn to for help. If you can recognize the true nature of the problem, help to determine its cause, and facilitate the needed management, you will have effectively treated what can become a disabling problem for vulnerable young people.

School refusal is happening when a child has major difficulty attending school, associated with intense emotional distress. It can be a refusal to attend school or difficulty remaining in school for an entire day. It is distinct (but not mutually exclusive) from truancy, which is a failure to attend school associated with antisocial behavior or other conduct problems. In the pediatrician’s office, school refusal sounds like, “He was moaning about a stomachache yesterday, I kept him home, but he had no fever and ate okay. Then it all repeated again this morning.” Or you might hear, “She was whining about a headache, but when I said she had to go to school, she started crying and couldn’t stop. She was hysterical!” In teenagers, there may be somatic complaints or just a sleepy, sulky refusal to get out of bed. Children with truancy might fake illness (as compared with feeling sick), or simply leave school. Truant children often want to be out of school doing other things, and may keep their whereabouts a secret from their parents. While it might seem like just one tough morning that can be shrugged off, true school refusal will continue or escalate unless it is properly managed.

School refusal affects approximately 5% of all children annually, affecting girls and boys in equal numbers and with peaks in incidence at the ages of 5 to 6 years and again at 10 to 11 years. Approximately half of children and teenagers with school refusal have a treatable psychiatric illness. In the Great Smoky Mountain Study of 2003, where more than 1,400 children were observed, they categorized children as being anxious school refusers, truant, or “mixed school refusers,” with features of both truancy and anxiety. In children with truancy or anxious school refusal, 25% had a psychiatric illness. In the mixed school refusers, they found 88% had at least one psychiatric diagnosis and 42% had somatic complaints. While pure truancy will require different management strategies from school and parents, those young people who display features of both anxiety and truancy around school attendance are most likely to be suffering from a psychiatric illness. Those illnesses most commonly associated with difficulty attending school include anxiety disorders (separation anxiety, social phobia, generalized anxiety disorder) and depression.

While psychiatric illness is a common factor, there is also always a behavioral component to school refusal. This simply means that children are either avoiding unpleasant feelings associated with school, such as anxiety, or escaping uncomfortable situations, such as bullying or the stress of performance. On the positive side, children may be refusing school because they are pursuing the attention of important people (parents, peers) or pursuing pleasurable activities (playing video games, surfing the web or hanging out in town). Beyond an internal anxiety disorder, some children may be facing bullying or threats at school or may have to walk through a dangerous neighborhood to get to school. Some children may be missing school because of significant stress or transitions at home, such as financial difficulties or divorce. Other children may be staying home to take care of younger siblings because of a parent’s medical illness or substance abuse problem. Children who are being abused may be kept home to prevent suspicion about bruises. Lastly, some children feel they have to stay home to be with a lonely or depressed parent. Gently asking about these very real concerns will help determine the necessary course of action.

Pediatricians can play a central role in the management of school refusal. Often, the most important step is helping parents to understand that there is not an insidious medical problem driving the morning stomachaches and headaches. It is critical to clarify that (usually) their child is not feigning illness, but that there is significant distress around school that has led to this behavioral problem. Even children who have a genuine medical problem also can have school refusal. Once parents understand that without proper management, this behavior will continue or worsen, they usually are ready to collaborate on effective management. Their child may need a thorough psychiatric evaluation to rule out a treatable underlying psychiatric diagnosis, particularly if they have both anxious and truant behaviors. Most of the psychiatric problems associated with school refusal will require therapy and some may require medications for effective treatment.

Successfully getting children back to school will require a behavior plan that is agreed upon by the parents and the school, and then used consistently. This plan will simply detail strategies to “demagnetize” the home and “remagnetize” the school. Such strategies might include ensuring that children are not allowed “screen time” when home from school, and that their homework expectations continue. It should support healthy routines, including a regular sleep schedule and exercise. It should facilitate their being able to gradually manage any anxiety associated with school (shorter days initially, the option to have time-outs in a favorite part of the school or with a favorite teacher). A behavior plan should detail strategies for the child to manage stress (relaxation strategies, connecting with supportive individuals, even singing a favorite song). This plan can detail reasonable accommodations for a medical or psychiatric condition and appropriate rewards for regular attendance, such as being able to go on a class trip.

Through all of this, the pediatrician is in a uniquely authoritative position to provide support and reassurance to parents of a school refusing child. The pediatrician has a unique ability to clarify for parents the seriousness of the behavioral problem, even if there is no medical problem. Compassionately acknowledging how much a child is suffering (and the parents, as well) is powerful. Remind parents that accommodating anxiety only shows a child you don’t think they can master it, and often keeps them from trying. Express confidence that this is a relatively common and treatable phenomenon. If a pediatrician’s and parents’ efforts do not work quickly, in a matter of a few days, urgent referral to a mental health consultant is indicated, as falling behind in school and any acceptance of staying home makes return to school more difficult every day.

Dr. Swick is an attending psychiatrist in the division of child psychiatry at Massachusetts General Hospital, Boston, and director of the Parenting at a Challenging Time (PACT) Program at the Vernon Cancer Center at Newton Wellesley Hospital, also in Boston. Dr. Jellinek is professor emeritus of psychiatry and pediatrics, Harvard Medical School, Boston.

It is important to step back occasionally to survey where one has been and to plot a new heading. In an online Aug. 10, 2016, release, the New England Journal of Medicine posted two opinion pieces that provide perspective on hospital medicine. As is often the case when journalism presents two opinions, the viewpoints represent opposite ends of a spectrum and the truth lies somewhere in between.

In one essay, Robert Wachter, MD, and Lee Goldman, MD, highlight the successful growth of hospital medicine (N Eng J Med. 2016, Aug 10. doi: 10.1056/NEJMp1607958). In just 2 decades, more than 50,000 physicians have changed their focus to the care of inpatients. The authors state that “many stars had to align” for hospital medicine to grow as rapidly as it has. I would argue instead that many talented leaders of the field have moved heaven and earth to create that alignment and birth this field.

In the other essay, Richard Gunderman, MD, focuses on what he sees as having been lost in this evolution (N Eng J Med. 2016, Aug 10. doi: 10.1056/NEJMp1608289). I believe Dr. Gunderman’s viewpoint nostalgically longs for the good old days and a model of an interpersonal doctor-patient relationship that never really existed for a large portion of the population. If you were wealthy, lived most of your life in one location, and had only intermittent or common diseases, then perhaps you had a trusted general internist to provide your medical care and provide the emotional reassurance that nourished both patient and doctor. But in modern medicine, that scenario is uncommon. With large group practices, there is only a small chance that your personal physician will be on call on the night of your admission to a hospital. The next day, as test results and specialty consults trickle in, that personal physician will be trapped in a busy outpatient clinic and not truly available at hospital bedside in “your moment of greatest need,” as Dr. Gunderman phrased it. When your personal physician finally does make rounds, s/he will find the hospital environment inefficient and repeating the same small mistakes that happened to his/her last patient.

I’ve been writing about and teaching professionalism for years. I agree with Dr. Gunderman about the importance of a doctor-patient relationship. I believe reducing physicians to being automatons in a hospital assembly line would be a bad idea. But this essay’s rose-colored and sienna-colored portrait of that relationship is not helpful guidance in the modern world. Surveyors and navigators need sharp, clear vision.

Trade-offs are being made. Many pediatricians in affluent communities do have the opportunity to establish long-term relationships with families, sometimes for multiple generations of children. Those relationships attract medical students into pediatrics and family medicine. I was fortunate enough to establish many of those relationships when I practiced outpatient pediatrics. During my last interstate move, the man packing the picture frames was amused to find amidst my many diplomas a framed crayon drawing. It was a gift to me from a young patient. I told the mover that I would be sadder to have that drawing damaged than if a diploma was damaged in the move. So he wrapped it with extra padding.

Those bonds established with families make up the emotional sustenance throughout a career that justifies the years of sacrifice spent becoming a physician. There is no doubt that it is easier to form those bonds in outpatient pediatrics. At a community hospital, with 7 days on/7 days off scheduling, I usually provide care for the entire hospitalization of a child. That provides emotional satisfaction for both the parents and for me as a physician in ways that 12-hour shifts usually don’t.

The diminishment of those relationships needs to be acknowledged, but not to the exclusion of what a hospitalist can provide. When I practiced general pediatrics and only admitted 1 or 2 children each week, I was often frustrated by inefficiency and errors in the hospital, but I had little recourse for changing it. As a hospitalist admitting 500 patients per year, I can perform problem solving and devote resources to continuously improve the quality and safety of inpatient care. I provide those improvements to all patients admitted to the hospital, whether they have a medical home or not. That fosters social justice. As a function-over-fashion person, that success is emotionally rewarding, too.

Dr. Powell is a pediatric hospitalist and clinical ethics consultant living in St. Louis. Email him at [email protected].

It is important to step back occasionally to survey where one has been and to plot a new heading. In an online Aug. 10, 2016, release, the New England Journal of Medicine posted two opinion pieces that provide perspective on hospital medicine. As is often the case when journalism presents two opinions, the viewpoints represent opposite ends of a spectrum and the truth lies somewhere in between.

In one essay, Robert Wachter, MD, and Lee Goldman, MD, highlight the successful growth of hospital medicine (N Eng J Med. 2016, Aug 10. doi: 10.1056/NEJMp1607958). In just 2 decades, more than 50,000 physicians have changed their focus to the care of inpatients. The authors state that “many stars had to align” for hospital medicine to grow as rapidly as it has. I would argue instead that many talented leaders of the field have moved heaven and earth to create that alignment and birth this field.

In the other essay, Richard Gunderman, MD, focuses on what he sees as having been lost in this evolution (N Eng J Med. 2016, Aug 10. doi: 10.1056/NEJMp1608289). I believe Dr. Gunderman’s viewpoint nostalgically longs for the good old days and a model of an interpersonal doctor-patient relationship that never really existed for a large portion of the population. If you were wealthy, lived most of your life in one location, and had only intermittent or common diseases, then perhaps you had a trusted general internist to provide your medical care and provide the emotional reassurance that nourished both patient and doctor. But in modern medicine, that scenario is uncommon. With large group practices, there is only a small chance that your personal physician will be on call on the night of your admission to a hospital. The next day, as test results and specialty consults trickle in, that personal physician will be trapped in a busy outpatient clinic and not truly available at hospital bedside in “your moment of greatest need,” as Dr. Gunderman phrased it. When your personal physician finally does make rounds, s/he will find the hospital environment inefficient and repeating the same small mistakes that happened to his/her last patient.

I’ve been writing about and teaching professionalism for years. I agree with Dr. Gunderman about the importance of a doctor-patient relationship. I believe reducing physicians to being automatons in a hospital assembly line would be a bad idea. But this essay’s rose-colored and sienna-colored portrait of that relationship is not helpful guidance in the modern world. Surveyors and navigators need sharp, clear vision.

Trade-offs are being made. Many pediatricians in affluent communities do have the opportunity to establish long-term relationships with families, sometimes for multiple generations of children. Those relationships attract medical students into pediatrics and family medicine. I was fortunate enough to establish many of those relationships when I practiced outpatient pediatrics. During my last interstate move, the man packing the picture frames was amused to find amidst my many diplomas a framed crayon drawing. It was a gift to me from a young patient. I told the mover that I would be sadder to have that drawing damaged than if a diploma was damaged in the move. So he wrapped it with extra padding.

Those bonds established with families make up the emotional sustenance throughout a career that justifies the years of sacrifice spent becoming a physician. There is no doubt that it is easier to form those bonds in outpatient pediatrics. At a community hospital, with 7 days on/7 days off scheduling, I usually provide care for the entire hospitalization of a child. That provides emotional satisfaction for both the parents and for me as a physician in ways that 12-hour shifts usually don’t.

The diminishment of those relationships needs to be acknowledged, but not to the exclusion of what a hospitalist can provide. When I practiced general pediatrics and only admitted 1 or 2 children each week, I was often frustrated by inefficiency and errors in the hospital, but I had little recourse for changing it. As a hospitalist admitting 500 patients per year, I can perform problem solving and devote resources to continuously improve the quality and safety of inpatient care. I provide those improvements to all patients admitted to the hospital, whether they have a medical home or not. That fosters social justice. As a function-over-fashion person, that success is emotionally rewarding, too.

Dr. Powell is a pediatric hospitalist and clinical ethics consultant living in St. Louis. Email him at [email protected].

It is important to step back occasionally to survey where one has been and to plot a new heading. In an online Aug. 10, 2016, release, the New England Journal of Medicine posted two opinion pieces that provide perspective on hospital medicine. As is often the case when journalism presents two opinions, the viewpoints represent opposite ends of a spectrum and the truth lies somewhere in between.

In one essay, Robert Wachter, MD, and Lee Goldman, MD, highlight the successful growth of hospital medicine (N Eng J Med. 2016, Aug 10. doi: 10.1056/NEJMp1607958). In just 2 decades, more than 50,000 physicians have changed their focus to the care of inpatients. The authors state that “many stars had to align” for hospital medicine to grow as rapidly as it has. I would argue instead that many talented leaders of the field have moved heaven and earth to create that alignment and birth this field.

In the other essay, Richard Gunderman, MD, focuses on what he sees as having been lost in this evolution (N Eng J Med. 2016, Aug 10. doi: 10.1056/NEJMp1608289). I believe Dr. Gunderman’s viewpoint nostalgically longs for the good old days and a model of an interpersonal doctor-patient relationship that never really existed for a large portion of the population. If you were wealthy, lived most of your life in one location, and had only intermittent or common diseases, then perhaps you had a trusted general internist to provide your medical care and provide the emotional reassurance that nourished both patient and doctor. But in modern medicine, that scenario is uncommon. With large group practices, there is only a small chance that your personal physician will be on call on the night of your admission to a hospital. The next day, as test results and specialty consults trickle in, that personal physician will be trapped in a busy outpatient clinic and not truly available at hospital bedside in “your moment of greatest need,” as Dr. Gunderman phrased it. When your personal physician finally does make rounds, s/he will find the hospital environment inefficient and repeating the same small mistakes that happened to his/her last patient.

I’ve been writing about and teaching professionalism for years. I agree with Dr. Gunderman about the importance of a doctor-patient relationship. I believe reducing physicians to being automatons in a hospital assembly line would be a bad idea. But this essay’s rose-colored and sienna-colored portrait of that relationship is not helpful guidance in the modern world. Surveyors and navigators need sharp, clear vision.

Trade-offs are being made. Many pediatricians in affluent communities do have the opportunity to establish long-term relationships with families, sometimes for multiple generations of children. Those relationships attract medical students into pediatrics and family medicine. I was fortunate enough to establish many of those relationships when I practiced outpatient pediatrics. During my last interstate move, the man packing the picture frames was amused to find amidst my many diplomas a framed crayon drawing. It was a gift to me from a young patient. I told the mover that I would be sadder to have that drawing damaged than if a diploma was damaged in the move. So he wrapped it with extra padding.

Those bonds established with families make up the emotional sustenance throughout a career that justifies the years of sacrifice spent becoming a physician. There is no doubt that it is easier to form those bonds in outpatient pediatrics. At a community hospital, with 7 days on/7 days off scheduling, I usually provide care for the entire hospitalization of a child. That provides emotional satisfaction for both the parents and for me as a physician in ways that 12-hour shifts usually don’t.

The diminishment of those relationships needs to be acknowledged, but not to the exclusion of what a hospitalist can provide. When I practiced general pediatrics and only admitted 1 or 2 children each week, I was often frustrated by inefficiency and errors in the hospital, but I had little recourse for changing it. As a hospitalist admitting 500 patients per year, I can perform problem solving and devote resources to continuously improve the quality and safety of inpatient care. I provide those improvements to all patients admitted to the hospital, whether they have a medical home or not. That fosters social justice. As a function-over-fashion person, that success is emotionally rewarding, too.

Dr. Powell is a pediatric hospitalist and clinical ethics consultant living in St. Louis. Email him at [email protected].

At the summer meetings of the American Academy of Dermatology, AAD President Abel Torres screened a video of members responding to the question, “What keeps you up at night?” A recurring refrain in many of their responses was, “loss of autonomy.”

Many physicians feel they are losing autonomy. No doubt they are right. But physicians are not alone in their loss.

A young academic friend of mine had a similar lament. “Some assistant dean sent me an email ordering me to grade my students in a way that made no sense,” he said. “I challenged him to explain why. He answered that my school was following the guidelines of some organization I’d never heard of.”

“Academics used to be autonomous,” he said. “No more.”

Another professor friend decided to retire. “Forty years in the department,” he said, “10 as chair. Now a junior administrator tells me that I have to spend more hours on campus, even though I don’t have anything useful to do when I’m there. She said there are new rules for more academic efficiency.”

New administrators. Guidelines. Efficiency. Experienced hands dropping out or retiring out of frustration. Any of these sound familiar?

Teachers also complain to me about their loss of autonomy. “I used to be able to use judgment,” said one. “I knew what worked for a specific student. Now I just teach to the standardized test.

“For every one of my 23 kindergartners, I spent 1 hour filling out an iPad questionnaire on reading readiness. I’ve had it.”

“What will you do instead?” I asked him.

“Something with dogs,” he said.

And so it goes. Accountants and attorneys complain about heavy reporting regulations, with new ones added each year. Judges in Wisconsin make sentencing decisions using proprietary algorithms that no one outside the company that sells the algorithms has validated. Financial advisers have clients sign boilerplate statements documenting that they accept a certain level of risk. These clients may or may not understand what “level of risk” really implies, but either way they must sign a form, and the form must be filed. If you didn’t document it, you didn’t do it. If you documented it, you did it, even though you may not have really done anything meaningful.

An internist told me how things are in her new dispensation.

“They allow 15 minutes for a physical,” she said, “which is not enough anyway. But I also have to check off boxes for the EMR that add nothing to patient care. Last year we had to start asking about gender status. ‘What was your gender assignment at birth?’ ‘What is it now?’ We have to ask that every year – and click the box that says we did it.

“Several docs in our group retired. Another bunch went concierge. They couldn’t deal with it anymore.”

Metrics. Algorithms. Higher authorities who tell professionals what to do, how to do it, how to record it, business quants with scant understanding of what professionals actually profess. All so familiar and tiresome. It’s everywhere, and it’s bigger than any of us.

Loss of autonomy by professionals across the board reflects a changed understanding by society at large of what quality service is and how it should be judged. Numbers are in. Personal judgment – in our case, clinical judgment – is out. Since judgment can’t be measured, it cannot be trusted.

To a certain extent, autonomy is an illusion. We can do what we want as long as powers larger than we are – natural, social, political – let us do it. Those powers may lie dormant for a while, but they’re always there, and always have been. When they wake up and change the rules of the game, everyone has to adapt. New burdens in the practice of medicine are just one instance of a much broader trend.

Our professional organizations know this well. They are hard at work giving the authorities, government, and insurance administrators what they demand: data showing that what we do is useful, in the quantitative terms the authorities will accept.

To the extent that they succeed, we will be able to do some of what we want to do. Young people entering the medical field will expect nothing more. Some of their older colleagues will be satisfied that they are autonomous enough. The rest will have to find something else to do.

Dr. Rockoff practices dermatology in Brookline, Mass. He is on the clinical faculty at Tufts University School of Medicine, Boston, and has taught senior medical students and other trainees for 30 years.

At the summer meetings of the American Academy of Dermatology, AAD President Abel Torres screened a video of members responding to the question, “What keeps you up at night?” A recurring refrain in many of their responses was, “loss of autonomy.”

Many physicians feel they are losing autonomy. No doubt they are right. But physicians are not alone in their loss.

A young academic friend of mine had a similar lament. “Some assistant dean sent me an email ordering me to grade my students in a way that made no sense,” he said. “I challenged him to explain why. He answered that my school was following the guidelines of some organization I’d never heard of.”

“Academics used to be autonomous,” he said. “No more.”

Another professor friend decided to retire. “Forty years in the department,” he said, “10 as chair. Now a junior administrator tells me that I have to spend more hours on campus, even though I don’t have anything useful to do when I’m there. She said there are new rules for more academic efficiency.”

New administrators. Guidelines. Efficiency. Experienced hands dropping out or retiring out of frustration. Any of these sound familiar?

Teachers also complain to me about their loss of autonomy. “I used to be able to use judgment,” said one. “I knew what worked for a specific student. Now I just teach to the standardized test.

“For every one of my 23 kindergartners, I spent 1 hour filling out an iPad questionnaire on reading readiness. I’ve had it.”

“What will you do instead?” I asked him.

“Something with dogs,” he said.

And so it goes. Accountants and attorneys complain about heavy reporting regulations, with new ones added each year. Judges in Wisconsin make sentencing decisions using proprietary algorithms that no one outside the company that sells the algorithms has validated. Financial advisers have clients sign boilerplate statements documenting that they accept a certain level of risk. These clients may or may not understand what “level of risk” really implies, but either way they must sign a form, and the form must be filed. If you didn’t document it, you didn’t do it. If you documented it, you did it, even though you may not have really done anything meaningful.

An internist told me how things are in her new dispensation.

“They allow 15 minutes for a physical,” she said, “which is not enough anyway. But I also have to check off boxes for the EMR that add nothing to patient care. Last year we had to start asking about gender status. ‘What was your gender assignment at birth?’ ‘What is it now?’ We have to ask that every year – and click the box that says we did it.

“Several docs in our group retired. Another bunch went concierge. They couldn’t deal with it anymore.”

Metrics. Algorithms. Higher authorities who tell professionals what to do, how to do it, how to record it, business quants with scant understanding of what professionals actually profess. All so familiar and tiresome. It’s everywhere, and it’s bigger than any of us.

Loss of autonomy by professionals across the board reflects a changed understanding by society at large of what quality service is and how it should be judged. Numbers are in. Personal judgment – in our case, clinical judgment – is out. Since judgment can’t be measured, it cannot be trusted.

To a certain extent, autonomy is an illusion. We can do what we want as long as powers larger than we are – natural, social, political – let us do it. Those powers may lie dormant for a while, but they’re always there, and always have been. When they wake up and change the rules of the game, everyone has to adapt. New burdens in the practice of medicine are just one instance of a much broader trend.

Our professional organizations know this well. They are hard at work giving the authorities, government, and insurance administrators what they demand: data showing that what we do is useful, in the quantitative terms the authorities will accept.

To the extent that they succeed, we will be able to do some of what we want to do. Young people entering the medical field will expect nothing more. Some of their older colleagues will be satisfied that they are autonomous enough. The rest will have to find something else to do.

Dr. Rockoff practices dermatology in Brookline, Mass. He is on the clinical faculty at Tufts University School of Medicine, Boston, and has taught senior medical students and other trainees for 30 years.

At the summer meetings of the American Academy of Dermatology, AAD President Abel Torres screened a video of members responding to the question, “What keeps you up at night?” A recurring refrain in many of their responses was, “loss of autonomy.”

Many physicians feel they are losing autonomy. No doubt they are right. But physicians are not alone in their loss.

A young academic friend of mine had a similar lament. “Some assistant dean sent me an email ordering me to grade my students in a way that made no sense,” he said. “I challenged him to explain why. He answered that my school was following the guidelines of some organization I’d never heard of.”

“Academics used to be autonomous,” he said. “No more.”

Another professor friend decided to retire. “Forty years in the department,” he said, “10 as chair. Now a junior administrator tells me that I have to spend more hours on campus, even though I don’t have anything useful to do when I’m there. She said there are new rules for more academic efficiency.”

New administrators. Guidelines. Efficiency. Experienced hands dropping out or retiring out of frustration. Any of these sound familiar?

Teachers also complain to me about their loss of autonomy. “I used to be able to use judgment,” said one. “I knew what worked for a specific student. Now I just teach to the standardized test.

“For every one of my 23 kindergartners, I spent 1 hour filling out an iPad questionnaire on reading readiness. I’ve had it.”

“What will you do instead?” I asked him.

“Something with dogs,” he said.

And so it goes. Accountants and attorneys complain about heavy reporting regulations, with new ones added each year. Judges in Wisconsin make sentencing decisions using proprietary algorithms that no one outside the company that sells the algorithms has validated. Financial advisers have clients sign boilerplate statements documenting that they accept a certain level of risk. These clients may or may not understand what “level of risk” really implies, but either way they must sign a form, and the form must be filed. If you didn’t document it, you didn’t do it. If you documented it, you did it, even though you may not have really done anything meaningful.

An internist told me how things are in her new dispensation.

“They allow 15 minutes for a physical,” she said, “which is not enough anyway. But I also have to check off boxes for the EMR that add nothing to patient care. Last year we had to start asking about gender status. ‘What was your gender assignment at birth?’ ‘What is it now?’ We have to ask that every year – and click the box that says we did it.

“Several docs in our group retired. Another bunch went concierge. They couldn’t deal with it anymore.”

Metrics. Algorithms. Higher authorities who tell professionals what to do, how to do it, how to record it, business quants with scant understanding of what professionals actually profess. All so familiar and tiresome. It’s everywhere, and it’s bigger than any of us.

Loss of autonomy by professionals across the board reflects a changed understanding by society at large of what quality service is and how it should be judged. Numbers are in. Personal judgment – in our case, clinical judgment – is out. Since judgment can’t be measured, it cannot be trusted.

To a certain extent, autonomy is an illusion. We can do what we want as long as powers larger than we are – natural, social, political – let us do it. Those powers may lie dormant for a while, but they’re always there, and always have been. When they wake up and change the rules of the game, everyone has to adapt. New burdens in the practice of medicine are just one instance of a much broader trend.

Our professional organizations know this well. They are hard at work giving the authorities, government, and insurance administrators what they demand: data showing that what we do is useful, in the quantitative terms the authorities will accept.

To the extent that they succeed, we will be able to do some of what we want to do. Young people entering the medical field will expect nothing more. Some of their older colleagues will be satisfied that they are autonomous enough. The rest will have to find something else to do.

Dr. Rockoff practices dermatology in Brookline, Mass. He is on the clinical faculty at Tufts University School of Medicine, Boston, and has taught senior medical students and other trainees for 30 years.