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Suicide barriers on the Golden Gate Bridge: Will they save lives?
Ultimately, we need to find better treatments for depression and anxiety
San Francisco entrances people. Photographers capture more images of the Golden Gate Bridge than any other bridge in the world.1 And only the Nanjing Yangtze River Bridge in China surpasses the Golden Gate as a destination for dying by suicide.2 At least 1,700 people reportedly have plunged from the bridge to their deaths since its opening in 1937.3
Despite concerted efforts by bridge security, the local mental health community, and a volunteer organization – Bridgewatch Angels – suicides continue at the pace of about 1 every 2 weeks. After more than 60 years of discussion, transportation officials allocated funding and have started building a suicide prevention barrier system on the Golden Gate.
Extrapolating from the success of barriers built on other bridges that were “suicide magnets,” we should be able to assure people that suicide deaths from the Golden Gate will dramatically decrease, and perhaps cease completely.4 Certainly, some in the mental health community think this barrier will save lives. They support this claim by citing research showing that removing highly accessible and lethal means of suicide reduces overall suicide rates, and that suicidal individuals, when thwarted, do not seek alternate modes of death.
I support building the Golden Gate suicide barrier, partly because symbolically, it should deliver a powerful message that we value all human life. But will the barrier save lives? I don’t think it will. As the American Psychiatric Association prepares to gather for its annual meeting in San Francisco, I would like to share my reasoning.
What the evidence shows
The most robust evidence that restricting availability of highly lethal and accessible means of suicide reduces overall suicide deaths comes from studies looking at self-poisoning in Asian countries and Great Britain. In many parts of Asia, ingestion of pesticides constitutes a significant proportion of suicide deaths, and several studies have found that, in localities where sales of highly lethal pesticides were restricted, overall suicide deaths decreased.5,6 Conversely, suicide rates increased when more lethal varieties of pesticides became more available. In Great Britain, overall suicide rates decreased when natural gas replaced coal gas for home heating and cooking.7 For decades preceding this change, more Britons had killed themselves by inhaling coal gas than by any other method.
Strong correlations exist between regional levels of gun ownership and suicide rates by shooting,8 but several potentially confounding sociopolitical factors explain some portion of this connection. Stronger evidence of gun availability affecting suicide rates has been demonstrated by decreases in suicide rates after restrictions in gun access in Switzerland,9 Israel,10 and other areas. These studies show correlations – not causality. However, the number of studies, links between increases and decreases in suicide rates with changes in access to guns, absence of changes in suicide rates during the same time periods among ostensibly similar control populations, and lack of other compelling explanations support the argument that restricting access to highly lethal and accessible means of suicide prevents suicide deaths overall.
The installation of suicide barriers on bridges that have been the sites of multiple suicides robustly reduces or even eliminates suicide deaths from those bridges,11 but the effect on overall suicide rates remains less clear. Various studies have found subsequent increases or no changes12-14 in suicide deaths from other bridges or tall buildings in the vicinity after the installation of suicide barriers on a “suicide magnet.” Many of the studies failed to find any impact on overall suicide rates in the regions investigated. Deaths from jumping off tall structures constitute a tiny proportion of total suicide deaths, making it difficult to detect any changes in overall suicide rates. In the United States, suicides by jumping/falling constituted 1%-2% of total suicides over the last several decades.15
If we know that restricting highly lethal and accessible methods of killing reduces suicide deaths, why would I question the value of the Golden Gate suicide barrier in preventing overall suicide deaths?
Unique aspects of the bridge
The World High Dive Federation recommends keeping dives to less than 20 meters (65.5 feet), with a few exceptions.16 The rail of the Golden Gate Bridge stands 67 meters (220 feet) above the water, and assuming minimal wind resistance, a falling person traverses that distance in about 3.7 seconds and lands with an impact of 130 km/hour (81 miles per hour).17 Only about 1%-2% of those jumping from the Golden Gate survive that fall.18
A 99% likelihood of death sounds pretty lethal; however, death by jumping from the Golden Gate inherently takes place in a public space, with the opportunity for interventions by other people. A more realistic calculation of the lethality would start the instant that someone initiates a sequence of behaviors leading to the intended death. By that criteria, measuring the lethality of the Golden Gate would begin when an individual enters a vehicle or sets off on foot with the plan of going over the railing.
Unless our surveillance-oriented society makes substantially greater advances (which I oppose), we will remain unable to assess suicide lethality by starting at the moment of inception. However, we do have data showing what happens once someone with suicidal intentions walks onto the bridge.
Between 2000 and 2018, observers noted 2,546 people on the Golden Gate who appeared to be considering a suicide attempt, the San Francisco Chronicle has reported. Five hundred sixty-four confirmed suicides occurred. In an additional 71 cases, suicide is presumed but bodies were not recovered. In the 1,911 remaining instances, mental health interventions were made, with individuals taken to local hospitals and psychiatric wards, and released when no longer overtly suicidal. Interventions successfully diverted 75% (1,911/2,546) of those intending to end their own lives, which suggests that the current lethality of the Golden Gate as a means of suicide is only 25%. Even in the bridge’s first half-century, without constant camera monitoring, and a cadre of volunteers and professionals scanning for those attempting suicide, the lethality rate approached about 50%.19
We face even more difficulties measuring accessibility than in determining lethality. The Golden Gate appears to be accessible to almost anyone – drivers have to pay a toll only when traveling from the north, and then only after they have traversed the span. Pedestrians retain unfettered admittance to the east sidewalk (facing San Francisco city and bay) throughout daylight hours. But any determination of accessibility must include how quickly and easily one can make use of an opportunity.
Both entrances to the Golden Gate are embedded in the Golden Gate National Recreational Area, part of the National Park system. The south entrance to the bridge arises from The Presidio, a former military installation that housed about 4,000 people.20 Even fewer people live in the parklands at the north end of the bridge. The Presidio extends far enough so that the closest San Francisco neighborhoods outside of the park are a full 2.2 km (1.36 miles) from the bridge railing. A brisk walk would still require a minimum of about 20 minutes to get to the bridge; it is difficult to arrive at the bridge without a trek.
Researchers define impulsivity, like accessibility, inconsistently – and often imprecisely. Impulsivity, which clearly exists on a spectrum, connotes overvaluing of immediate feelings and thoughts at the expense of longer term goals and aspirations. Some suicide research appears to define impulsivity as the antithesis of planned behavior;21,22 others define it pragmatically as behaviors executed within 5 minutes of a decision,23 and still others contend that “suicidal behavior is rarely if ever impulsive.”24 Furthermore, when we assess impulsivity, we must acknowledge a fundamental difference between “impulsive” shootings and poisonings that are accomplished at home and within seconds or minutes, from “impulsive” Golden Gate Bridge suicide attempts, which require substantial travel and time commitments, and inherently involve the potential for others to intervene.
Those arguing that the bridge suicide barrier will save lives often bring up two additional sets of numbers to back up their assertions. They provide evidence that most of those people who were stopped in their attempts at suicide at the Golden Gate do not go on to commit suicide elsewhere, and that many of those who survived their attempts express regret at having tried to kill themselves. Specifically, 94% of those who were prevented from jumping from the Golden Gate had not committed suicide after a median follow-up of 26 years, according to a follow-up study published a few years ago. On the other hand, those who have made a serious suicide attempt have a substantially increased risk, relative to the general population, of dying from a later attempt,25,26 and the strongest predictor for death by suicide is having made a previous, serious suicide attempt.27
While all of these studies provide important and interesting information regarding suicide, none directly address the question of whether individuals will substitute attempts by other methods if the Golden Gate Bridge were no longer available. Many discussions blur the distinction between how individuals behave after a thwarted Golden Gate suicide attempt and how other people might act if we secured the bridge from any potential future suicide attempts. I hope that the following analogy makes this distinction clearer without trivializing: Imagine that we know that everyone who was interrupted while eating their dinner in a particular restaurant never went back and ate out anywhere, ever again. We could not conclude from this that another individual, who learned that the intended restaurant was indefinitely closed, would never dine out again. Once effective suicide barriers exist on the Golden Gate, this will likely become widely known, thereby greatly reducing the likelihood that any individuals will consider the possibility of jumping from the bridge. But it seems very unlikely that this would vanquish all suicidal impulses from the northern California population.
Lessons from patients
Two former patients of mine ended their lives by suicide from the Golden Gate. P, a solitary and lonely man in his 50s, was referred to me by his neighbor, Q, one of my long-term patients. P had a history of repeated assessments for lifelong depression, with minimal follow-up. I made a treatment plan with P that we hoped would address both his depression and his reluctance to engage with mental health professionals. He did not return for his follow-up appointment and ignored all my attempts to contact him.
P continued to have intermittent contact with Q. A decade after I had evaluated him, P was finally hospitalized for depression. Since P had no local family or friends, he asked Q to pick him up from the hospital at the time of his discharge. P asked Q to drive him to the Golden Gate Bridge, ostensibly to relish his release by partaking of the panoramic view of San Francisco from the bridge. They parked in the lot at the north end of the bridge, where Q stayed with the car at the vista point. The last that anyone saw of P was when Q noticed him walking on the bridge; nobody saw him go over and his body was not recovered.
In contrast to my brief connection with P, I worked with S over the course of 8 years to deal with her very severe attention-deficit/hyperactivity disorder and associated depression, which destroyed jobs and friendships, and estranged her from her family. She moved to Hawaii in hopes of “starting over with less baggage,” but I received a few phone calls over the next few years detailing suicide attempts, including driving her car off a bridge. Floundering in life, she returned to San Francisco and was hospitalized with suicidal ideation. The inpatient team sedated her heavily, ignored her past treatments and diagnoses, and discharged her after several days. Within a day of discharge, S’s sister called to say that S’s body had been recovered from the water below the bridge.
I don’t think that suicide was inevitable for either P or S, but I also lack any indication that either would be alive today had we installed suicide barriers on the Golden Gate years ago. Unless we eliminate access to guns, cars, trains, poisons, ropes, tall buildings and cliffs, people contemplating suicide will have numerous options at their disposal. We are likely to save lives by continuing to find ways to restrict access to means of death that can be used within seconds and have a high degree of lethality, and we should persist with such efforts. Buying a $5 trigger lock for every gun in California, and spending tens of millions on a public service campaign would cost less and may well save more lives than the Golden Gate suicide barrier. Unfortunately, we still possess very limited knowledge regarding which suicide prevention measures have an “impact on actual deaths or behavior.”28
To increase our efficacy in reducing suicide, we need to find better treatments for depression and anxiety. We also need to identify better ways of targeting those most at risk for suicide,29 improve our delivery of such treatments, and mitigate the social factors that contribute to such misery and unhappiness.
As a psychiatrist who has lost not only patients but also family members to suicide, I appreciate the hole in the soul these deaths create. I understand the drive to find ways to prevent additional deaths and save future survivors from such grief. But we must design psychiatric interventions that do the maximum good. To be imprecise in the lessons we learn from those who have killed themselves doubles down on the disservice to those lives already lost.
Dr. Kruse is a psychiatrist who practices in San Francisco. Several key details about the patients were changed to protect confidentiality.
References
1. Frommer’s Comprehensive Travel Guide, California. New York: Prentice Hall Travel, 1993.
2. “Chen Si, the ‘Angel of Nanjing,’ has saved more than 330 people from suicide,” by Matt Young, News.com.au. May 14, 2017.
3. “Finding Kyle,” by Lizzie Johnson, San Francisco Chronicle. Feb 8, 2019.
4. Beautrais A. Suicide by jumping. A review of research and prevention strategies. Crisis. 2007 Jan;28 Suppl 1:58-63. Crisis: The J of Crisis Interven Suicide Preven. 2007 Jan. (28)[Suppl1]:58-63.
5. Gunnell D et al. The global distribution of fatal pesticide self-poisoning: Systematic review. BMC Public Health. 2007 Dec. 21;7:357.
6. Vijayakumar L and Satheesh-Babu R. Does ‘no pesticide’ reduce suicides? Int J Soc Psychiatry. 2009 Jul 17;55:401-6.
7. Kreitman N. The coal gas story. United Kingdom suicide rates, 1960-71. Br J Prev Soc Med. 1976 Jun;30(2)86-93.
8. Ajdacic-Gross V et al. Changing times: A longitudinal analysis of international firearm suicide data. Am J Public Health. 2006 Oct;96(10):1752-5.
9. Reisch T et al. Change in suicide rates in Switzerland before and after firearm restriction resulting from the 2003 “Army XXI” reform. Am J Psychiatry. 2013 Sep170(9):977-84.
10. Lubin G et al. Decrease in suicide rates after a change of policy reducing access to firearms in adolescents: A naturalistic epidemiological study. Suicide Life Threat Behav. 2010 Oct;40(5):421-4.
11. Sinyor M and Levitt A. Effect of a barrier at Bloor Street Viaduct on suicide rates in Toronto: Natural experiment BMJ. 2010;341. doi: 1136/bmjc2884.
12. O’Carroll P and Silverman M. Community suicide prevention: The effectiveness of bridge barriers. Suicide Life Threat Behav. 1994 Spring;24(1):89-91; discussion 91-9.
13. Pelletier A. Preventing suicide by jumping: The effect of a bridge safety fence. Inj Prev. 2007 Feb;13(1):57-9.
14. Bennewith O et al. Effect of barriers on the Clifton suspension bridge, England, on local patterns of suicide: Implications for prevention. Br J Psychiatry. 2007 Mar;190:266-7.
15. Harvard T.H. Chan School of Public Health. 2004. “How do people most commonly complete suicide?”
16. “How cliff diving works,” by Heather Kolich, HowStuffWorks.com. Oct 5, 2009.
17. “Bridge design and construction statistics.” Goldengate.org
18. “How did teen survive fall from Golden Gate Bridge?” by Remy Molina, Live Science. Apr 19, 2011.
19. Seiden R. Where are they now? A follow-up study of suicide attempters from the Golden Gate Bridge. Suicide Life Threat Behav. 1978 Winter;8(4):203-16.
20. Presidio demographics. Point2homes.com.
21. Baca-García E et al. A prospective study of the paradoxical relationship between impulsivity and lethality of suicide attempts. J Clin Psychiatry. 2001 Jul;62(7):560-4.
22. Lim M et al. Differences between impulsive and non-impulsive suicide attempts among individuals treated in emergency rooms of South Korea. Psychiatry Investig. 2016 Jul;13(4):389-96.
23. Simon O et al. Characteristics of impulsive suicide attempts and attempters. Suicide Life Threat Behav. 2001;32(1 Suppl):49-59.
24. Anestis M et al. Reconsidering the link between impulsivity and suicidal behavior. Pers Soc Psychol Rev. 2014 Nov;18(4):366-86.
25. Ostamo A et al. Excess mortality of suicide attempters. Psychiatry Psychiatr Epidemiol. 2001 Jan;36(1):29-35.
26. Leon A et al. Statistical issues in the identification of risk factors for suicidal behavior: The application of survival analysis. Psychiatry Res. 1990 Jan;31(1):99-108.
27. Bostwick J et al. Suicide attempt as a risk factor for completed suicide: Even more lethal than we knew. Am J Psychiatry. 2016 Nov 1;173(11):1094-100.
28. Stone D and Crosby A. Suicide prevention. Am J Lifestyle Med. 2014;8(6):404-20.
29. Belsher B et al. Prediction models for suicide attempts and deaths: A systematic review and simulation. JAMA Psychiatry. 2019 Mar 13. doi: 10.1001/jamapsychiatry.2019.0174.
Ultimately, we need to find better treatments for depression and anxiety
Ultimately, we need to find better treatments for depression and anxiety
San Francisco entrances people. Photographers capture more images of the Golden Gate Bridge than any other bridge in the world.1 And only the Nanjing Yangtze River Bridge in China surpasses the Golden Gate as a destination for dying by suicide.2 At least 1,700 people reportedly have plunged from the bridge to their deaths since its opening in 1937.3
Despite concerted efforts by bridge security, the local mental health community, and a volunteer organization – Bridgewatch Angels – suicides continue at the pace of about 1 every 2 weeks. After more than 60 years of discussion, transportation officials allocated funding and have started building a suicide prevention barrier system on the Golden Gate.
Extrapolating from the success of barriers built on other bridges that were “suicide magnets,” we should be able to assure people that suicide deaths from the Golden Gate will dramatically decrease, and perhaps cease completely.4 Certainly, some in the mental health community think this barrier will save lives. They support this claim by citing research showing that removing highly accessible and lethal means of suicide reduces overall suicide rates, and that suicidal individuals, when thwarted, do not seek alternate modes of death.
I support building the Golden Gate suicide barrier, partly because symbolically, it should deliver a powerful message that we value all human life. But will the barrier save lives? I don’t think it will. As the American Psychiatric Association prepares to gather for its annual meeting in San Francisco, I would like to share my reasoning.
What the evidence shows
The most robust evidence that restricting availability of highly lethal and accessible means of suicide reduces overall suicide deaths comes from studies looking at self-poisoning in Asian countries and Great Britain. In many parts of Asia, ingestion of pesticides constitutes a significant proportion of suicide deaths, and several studies have found that, in localities where sales of highly lethal pesticides were restricted, overall suicide deaths decreased.5,6 Conversely, suicide rates increased when more lethal varieties of pesticides became more available. In Great Britain, overall suicide rates decreased when natural gas replaced coal gas for home heating and cooking.7 For decades preceding this change, more Britons had killed themselves by inhaling coal gas than by any other method.
Strong correlations exist between regional levels of gun ownership and suicide rates by shooting,8 but several potentially confounding sociopolitical factors explain some portion of this connection. Stronger evidence of gun availability affecting suicide rates has been demonstrated by decreases in suicide rates after restrictions in gun access in Switzerland,9 Israel,10 and other areas. These studies show correlations – not causality. However, the number of studies, links between increases and decreases in suicide rates with changes in access to guns, absence of changes in suicide rates during the same time periods among ostensibly similar control populations, and lack of other compelling explanations support the argument that restricting access to highly lethal and accessible means of suicide prevents suicide deaths overall.
The installation of suicide barriers on bridges that have been the sites of multiple suicides robustly reduces or even eliminates suicide deaths from those bridges,11 but the effect on overall suicide rates remains less clear. Various studies have found subsequent increases or no changes12-14 in suicide deaths from other bridges or tall buildings in the vicinity after the installation of suicide barriers on a “suicide magnet.” Many of the studies failed to find any impact on overall suicide rates in the regions investigated. Deaths from jumping off tall structures constitute a tiny proportion of total suicide deaths, making it difficult to detect any changes in overall suicide rates. In the United States, suicides by jumping/falling constituted 1%-2% of total suicides over the last several decades.15
If we know that restricting highly lethal and accessible methods of killing reduces suicide deaths, why would I question the value of the Golden Gate suicide barrier in preventing overall suicide deaths?
Unique aspects of the bridge
The World High Dive Federation recommends keeping dives to less than 20 meters (65.5 feet), with a few exceptions.16 The rail of the Golden Gate Bridge stands 67 meters (220 feet) above the water, and assuming minimal wind resistance, a falling person traverses that distance in about 3.7 seconds and lands with an impact of 130 km/hour (81 miles per hour).17 Only about 1%-2% of those jumping from the Golden Gate survive that fall.18
A 99% likelihood of death sounds pretty lethal; however, death by jumping from the Golden Gate inherently takes place in a public space, with the opportunity for interventions by other people. A more realistic calculation of the lethality would start the instant that someone initiates a sequence of behaviors leading to the intended death. By that criteria, measuring the lethality of the Golden Gate would begin when an individual enters a vehicle or sets off on foot with the plan of going over the railing.
Unless our surveillance-oriented society makes substantially greater advances (which I oppose), we will remain unable to assess suicide lethality by starting at the moment of inception. However, we do have data showing what happens once someone with suicidal intentions walks onto the bridge.
Between 2000 and 2018, observers noted 2,546 people on the Golden Gate who appeared to be considering a suicide attempt, the San Francisco Chronicle has reported. Five hundred sixty-four confirmed suicides occurred. In an additional 71 cases, suicide is presumed but bodies were not recovered. In the 1,911 remaining instances, mental health interventions were made, with individuals taken to local hospitals and psychiatric wards, and released when no longer overtly suicidal. Interventions successfully diverted 75% (1,911/2,546) of those intending to end their own lives, which suggests that the current lethality of the Golden Gate as a means of suicide is only 25%. Even in the bridge’s first half-century, without constant camera monitoring, and a cadre of volunteers and professionals scanning for those attempting suicide, the lethality rate approached about 50%.19
We face even more difficulties measuring accessibility than in determining lethality. The Golden Gate appears to be accessible to almost anyone – drivers have to pay a toll only when traveling from the north, and then only after they have traversed the span. Pedestrians retain unfettered admittance to the east sidewalk (facing San Francisco city and bay) throughout daylight hours. But any determination of accessibility must include how quickly and easily one can make use of an opportunity.
Both entrances to the Golden Gate are embedded in the Golden Gate National Recreational Area, part of the National Park system. The south entrance to the bridge arises from The Presidio, a former military installation that housed about 4,000 people.20 Even fewer people live in the parklands at the north end of the bridge. The Presidio extends far enough so that the closest San Francisco neighborhoods outside of the park are a full 2.2 km (1.36 miles) from the bridge railing. A brisk walk would still require a minimum of about 20 minutes to get to the bridge; it is difficult to arrive at the bridge without a trek.
Researchers define impulsivity, like accessibility, inconsistently – and often imprecisely. Impulsivity, which clearly exists on a spectrum, connotes overvaluing of immediate feelings and thoughts at the expense of longer term goals and aspirations. Some suicide research appears to define impulsivity as the antithesis of planned behavior;21,22 others define it pragmatically as behaviors executed within 5 minutes of a decision,23 and still others contend that “suicidal behavior is rarely if ever impulsive.”24 Furthermore, when we assess impulsivity, we must acknowledge a fundamental difference between “impulsive” shootings and poisonings that are accomplished at home and within seconds or minutes, from “impulsive” Golden Gate Bridge suicide attempts, which require substantial travel and time commitments, and inherently involve the potential for others to intervene.
Those arguing that the bridge suicide barrier will save lives often bring up two additional sets of numbers to back up their assertions. They provide evidence that most of those people who were stopped in their attempts at suicide at the Golden Gate do not go on to commit suicide elsewhere, and that many of those who survived their attempts express regret at having tried to kill themselves. Specifically, 94% of those who were prevented from jumping from the Golden Gate had not committed suicide after a median follow-up of 26 years, according to a follow-up study published a few years ago. On the other hand, those who have made a serious suicide attempt have a substantially increased risk, relative to the general population, of dying from a later attempt,25,26 and the strongest predictor for death by suicide is having made a previous, serious suicide attempt.27
While all of these studies provide important and interesting information regarding suicide, none directly address the question of whether individuals will substitute attempts by other methods if the Golden Gate Bridge were no longer available. Many discussions blur the distinction between how individuals behave after a thwarted Golden Gate suicide attempt and how other people might act if we secured the bridge from any potential future suicide attempts. I hope that the following analogy makes this distinction clearer without trivializing: Imagine that we know that everyone who was interrupted while eating their dinner in a particular restaurant never went back and ate out anywhere, ever again. We could not conclude from this that another individual, who learned that the intended restaurant was indefinitely closed, would never dine out again. Once effective suicide barriers exist on the Golden Gate, this will likely become widely known, thereby greatly reducing the likelihood that any individuals will consider the possibility of jumping from the bridge. But it seems very unlikely that this would vanquish all suicidal impulses from the northern California population.
Lessons from patients
Two former patients of mine ended their lives by suicide from the Golden Gate. P, a solitary and lonely man in his 50s, was referred to me by his neighbor, Q, one of my long-term patients. P had a history of repeated assessments for lifelong depression, with minimal follow-up. I made a treatment plan with P that we hoped would address both his depression and his reluctance to engage with mental health professionals. He did not return for his follow-up appointment and ignored all my attempts to contact him.
P continued to have intermittent contact with Q. A decade after I had evaluated him, P was finally hospitalized for depression. Since P had no local family or friends, he asked Q to pick him up from the hospital at the time of his discharge. P asked Q to drive him to the Golden Gate Bridge, ostensibly to relish his release by partaking of the panoramic view of San Francisco from the bridge. They parked in the lot at the north end of the bridge, where Q stayed with the car at the vista point. The last that anyone saw of P was when Q noticed him walking on the bridge; nobody saw him go over and his body was not recovered.
In contrast to my brief connection with P, I worked with S over the course of 8 years to deal with her very severe attention-deficit/hyperactivity disorder and associated depression, which destroyed jobs and friendships, and estranged her from her family. She moved to Hawaii in hopes of “starting over with less baggage,” but I received a few phone calls over the next few years detailing suicide attempts, including driving her car off a bridge. Floundering in life, she returned to San Francisco and was hospitalized with suicidal ideation. The inpatient team sedated her heavily, ignored her past treatments and diagnoses, and discharged her after several days. Within a day of discharge, S’s sister called to say that S’s body had been recovered from the water below the bridge.
I don’t think that suicide was inevitable for either P or S, but I also lack any indication that either would be alive today had we installed suicide barriers on the Golden Gate years ago. Unless we eliminate access to guns, cars, trains, poisons, ropes, tall buildings and cliffs, people contemplating suicide will have numerous options at their disposal. We are likely to save lives by continuing to find ways to restrict access to means of death that can be used within seconds and have a high degree of lethality, and we should persist with such efforts. Buying a $5 trigger lock for every gun in California, and spending tens of millions on a public service campaign would cost less and may well save more lives than the Golden Gate suicide barrier. Unfortunately, we still possess very limited knowledge regarding which suicide prevention measures have an “impact on actual deaths or behavior.”28
To increase our efficacy in reducing suicide, we need to find better treatments for depression and anxiety. We also need to identify better ways of targeting those most at risk for suicide,29 improve our delivery of such treatments, and mitigate the social factors that contribute to such misery and unhappiness.
As a psychiatrist who has lost not only patients but also family members to suicide, I appreciate the hole in the soul these deaths create. I understand the drive to find ways to prevent additional deaths and save future survivors from such grief. But we must design psychiatric interventions that do the maximum good. To be imprecise in the lessons we learn from those who have killed themselves doubles down on the disservice to those lives already lost.
Dr. Kruse is a psychiatrist who practices in San Francisco. Several key details about the patients were changed to protect confidentiality.
References
1. Frommer’s Comprehensive Travel Guide, California. New York: Prentice Hall Travel, 1993.
2. “Chen Si, the ‘Angel of Nanjing,’ has saved more than 330 people from suicide,” by Matt Young, News.com.au. May 14, 2017.
3. “Finding Kyle,” by Lizzie Johnson, San Francisco Chronicle. Feb 8, 2019.
4. Beautrais A. Suicide by jumping. A review of research and prevention strategies. Crisis. 2007 Jan;28 Suppl 1:58-63. Crisis: The J of Crisis Interven Suicide Preven. 2007 Jan. (28)[Suppl1]:58-63.
5. Gunnell D et al. The global distribution of fatal pesticide self-poisoning: Systematic review. BMC Public Health. 2007 Dec. 21;7:357.
6. Vijayakumar L and Satheesh-Babu R. Does ‘no pesticide’ reduce suicides? Int J Soc Psychiatry. 2009 Jul 17;55:401-6.
7. Kreitman N. The coal gas story. United Kingdom suicide rates, 1960-71. Br J Prev Soc Med. 1976 Jun;30(2)86-93.
8. Ajdacic-Gross V et al. Changing times: A longitudinal analysis of international firearm suicide data. Am J Public Health. 2006 Oct;96(10):1752-5.
9. Reisch T et al. Change in suicide rates in Switzerland before and after firearm restriction resulting from the 2003 “Army XXI” reform. Am J Psychiatry. 2013 Sep170(9):977-84.
10. Lubin G et al. Decrease in suicide rates after a change of policy reducing access to firearms in adolescents: A naturalistic epidemiological study. Suicide Life Threat Behav. 2010 Oct;40(5):421-4.
11. Sinyor M and Levitt A. Effect of a barrier at Bloor Street Viaduct on suicide rates in Toronto: Natural experiment BMJ. 2010;341. doi: 1136/bmjc2884.
12. O’Carroll P and Silverman M. Community suicide prevention: The effectiveness of bridge barriers. Suicide Life Threat Behav. 1994 Spring;24(1):89-91; discussion 91-9.
13. Pelletier A. Preventing suicide by jumping: The effect of a bridge safety fence. Inj Prev. 2007 Feb;13(1):57-9.
14. Bennewith O et al. Effect of barriers on the Clifton suspension bridge, England, on local patterns of suicide: Implications for prevention. Br J Psychiatry. 2007 Mar;190:266-7.
15. Harvard T.H. Chan School of Public Health. 2004. “How do people most commonly complete suicide?”
16. “How cliff diving works,” by Heather Kolich, HowStuffWorks.com. Oct 5, 2009.
17. “Bridge design and construction statistics.” Goldengate.org
18. “How did teen survive fall from Golden Gate Bridge?” by Remy Molina, Live Science. Apr 19, 2011.
19. Seiden R. Where are they now? A follow-up study of suicide attempters from the Golden Gate Bridge. Suicide Life Threat Behav. 1978 Winter;8(4):203-16.
20. Presidio demographics. Point2homes.com.
21. Baca-García E et al. A prospective study of the paradoxical relationship between impulsivity and lethality of suicide attempts. J Clin Psychiatry. 2001 Jul;62(7):560-4.
22. Lim M et al. Differences between impulsive and non-impulsive suicide attempts among individuals treated in emergency rooms of South Korea. Psychiatry Investig. 2016 Jul;13(4):389-96.
23. Simon O et al. Characteristics of impulsive suicide attempts and attempters. Suicide Life Threat Behav. 2001;32(1 Suppl):49-59.
24. Anestis M et al. Reconsidering the link between impulsivity and suicidal behavior. Pers Soc Psychol Rev. 2014 Nov;18(4):366-86.
25. Ostamo A et al. Excess mortality of suicide attempters. Psychiatry Psychiatr Epidemiol. 2001 Jan;36(1):29-35.
26. Leon A et al. Statistical issues in the identification of risk factors for suicidal behavior: The application of survival analysis. Psychiatry Res. 1990 Jan;31(1):99-108.
27. Bostwick J et al. Suicide attempt as a risk factor for completed suicide: Even more lethal than we knew. Am J Psychiatry. 2016 Nov 1;173(11):1094-100.
28. Stone D and Crosby A. Suicide prevention. Am J Lifestyle Med. 2014;8(6):404-20.
29. Belsher B et al. Prediction models for suicide attempts and deaths: A systematic review and simulation. JAMA Psychiatry. 2019 Mar 13. doi: 10.1001/jamapsychiatry.2019.0174.
San Francisco entrances people. Photographers capture more images of the Golden Gate Bridge than any other bridge in the world.1 And only the Nanjing Yangtze River Bridge in China surpasses the Golden Gate as a destination for dying by suicide.2 At least 1,700 people reportedly have plunged from the bridge to their deaths since its opening in 1937.3
Despite concerted efforts by bridge security, the local mental health community, and a volunteer organization – Bridgewatch Angels – suicides continue at the pace of about 1 every 2 weeks. After more than 60 years of discussion, transportation officials allocated funding and have started building a suicide prevention barrier system on the Golden Gate.
Extrapolating from the success of barriers built on other bridges that were “suicide magnets,” we should be able to assure people that suicide deaths from the Golden Gate will dramatically decrease, and perhaps cease completely.4 Certainly, some in the mental health community think this barrier will save lives. They support this claim by citing research showing that removing highly accessible and lethal means of suicide reduces overall suicide rates, and that suicidal individuals, when thwarted, do not seek alternate modes of death.
I support building the Golden Gate suicide barrier, partly because symbolically, it should deliver a powerful message that we value all human life. But will the barrier save lives? I don’t think it will. As the American Psychiatric Association prepares to gather for its annual meeting in San Francisco, I would like to share my reasoning.
What the evidence shows
The most robust evidence that restricting availability of highly lethal and accessible means of suicide reduces overall suicide deaths comes from studies looking at self-poisoning in Asian countries and Great Britain. In many parts of Asia, ingestion of pesticides constitutes a significant proportion of suicide deaths, and several studies have found that, in localities where sales of highly lethal pesticides were restricted, overall suicide deaths decreased.5,6 Conversely, suicide rates increased when more lethal varieties of pesticides became more available. In Great Britain, overall suicide rates decreased when natural gas replaced coal gas for home heating and cooking.7 For decades preceding this change, more Britons had killed themselves by inhaling coal gas than by any other method.
Strong correlations exist between regional levels of gun ownership and suicide rates by shooting,8 but several potentially confounding sociopolitical factors explain some portion of this connection. Stronger evidence of gun availability affecting suicide rates has been demonstrated by decreases in suicide rates after restrictions in gun access in Switzerland,9 Israel,10 and other areas. These studies show correlations – not causality. However, the number of studies, links between increases and decreases in suicide rates with changes in access to guns, absence of changes in suicide rates during the same time periods among ostensibly similar control populations, and lack of other compelling explanations support the argument that restricting access to highly lethal and accessible means of suicide prevents suicide deaths overall.
The installation of suicide barriers on bridges that have been the sites of multiple suicides robustly reduces or even eliminates suicide deaths from those bridges,11 but the effect on overall suicide rates remains less clear. Various studies have found subsequent increases or no changes12-14 in suicide deaths from other bridges or tall buildings in the vicinity after the installation of suicide barriers on a “suicide magnet.” Many of the studies failed to find any impact on overall suicide rates in the regions investigated. Deaths from jumping off tall structures constitute a tiny proportion of total suicide deaths, making it difficult to detect any changes in overall suicide rates. In the United States, suicides by jumping/falling constituted 1%-2% of total suicides over the last several decades.15
If we know that restricting highly lethal and accessible methods of killing reduces suicide deaths, why would I question the value of the Golden Gate suicide barrier in preventing overall suicide deaths?
Unique aspects of the bridge
The World High Dive Federation recommends keeping dives to less than 20 meters (65.5 feet), with a few exceptions.16 The rail of the Golden Gate Bridge stands 67 meters (220 feet) above the water, and assuming minimal wind resistance, a falling person traverses that distance in about 3.7 seconds and lands with an impact of 130 km/hour (81 miles per hour).17 Only about 1%-2% of those jumping from the Golden Gate survive that fall.18
A 99% likelihood of death sounds pretty lethal; however, death by jumping from the Golden Gate inherently takes place in a public space, with the opportunity for interventions by other people. A more realistic calculation of the lethality would start the instant that someone initiates a sequence of behaviors leading to the intended death. By that criteria, measuring the lethality of the Golden Gate would begin when an individual enters a vehicle or sets off on foot with the plan of going over the railing.
Unless our surveillance-oriented society makes substantially greater advances (which I oppose), we will remain unable to assess suicide lethality by starting at the moment of inception. However, we do have data showing what happens once someone with suicidal intentions walks onto the bridge.
Between 2000 and 2018, observers noted 2,546 people on the Golden Gate who appeared to be considering a suicide attempt, the San Francisco Chronicle has reported. Five hundred sixty-four confirmed suicides occurred. In an additional 71 cases, suicide is presumed but bodies were not recovered. In the 1,911 remaining instances, mental health interventions were made, with individuals taken to local hospitals and psychiatric wards, and released when no longer overtly suicidal. Interventions successfully diverted 75% (1,911/2,546) of those intending to end their own lives, which suggests that the current lethality of the Golden Gate as a means of suicide is only 25%. Even in the bridge’s first half-century, without constant camera monitoring, and a cadre of volunteers and professionals scanning for those attempting suicide, the lethality rate approached about 50%.19
We face even more difficulties measuring accessibility than in determining lethality. The Golden Gate appears to be accessible to almost anyone – drivers have to pay a toll only when traveling from the north, and then only after they have traversed the span. Pedestrians retain unfettered admittance to the east sidewalk (facing San Francisco city and bay) throughout daylight hours. But any determination of accessibility must include how quickly and easily one can make use of an opportunity.
Both entrances to the Golden Gate are embedded in the Golden Gate National Recreational Area, part of the National Park system. The south entrance to the bridge arises from The Presidio, a former military installation that housed about 4,000 people.20 Even fewer people live in the parklands at the north end of the bridge. The Presidio extends far enough so that the closest San Francisco neighborhoods outside of the park are a full 2.2 km (1.36 miles) from the bridge railing. A brisk walk would still require a minimum of about 20 minutes to get to the bridge; it is difficult to arrive at the bridge without a trek.
Researchers define impulsivity, like accessibility, inconsistently – and often imprecisely. Impulsivity, which clearly exists on a spectrum, connotes overvaluing of immediate feelings and thoughts at the expense of longer term goals and aspirations. Some suicide research appears to define impulsivity as the antithesis of planned behavior;21,22 others define it pragmatically as behaviors executed within 5 minutes of a decision,23 and still others contend that “suicidal behavior is rarely if ever impulsive.”24 Furthermore, when we assess impulsivity, we must acknowledge a fundamental difference between “impulsive” shootings and poisonings that are accomplished at home and within seconds or minutes, from “impulsive” Golden Gate Bridge suicide attempts, which require substantial travel and time commitments, and inherently involve the potential for others to intervene.
Those arguing that the bridge suicide barrier will save lives often bring up two additional sets of numbers to back up their assertions. They provide evidence that most of those people who were stopped in their attempts at suicide at the Golden Gate do not go on to commit suicide elsewhere, and that many of those who survived their attempts express regret at having tried to kill themselves. Specifically, 94% of those who were prevented from jumping from the Golden Gate had not committed suicide after a median follow-up of 26 years, according to a follow-up study published a few years ago. On the other hand, those who have made a serious suicide attempt have a substantially increased risk, relative to the general population, of dying from a later attempt,25,26 and the strongest predictor for death by suicide is having made a previous, serious suicide attempt.27
While all of these studies provide important and interesting information regarding suicide, none directly address the question of whether individuals will substitute attempts by other methods if the Golden Gate Bridge were no longer available. Many discussions blur the distinction between how individuals behave after a thwarted Golden Gate suicide attempt and how other people might act if we secured the bridge from any potential future suicide attempts. I hope that the following analogy makes this distinction clearer without trivializing: Imagine that we know that everyone who was interrupted while eating their dinner in a particular restaurant never went back and ate out anywhere, ever again. We could not conclude from this that another individual, who learned that the intended restaurant was indefinitely closed, would never dine out again. Once effective suicide barriers exist on the Golden Gate, this will likely become widely known, thereby greatly reducing the likelihood that any individuals will consider the possibility of jumping from the bridge. But it seems very unlikely that this would vanquish all suicidal impulses from the northern California population.
Lessons from patients
Two former patients of mine ended their lives by suicide from the Golden Gate. P, a solitary and lonely man in his 50s, was referred to me by his neighbor, Q, one of my long-term patients. P had a history of repeated assessments for lifelong depression, with minimal follow-up. I made a treatment plan with P that we hoped would address both his depression and his reluctance to engage with mental health professionals. He did not return for his follow-up appointment and ignored all my attempts to contact him.
P continued to have intermittent contact with Q. A decade after I had evaluated him, P was finally hospitalized for depression. Since P had no local family or friends, he asked Q to pick him up from the hospital at the time of his discharge. P asked Q to drive him to the Golden Gate Bridge, ostensibly to relish his release by partaking of the panoramic view of San Francisco from the bridge. They parked in the lot at the north end of the bridge, where Q stayed with the car at the vista point. The last that anyone saw of P was when Q noticed him walking on the bridge; nobody saw him go over and his body was not recovered.
In contrast to my brief connection with P, I worked with S over the course of 8 years to deal with her very severe attention-deficit/hyperactivity disorder and associated depression, which destroyed jobs and friendships, and estranged her from her family. She moved to Hawaii in hopes of “starting over with less baggage,” but I received a few phone calls over the next few years detailing suicide attempts, including driving her car off a bridge. Floundering in life, she returned to San Francisco and was hospitalized with suicidal ideation. The inpatient team sedated her heavily, ignored her past treatments and diagnoses, and discharged her after several days. Within a day of discharge, S’s sister called to say that S’s body had been recovered from the water below the bridge.
I don’t think that suicide was inevitable for either P or S, but I also lack any indication that either would be alive today had we installed suicide barriers on the Golden Gate years ago. Unless we eliminate access to guns, cars, trains, poisons, ropes, tall buildings and cliffs, people contemplating suicide will have numerous options at their disposal. We are likely to save lives by continuing to find ways to restrict access to means of death that can be used within seconds and have a high degree of lethality, and we should persist with such efforts. Buying a $5 trigger lock for every gun in California, and spending tens of millions on a public service campaign would cost less and may well save more lives than the Golden Gate suicide barrier. Unfortunately, we still possess very limited knowledge regarding which suicide prevention measures have an “impact on actual deaths or behavior.”28
To increase our efficacy in reducing suicide, we need to find better treatments for depression and anxiety. We also need to identify better ways of targeting those most at risk for suicide,29 improve our delivery of such treatments, and mitigate the social factors that contribute to such misery and unhappiness.
As a psychiatrist who has lost not only patients but also family members to suicide, I appreciate the hole in the soul these deaths create. I understand the drive to find ways to prevent additional deaths and save future survivors from such grief. But we must design psychiatric interventions that do the maximum good. To be imprecise in the lessons we learn from those who have killed themselves doubles down on the disservice to those lives already lost.
Dr. Kruse is a psychiatrist who practices in San Francisco. Several key details about the patients were changed to protect confidentiality.
References
1. Frommer’s Comprehensive Travel Guide, California. New York: Prentice Hall Travel, 1993.
2. “Chen Si, the ‘Angel of Nanjing,’ has saved more than 330 people from suicide,” by Matt Young, News.com.au. May 14, 2017.
3. “Finding Kyle,” by Lizzie Johnson, San Francisco Chronicle. Feb 8, 2019.
4. Beautrais A. Suicide by jumping. A review of research and prevention strategies. Crisis. 2007 Jan;28 Suppl 1:58-63. Crisis: The J of Crisis Interven Suicide Preven. 2007 Jan. (28)[Suppl1]:58-63.
5. Gunnell D et al. The global distribution of fatal pesticide self-poisoning: Systematic review. BMC Public Health. 2007 Dec. 21;7:357.
6. Vijayakumar L and Satheesh-Babu R. Does ‘no pesticide’ reduce suicides? Int J Soc Psychiatry. 2009 Jul 17;55:401-6.
7. Kreitman N. The coal gas story. United Kingdom suicide rates, 1960-71. Br J Prev Soc Med. 1976 Jun;30(2)86-93.
8. Ajdacic-Gross V et al. Changing times: A longitudinal analysis of international firearm suicide data. Am J Public Health. 2006 Oct;96(10):1752-5.
9. Reisch T et al. Change in suicide rates in Switzerland before and after firearm restriction resulting from the 2003 “Army XXI” reform. Am J Psychiatry. 2013 Sep170(9):977-84.
10. Lubin G et al. Decrease in suicide rates after a change of policy reducing access to firearms in adolescents: A naturalistic epidemiological study. Suicide Life Threat Behav. 2010 Oct;40(5):421-4.
11. Sinyor M and Levitt A. Effect of a barrier at Bloor Street Viaduct on suicide rates in Toronto: Natural experiment BMJ. 2010;341. doi: 1136/bmjc2884.
12. O’Carroll P and Silverman M. Community suicide prevention: The effectiveness of bridge barriers. Suicide Life Threat Behav. 1994 Spring;24(1):89-91; discussion 91-9.
13. Pelletier A. Preventing suicide by jumping: The effect of a bridge safety fence. Inj Prev. 2007 Feb;13(1):57-9.
14. Bennewith O et al. Effect of barriers on the Clifton suspension bridge, England, on local patterns of suicide: Implications for prevention. Br J Psychiatry. 2007 Mar;190:266-7.
15. Harvard T.H. Chan School of Public Health. 2004. “How do people most commonly complete suicide?”
16. “How cliff diving works,” by Heather Kolich, HowStuffWorks.com. Oct 5, 2009.
17. “Bridge design and construction statistics.” Goldengate.org
18. “How did teen survive fall from Golden Gate Bridge?” by Remy Molina, Live Science. Apr 19, 2011.
19. Seiden R. Where are they now? A follow-up study of suicide attempters from the Golden Gate Bridge. Suicide Life Threat Behav. 1978 Winter;8(4):203-16.
20. Presidio demographics. Point2homes.com.
21. Baca-García E et al. A prospective study of the paradoxical relationship between impulsivity and lethality of suicide attempts. J Clin Psychiatry. 2001 Jul;62(7):560-4.
22. Lim M et al. Differences between impulsive and non-impulsive suicide attempts among individuals treated in emergency rooms of South Korea. Psychiatry Investig. 2016 Jul;13(4):389-96.
23. Simon O et al. Characteristics of impulsive suicide attempts and attempters. Suicide Life Threat Behav. 2001;32(1 Suppl):49-59.
24. Anestis M et al. Reconsidering the link between impulsivity and suicidal behavior. Pers Soc Psychol Rev. 2014 Nov;18(4):366-86.
25. Ostamo A et al. Excess mortality of suicide attempters. Psychiatry Psychiatr Epidemiol. 2001 Jan;36(1):29-35.
26. Leon A et al. Statistical issues in the identification of risk factors for suicidal behavior: The application of survival analysis. Psychiatry Res. 1990 Jan;31(1):99-108.
27. Bostwick J et al. Suicide attempt as a risk factor for completed suicide: Even more lethal than we knew. Am J Psychiatry. 2016 Nov 1;173(11):1094-100.
28. Stone D and Crosby A. Suicide prevention. Am J Lifestyle Med. 2014;8(6):404-20.
29. Belsher B et al. Prediction models for suicide attempts and deaths: A systematic review and simulation. JAMA Psychiatry. 2019 Mar 13. doi: 10.1001/jamapsychiatry.2019.0174.
Make your evaluations and progress notes sing
I was talking to a physical therapy (PT) colleague and she was lamenting how much she hated doing documentation on patients she was treating. I suggested to her that she make her evaluations and progress notes sing. This is a concept I would sometimes use with patients who might be depressed, for example, I would ask them if anything made their heart sing to get an idea how “depressed” they might be. If they were unhappy or sad, I would advise that they engage in “heart singing” activities and behaviors, as I believe it is the “simple pleasures” in life that keep us resilient and persistent.
It is funny, when I was a resident and working in Jackson Park Hospital’s first psychiatric ward in 1972, one day in a note I wrote “I am going to give this acutely psychotic patient the big T – Thorazine to help them get some sleep at night,” I did not really think much about it until one of the nurses brought it to my attention because she thought it was unique – and a funny way of reporting plans in my progress notes.
My PT colleague told me that she remembered the first time she read one of my notes on a patient we were treating together (she needed to know the patient’s psychiatric status before she engaged them in physical therapy), and it struck her that I reported the patient was “befuddled,” and she wondered who would use befuddled in a note (lately, I have started using “flummoxed”). Another time, I was charting on a patient, and I used the word “flapdoodle” to describe the nonsense the patient was spewing (I recall this particular patient told me they graduated from grammar school at 5 years old). Another favorite word of mine that I use to describe nonsense is “claptrap.”
So, I have been making my evaluations and progress notes sing for a very long time, as doing so improves my writing skills, stimulates my thinking, turns the drudgery of charting into some fun, and creates an adventure in writing.
I have also been a big user of mental status templates to cut down my time. The essential elements of a mental status are in the narrative template, and all I need to do is to edit the verbiage in the template to fit the patient’s presentation so that the mental status sings. Early on, I understood that, to be a good psychiatrist, you needed a good vocabulary so you can speak with as much precision as possible when describing a patient’s mental status.
I was seeing many Alzheimer’s patients at one point. So I developed a special mental status template for them (female and male), so all I had to do to it was cut and paste, and then edit the template to fit the patient like a glove. Template example: This is a xx-year-old female who was appropriately groomed and who was cooperative with the interview, but she could not give much information. She was not hyperactive or lethargic. Her mood was bland, and her affect was flat and bland. Her speech did not contain any relevant information. Thought processes were not evident, although she was awake. I could not get a history of delusions or current auditory or visual hallucinations. Her thought content was nondescript. She was attentive, and her recent and remote memory were poor. Clinical estimate of her intelligence could not be determined. Her judgment and insight were poor. I could not determine whether there was any suicidal or homicidal ideation.
Formulation: This is a xx-year-old female who has a major neurocognitive disorder (formerly known as dementia). She is not overtly psychotic, suicidal, homicidal, or gravely disabled, but her level of functioning leaves a lot to be desired, which is why she needs a sheltered living circumstance.
Dx: Major neurocognitive disorder (formerly known as dementia).
Here’s another example: This is a xx-year-old male who was appropriately groomed and who was cooperative with the interview. He was not hyperactive or lethargic. His mood was euthymic and he had a wide range of affect as he was able to smile, get serious, and be sad (about xxx). His speech was relevant, linear, and goal directed. Thought processes did not show any signs of loose associations, tangentiality, or circumstantiality. He denies any delusions or current auditory or visual hallucinations. His thought content was surrounding xxx. He was attentive, and his recent and remote memory were intact. Clinical estimate of his intelligence was xxx average. His judgment and insight were poor as xxx. No report of suicidal or homicidal ideation.
Formulation: xxx. He is not overtly psychotic, suicidal, homicidal, or gravely disabled so I will clear him for psychiatric discharge.
Dx: xxx.
Just me trying to make work a little easier for myself and everyone else.
Dr. Bell is a staff psychiatrist at Jackson Park Hospital’s Medical/Surgical-Psychiatry Inpatient Unit in Chicago, clinical psychiatrist emeritus in the department of psychiatry at the University of Illinois at Chicago, former president/CEO of Community Mental Health Council, and former director of the Institute for Juvenile Research (birthplace of child psychiatry), also in Chicago.
I was talking to a physical therapy (PT) colleague and she was lamenting how much she hated doing documentation on patients she was treating. I suggested to her that she make her evaluations and progress notes sing. This is a concept I would sometimes use with patients who might be depressed, for example, I would ask them if anything made their heart sing to get an idea how “depressed” they might be. If they were unhappy or sad, I would advise that they engage in “heart singing” activities and behaviors, as I believe it is the “simple pleasures” in life that keep us resilient and persistent.
It is funny, when I was a resident and working in Jackson Park Hospital’s first psychiatric ward in 1972, one day in a note I wrote “I am going to give this acutely psychotic patient the big T – Thorazine to help them get some sleep at night,” I did not really think much about it until one of the nurses brought it to my attention because she thought it was unique – and a funny way of reporting plans in my progress notes.
My PT colleague told me that she remembered the first time she read one of my notes on a patient we were treating together (she needed to know the patient’s psychiatric status before she engaged them in physical therapy), and it struck her that I reported the patient was “befuddled,” and she wondered who would use befuddled in a note (lately, I have started using “flummoxed”). Another time, I was charting on a patient, and I used the word “flapdoodle” to describe the nonsense the patient was spewing (I recall this particular patient told me they graduated from grammar school at 5 years old). Another favorite word of mine that I use to describe nonsense is “claptrap.”
So, I have been making my evaluations and progress notes sing for a very long time, as doing so improves my writing skills, stimulates my thinking, turns the drudgery of charting into some fun, and creates an adventure in writing.
I have also been a big user of mental status templates to cut down my time. The essential elements of a mental status are in the narrative template, and all I need to do is to edit the verbiage in the template to fit the patient’s presentation so that the mental status sings. Early on, I understood that, to be a good psychiatrist, you needed a good vocabulary so you can speak with as much precision as possible when describing a patient’s mental status.
I was seeing many Alzheimer’s patients at one point. So I developed a special mental status template for them (female and male), so all I had to do to it was cut and paste, and then edit the template to fit the patient like a glove. Template example: This is a xx-year-old female who was appropriately groomed and who was cooperative with the interview, but she could not give much information. She was not hyperactive or lethargic. Her mood was bland, and her affect was flat and bland. Her speech did not contain any relevant information. Thought processes were not evident, although she was awake. I could not get a history of delusions or current auditory or visual hallucinations. Her thought content was nondescript. She was attentive, and her recent and remote memory were poor. Clinical estimate of her intelligence could not be determined. Her judgment and insight were poor. I could not determine whether there was any suicidal or homicidal ideation.
Formulation: This is a xx-year-old female who has a major neurocognitive disorder (formerly known as dementia). She is not overtly psychotic, suicidal, homicidal, or gravely disabled, but her level of functioning leaves a lot to be desired, which is why she needs a sheltered living circumstance.
Dx: Major neurocognitive disorder (formerly known as dementia).
Here’s another example: This is a xx-year-old male who was appropriately groomed and who was cooperative with the interview. He was not hyperactive or lethargic. His mood was euthymic and he had a wide range of affect as he was able to smile, get serious, and be sad (about xxx). His speech was relevant, linear, and goal directed. Thought processes did not show any signs of loose associations, tangentiality, or circumstantiality. He denies any delusions or current auditory or visual hallucinations. His thought content was surrounding xxx. He was attentive, and his recent and remote memory were intact. Clinical estimate of his intelligence was xxx average. His judgment and insight were poor as xxx. No report of suicidal or homicidal ideation.
Formulation: xxx. He is not overtly psychotic, suicidal, homicidal, or gravely disabled so I will clear him for psychiatric discharge.
Dx: xxx.
Just me trying to make work a little easier for myself and everyone else.
Dr. Bell is a staff psychiatrist at Jackson Park Hospital’s Medical/Surgical-Psychiatry Inpatient Unit in Chicago, clinical psychiatrist emeritus in the department of psychiatry at the University of Illinois at Chicago, former president/CEO of Community Mental Health Council, and former director of the Institute for Juvenile Research (birthplace of child psychiatry), also in Chicago.
I was talking to a physical therapy (PT) colleague and she was lamenting how much she hated doing documentation on patients she was treating. I suggested to her that she make her evaluations and progress notes sing. This is a concept I would sometimes use with patients who might be depressed, for example, I would ask them if anything made their heart sing to get an idea how “depressed” they might be. If they were unhappy or sad, I would advise that they engage in “heart singing” activities and behaviors, as I believe it is the “simple pleasures” in life that keep us resilient and persistent.
It is funny, when I was a resident and working in Jackson Park Hospital’s first psychiatric ward in 1972, one day in a note I wrote “I am going to give this acutely psychotic patient the big T – Thorazine to help them get some sleep at night,” I did not really think much about it until one of the nurses brought it to my attention because she thought it was unique – and a funny way of reporting plans in my progress notes.
My PT colleague told me that she remembered the first time she read one of my notes on a patient we were treating together (she needed to know the patient’s psychiatric status before she engaged them in physical therapy), and it struck her that I reported the patient was “befuddled,” and she wondered who would use befuddled in a note (lately, I have started using “flummoxed”). Another time, I was charting on a patient, and I used the word “flapdoodle” to describe the nonsense the patient was spewing (I recall this particular patient told me they graduated from grammar school at 5 years old). Another favorite word of mine that I use to describe nonsense is “claptrap.”
So, I have been making my evaluations and progress notes sing for a very long time, as doing so improves my writing skills, stimulates my thinking, turns the drudgery of charting into some fun, and creates an adventure in writing.
I have also been a big user of mental status templates to cut down my time. The essential elements of a mental status are in the narrative template, and all I need to do is to edit the verbiage in the template to fit the patient’s presentation so that the mental status sings. Early on, I understood that, to be a good psychiatrist, you needed a good vocabulary so you can speak with as much precision as possible when describing a patient’s mental status.
I was seeing many Alzheimer’s patients at one point. So I developed a special mental status template for them (female and male), so all I had to do to it was cut and paste, and then edit the template to fit the patient like a glove. Template example: This is a xx-year-old female who was appropriately groomed and who was cooperative with the interview, but she could not give much information. She was not hyperactive or lethargic. Her mood was bland, and her affect was flat and bland. Her speech did not contain any relevant information. Thought processes were not evident, although she was awake. I could not get a history of delusions or current auditory or visual hallucinations. Her thought content was nondescript. She was attentive, and her recent and remote memory were poor. Clinical estimate of her intelligence could not be determined. Her judgment and insight were poor. I could not determine whether there was any suicidal or homicidal ideation.
Formulation: This is a xx-year-old female who has a major neurocognitive disorder (formerly known as dementia). She is not overtly psychotic, suicidal, homicidal, or gravely disabled, but her level of functioning leaves a lot to be desired, which is why she needs a sheltered living circumstance.
Dx: Major neurocognitive disorder (formerly known as dementia).
Here’s another example: This is a xx-year-old male who was appropriately groomed and who was cooperative with the interview. He was not hyperactive or lethargic. His mood was euthymic and he had a wide range of affect as he was able to smile, get serious, and be sad (about xxx). His speech was relevant, linear, and goal directed. Thought processes did not show any signs of loose associations, tangentiality, or circumstantiality. He denies any delusions or current auditory or visual hallucinations. His thought content was surrounding xxx. He was attentive, and his recent and remote memory were intact. Clinical estimate of his intelligence was xxx average. His judgment and insight were poor as xxx. No report of suicidal or homicidal ideation.
Formulation: xxx. He is not overtly psychotic, suicidal, homicidal, or gravely disabled so I will clear him for psychiatric discharge.
Dx: xxx.
Just me trying to make work a little easier for myself and everyone else.
Dr. Bell is a staff psychiatrist at Jackson Park Hospital’s Medical/Surgical-Psychiatry Inpatient Unit in Chicago, clinical psychiatrist emeritus in the department of psychiatry at the University of Illinois at Chicago, former president/CEO of Community Mental Health Council, and former director of the Institute for Juvenile Research (birthplace of child psychiatry), also in Chicago.
Teen e-cigarette use: A public health crisis
After 2 decades of steady decline in adolescent and young adult use of tobacco products, e-cigarettes have dramatically altered the landscape of substance use in youth. E-cigarette use among teens has been on the rise for years but the recent exponential increase is unprecedented. From 2017 to 2018, adolescent e-cigarette use had the largest year-to-year increase (78%, from 12% to 21%) of any individual substance or class of substances at any time during the past 2 decades of nationwide monitoring.1 This has appropriately caught the nation’s attention. In 2016, Surgeon General Vivek H. Murthy, MD, commissioned an extensive report about electronic cigarettes, and in 2018 Surgeon General Jerome Adams, MD, MPH, issued an advisory declaring e-cigarettes a public health crisis for adolescents.2
E-cigarettes have received attention as a possible boon to adult cigarette smokers seeking a less hazardous product. We can consider the use of tobacco products along a continuum from smoked tobacco, dual use (both smoked tobacco and electronic nicotine delivery), electronic nicotine delivery only, and finally, nonuse. For some adults, transitioning from smoked tobacco products to electronic delivery systems has been a step toward less overall harm from substance use, with a small minority of that population going on to achieve abstinence from all nicotine products.3 For youth and teens, the story has been the opposite. With the rapid rise of e-cigarettes, adolescents overwhelmingly have been moving in the wrong direction at each potential step along this continuum.4 Less than 8% of teens who use e-cigarettes indicated that smoking cessation is a factor in their use.5 An estimated 1.3 million U.S. teens now are dependent or at high risk for dependence upon nicotine because of e-cigarette use. Furthermore, these teens are at a fourfold higher risk of progression to cigarette use, compared with their peers.6
One product in particular gives us information as to why this trend has accelerated so rapidly. Juul, now the sales leader among electronic nicotine delivery systems, rose from approximately 25% to a dominant 75% of market share in just over 1 fiscal year after a social media campaign targeted toward youth and young adults. The device is shaped like an elongated flash drive, is marketed as “sleek,” “looking cool,” and being “super easy” to use. This product touts its use of nicotine salts that can deliver higher concentrations of nicotine more rapidly to mimic the experience of smoking a cigarette as closely as possible. The fruity flavors in Juul “pods” and many other devices also appeal to teens. Many youth are left misinformed, thinking they are using a relatively harmless alternative to cigarettes.
E-cigarette use in youth carries many risks. Among the physical risks is exposure to harmful chemicals (even if less numerous than smoked tobacco products) such as diacetyl (a known cause of bronchiolitis obliterans, or “popcorn lung”), formaldehyde, acrolein, benzene, and metals such as nickel, tin and lead.7 “Safer than cigarettes” is a low bar indeed. Cognitive and emotional risks of early nicotine exposure include poor focus and attention, permanent lowering of impulse control, and a higher risk of mood and anxiety disorders.
Furthermore, nicotine is a gateway drug, with a clearly understood molecular basis for how it can potentiate the effects of later used substances, especially stimulants such as cocaine.8 The gateway and priming effect is compounded for youth because of ongoing brain development and plasticity during teen years. E-cigarette use also is associated with other risk behaviors including a manyfold higher likelihood of binge drinking, having multiple sexual partners in a short period of time, and using other substances such as cannabis, cocaine, methamphetamine, and heroin or nonprescribed opioids.9 An electronic system for vaporization also presents a risk for use of other substances. In just 1 year from 2017 to 2018, marijuana “vaping” increased by more than 50% among all ages surveyed.10
Pediatric health care providers are essential educators for both teens and parents regarding the risks of e-cigarette use. Many youth don’t know what they’re using; 66% of youth reported that the vapors they were inhaling contained only flavoring. Only 13% reported they were inhaling nicotine.10 In stark contrast to these self-reports, all Juul “pods” contain nicotine. As has been a pattern with nationwide surveys of substance use for decades, adolescent use is inversely correlated with perception of risk; 70% of 8th-12th graders do not foresee great harm in regular e-cigarette use. In addition, adolescents use substances less often when they know their parents disapprove. Parents also must be taught about the risks of e-cigarette use and can be provided with resources and taught effective strategies if they have difficulty communicating their disapproval to their children.
Age-appropriate screening in primary care settings must include specific language regarding the use of electronic cigarettes, with questions about “vaping” and “juuling.” Discussions with teens may be more effective with emphasis on issues that resonate with youth such as the financial cost, loss of freedom when dependence develops, and the fact that their generation is once again being targeted by the tobacco industry. Referral for further treatment, including individual and group therapy as well as family-focused interventions, should be considered for teens who use daily, use other substances regularly, or could benefit from treatment for co-occurring mental health disorders.
Electronic cigarette use should not be recommended as a smoking cessation strategy for teens.11 Pediatric health care providers must advocate for regulation of these products, including increasing the legal age of purchase and banning flavoring in e-cigarettes products, Internet sales, and advertisements targeted to youth.
The rapid rise in e-cigarette use among teens is of great concern. As with all classes of substances, early initiation of nicotine drastically increases the risk of developing a substance use disorder and portends a prolonged course and greater accumulation of adverse consequences. There is an urgent need for education, prevention, and early identification of e-cigarette use to protect the current and future well-being of children and adolescents.
Dr. Jackson is assistant professor of psychiatry at the University of Vermont, Burlington. He said he had no relevant financial disclosures. Email Dr. Jackson at [email protected].
References
1. MMWR Morb Mortal Wkly Rep. 2018;67:1276-7.
2. e-cigarettes.surgeongeneral.gov
3. N Engl J Med 2019;380:629-37.
4. Pediatrics. 2018 Dec; 142(6):e20180486.
5. MMWR Morb Mortal Wkly Rep 2018;67:196-200.
6. JAMA Pediatr. 2017 Aug 1;171(8):788-97.
7. “Public health consequences of e-cigarettes” (Washington, DC: National Academies Press, January 2018).
8. N Engl J Med 2014;371:932-43.
9. N Engl J Med 2019;380:689-90.
10. MMWR Morb Mortal Wkly Rep. 2016 Jan 8;64(52):1403-8.
11. Pediatrics. 2019 Feb;143(2). pii: e20183652.
After 2 decades of steady decline in adolescent and young adult use of tobacco products, e-cigarettes have dramatically altered the landscape of substance use in youth. E-cigarette use among teens has been on the rise for years but the recent exponential increase is unprecedented. From 2017 to 2018, adolescent e-cigarette use had the largest year-to-year increase (78%, from 12% to 21%) of any individual substance or class of substances at any time during the past 2 decades of nationwide monitoring.1 This has appropriately caught the nation’s attention. In 2016, Surgeon General Vivek H. Murthy, MD, commissioned an extensive report about electronic cigarettes, and in 2018 Surgeon General Jerome Adams, MD, MPH, issued an advisory declaring e-cigarettes a public health crisis for adolescents.2
E-cigarettes have received attention as a possible boon to adult cigarette smokers seeking a less hazardous product. We can consider the use of tobacco products along a continuum from smoked tobacco, dual use (both smoked tobacco and electronic nicotine delivery), electronic nicotine delivery only, and finally, nonuse. For some adults, transitioning from smoked tobacco products to electronic delivery systems has been a step toward less overall harm from substance use, with a small minority of that population going on to achieve abstinence from all nicotine products.3 For youth and teens, the story has been the opposite. With the rapid rise of e-cigarettes, adolescents overwhelmingly have been moving in the wrong direction at each potential step along this continuum.4 Less than 8% of teens who use e-cigarettes indicated that smoking cessation is a factor in their use.5 An estimated 1.3 million U.S. teens now are dependent or at high risk for dependence upon nicotine because of e-cigarette use. Furthermore, these teens are at a fourfold higher risk of progression to cigarette use, compared with their peers.6
One product in particular gives us information as to why this trend has accelerated so rapidly. Juul, now the sales leader among electronic nicotine delivery systems, rose from approximately 25% to a dominant 75% of market share in just over 1 fiscal year after a social media campaign targeted toward youth and young adults. The device is shaped like an elongated flash drive, is marketed as “sleek,” “looking cool,” and being “super easy” to use. This product touts its use of nicotine salts that can deliver higher concentrations of nicotine more rapidly to mimic the experience of smoking a cigarette as closely as possible. The fruity flavors in Juul “pods” and many other devices also appeal to teens. Many youth are left misinformed, thinking they are using a relatively harmless alternative to cigarettes.
E-cigarette use in youth carries many risks. Among the physical risks is exposure to harmful chemicals (even if less numerous than smoked tobacco products) such as diacetyl (a known cause of bronchiolitis obliterans, or “popcorn lung”), formaldehyde, acrolein, benzene, and metals such as nickel, tin and lead.7 “Safer than cigarettes” is a low bar indeed. Cognitive and emotional risks of early nicotine exposure include poor focus and attention, permanent lowering of impulse control, and a higher risk of mood and anxiety disorders.
Furthermore, nicotine is a gateway drug, with a clearly understood molecular basis for how it can potentiate the effects of later used substances, especially stimulants such as cocaine.8 The gateway and priming effect is compounded for youth because of ongoing brain development and plasticity during teen years. E-cigarette use also is associated with other risk behaviors including a manyfold higher likelihood of binge drinking, having multiple sexual partners in a short period of time, and using other substances such as cannabis, cocaine, methamphetamine, and heroin or nonprescribed opioids.9 An electronic system for vaporization also presents a risk for use of other substances. In just 1 year from 2017 to 2018, marijuana “vaping” increased by more than 50% among all ages surveyed.10
Pediatric health care providers are essential educators for both teens and parents regarding the risks of e-cigarette use. Many youth don’t know what they’re using; 66% of youth reported that the vapors they were inhaling contained only flavoring. Only 13% reported they were inhaling nicotine.10 In stark contrast to these self-reports, all Juul “pods” contain nicotine. As has been a pattern with nationwide surveys of substance use for decades, adolescent use is inversely correlated with perception of risk; 70% of 8th-12th graders do not foresee great harm in regular e-cigarette use. In addition, adolescents use substances less often when they know their parents disapprove. Parents also must be taught about the risks of e-cigarette use and can be provided with resources and taught effective strategies if they have difficulty communicating their disapproval to their children.
Age-appropriate screening in primary care settings must include specific language regarding the use of electronic cigarettes, with questions about “vaping” and “juuling.” Discussions with teens may be more effective with emphasis on issues that resonate with youth such as the financial cost, loss of freedom when dependence develops, and the fact that their generation is once again being targeted by the tobacco industry. Referral for further treatment, including individual and group therapy as well as family-focused interventions, should be considered for teens who use daily, use other substances regularly, or could benefit from treatment for co-occurring mental health disorders.
Electronic cigarette use should not be recommended as a smoking cessation strategy for teens.11 Pediatric health care providers must advocate for regulation of these products, including increasing the legal age of purchase and banning flavoring in e-cigarettes products, Internet sales, and advertisements targeted to youth.
The rapid rise in e-cigarette use among teens is of great concern. As with all classes of substances, early initiation of nicotine drastically increases the risk of developing a substance use disorder and portends a prolonged course and greater accumulation of adverse consequences. There is an urgent need for education, prevention, and early identification of e-cigarette use to protect the current and future well-being of children and adolescents.
Dr. Jackson is assistant professor of psychiatry at the University of Vermont, Burlington. He said he had no relevant financial disclosures. Email Dr. Jackson at [email protected].
References
1. MMWR Morb Mortal Wkly Rep. 2018;67:1276-7.
2. e-cigarettes.surgeongeneral.gov
3. N Engl J Med 2019;380:629-37.
4. Pediatrics. 2018 Dec; 142(6):e20180486.
5. MMWR Morb Mortal Wkly Rep 2018;67:196-200.
6. JAMA Pediatr. 2017 Aug 1;171(8):788-97.
7. “Public health consequences of e-cigarettes” (Washington, DC: National Academies Press, January 2018).
8. N Engl J Med 2014;371:932-43.
9. N Engl J Med 2019;380:689-90.
10. MMWR Morb Mortal Wkly Rep. 2016 Jan 8;64(52):1403-8.
11. Pediatrics. 2019 Feb;143(2). pii: e20183652.
After 2 decades of steady decline in adolescent and young adult use of tobacco products, e-cigarettes have dramatically altered the landscape of substance use in youth. E-cigarette use among teens has been on the rise for years but the recent exponential increase is unprecedented. From 2017 to 2018, adolescent e-cigarette use had the largest year-to-year increase (78%, from 12% to 21%) of any individual substance or class of substances at any time during the past 2 decades of nationwide monitoring.1 This has appropriately caught the nation’s attention. In 2016, Surgeon General Vivek H. Murthy, MD, commissioned an extensive report about electronic cigarettes, and in 2018 Surgeon General Jerome Adams, MD, MPH, issued an advisory declaring e-cigarettes a public health crisis for adolescents.2
E-cigarettes have received attention as a possible boon to adult cigarette smokers seeking a less hazardous product. We can consider the use of tobacco products along a continuum from smoked tobacco, dual use (both smoked tobacco and electronic nicotine delivery), electronic nicotine delivery only, and finally, nonuse. For some adults, transitioning from smoked tobacco products to electronic delivery systems has been a step toward less overall harm from substance use, with a small minority of that population going on to achieve abstinence from all nicotine products.3 For youth and teens, the story has been the opposite. With the rapid rise of e-cigarettes, adolescents overwhelmingly have been moving in the wrong direction at each potential step along this continuum.4 Less than 8% of teens who use e-cigarettes indicated that smoking cessation is a factor in their use.5 An estimated 1.3 million U.S. teens now are dependent or at high risk for dependence upon nicotine because of e-cigarette use. Furthermore, these teens are at a fourfold higher risk of progression to cigarette use, compared with their peers.6
One product in particular gives us information as to why this trend has accelerated so rapidly. Juul, now the sales leader among electronic nicotine delivery systems, rose from approximately 25% to a dominant 75% of market share in just over 1 fiscal year after a social media campaign targeted toward youth and young adults. The device is shaped like an elongated flash drive, is marketed as “sleek,” “looking cool,” and being “super easy” to use. This product touts its use of nicotine salts that can deliver higher concentrations of nicotine more rapidly to mimic the experience of smoking a cigarette as closely as possible. The fruity flavors in Juul “pods” and many other devices also appeal to teens. Many youth are left misinformed, thinking they are using a relatively harmless alternative to cigarettes.
E-cigarette use in youth carries many risks. Among the physical risks is exposure to harmful chemicals (even if less numerous than smoked tobacco products) such as diacetyl (a known cause of bronchiolitis obliterans, or “popcorn lung”), formaldehyde, acrolein, benzene, and metals such as nickel, tin and lead.7 “Safer than cigarettes” is a low bar indeed. Cognitive and emotional risks of early nicotine exposure include poor focus and attention, permanent lowering of impulse control, and a higher risk of mood and anxiety disorders.
Furthermore, nicotine is a gateway drug, with a clearly understood molecular basis for how it can potentiate the effects of later used substances, especially stimulants such as cocaine.8 The gateway and priming effect is compounded for youth because of ongoing brain development and plasticity during teen years. E-cigarette use also is associated with other risk behaviors including a manyfold higher likelihood of binge drinking, having multiple sexual partners in a short period of time, and using other substances such as cannabis, cocaine, methamphetamine, and heroin or nonprescribed opioids.9 An electronic system for vaporization also presents a risk for use of other substances. In just 1 year from 2017 to 2018, marijuana “vaping” increased by more than 50% among all ages surveyed.10
Pediatric health care providers are essential educators for both teens and parents regarding the risks of e-cigarette use. Many youth don’t know what they’re using; 66% of youth reported that the vapors they were inhaling contained only flavoring. Only 13% reported they were inhaling nicotine.10 In stark contrast to these self-reports, all Juul “pods” contain nicotine. As has been a pattern with nationwide surveys of substance use for decades, adolescent use is inversely correlated with perception of risk; 70% of 8th-12th graders do not foresee great harm in regular e-cigarette use. In addition, adolescents use substances less often when they know their parents disapprove. Parents also must be taught about the risks of e-cigarette use and can be provided with resources and taught effective strategies if they have difficulty communicating their disapproval to their children.
Age-appropriate screening in primary care settings must include specific language regarding the use of electronic cigarettes, with questions about “vaping” and “juuling.” Discussions with teens may be more effective with emphasis on issues that resonate with youth such as the financial cost, loss of freedom when dependence develops, and the fact that their generation is once again being targeted by the tobacco industry. Referral for further treatment, including individual and group therapy as well as family-focused interventions, should be considered for teens who use daily, use other substances regularly, or could benefit from treatment for co-occurring mental health disorders.
Electronic cigarette use should not be recommended as a smoking cessation strategy for teens.11 Pediatric health care providers must advocate for regulation of these products, including increasing the legal age of purchase and banning flavoring in e-cigarettes products, Internet sales, and advertisements targeted to youth.
The rapid rise in e-cigarette use among teens is of great concern. As with all classes of substances, early initiation of nicotine drastically increases the risk of developing a substance use disorder and portends a prolonged course and greater accumulation of adverse consequences. There is an urgent need for education, prevention, and early identification of e-cigarette use to protect the current and future well-being of children and adolescents.
Dr. Jackson is assistant professor of psychiatry at the University of Vermont, Burlington. He said he had no relevant financial disclosures. Email Dr. Jackson at [email protected].
References
1. MMWR Morb Mortal Wkly Rep. 2018;67:1276-7.
2. e-cigarettes.surgeongeneral.gov
3. N Engl J Med 2019;380:629-37.
4. Pediatrics. 2018 Dec; 142(6):e20180486.
5. MMWR Morb Mortal Wkly Rep 2018;67:196-200.
6. JAMA Pediatr. 2017 Aug 1;171(8):788-97.
7. “Public health consequences of e-cigarettes” (Washington, DC: National Academies Press, January 2018).
8. N Engl J Med 2014;371:932-43.
9. N Engl J Med 2019;380:689-90.
10. MMWR Morb Mortal Wkly Rep. 2016 Jan 8;64(52):1403-8.
11. Pediatrics. 2019 Feb;143(2). pii: e20183652.
Poster ads don’t belong in the clinic
In the last few months, I’ve received several posters. They’re always delivered by UPS, and come in a solid cardboard box to keep them from being crushed.
The boxes get opened, and once I know what they are, the whole thing gets tossed in the office recycling.
I know they’re presented as helpful patient information, with some bullet lists and glossy graphics showing brains, nerve transmitters, or patients. But the basic reality is that they’re just advertisements. Like infomercials on TV, they come across as professional and interesting, but at their heart and soul are just selling something.
No thanks.
Years ago, a company sent me a poster listing the warning signs of stroke. Although it was still an advertisement, I decided to hang it up in my exam room as a sort of public service announcement. Unfortunately, I soon discovered that any patient left staring at it for more than 1-2 minutes would start to complain of at least two of the symptoms listed. It got taken down after a few days.
I have nothing against advertising. It pays for websites, television shows, sporting events, newspapers, and magazines.
But my exam room isn’t the place for it. Patients are bombarded with direct-to-consumer advertising for many drugs in every media outlet. The doctor’s discussion room shouldn’t be one of the them.
The meeting between me and a patient should be frank, honest assessments about what should be done and what, specifically, is best for their individual case. I don’t need marketing for a drug that may or may not be appropriate, or easily covered by insurance, staring back at them.
It’s a thin line. Obviously, magazines out in my lobby are full of pharmaceutical ads, and that doesn’t bother me. But once a patient crosses the line into my consultation area it should just be between me and them.
Dr. Block has a solo neurology practice in Scottsdale, Ariz.
In the last few months, I’ve received several posters. They’re always delivered by UPS, and come in a solid cardboard box to keep them from being crushed.
The boxes get opened, and once I know what they are, the whole thing gets tossed in the office recycling.
I know they’re presented as helpful patient information, with some bullet lists and glossy graphics showing brains, nerve transmitters, or patients. But the basic reality is that they’re just advertisements. Like infomercials on TV, they come across as professional and interesting, but at their heart and soul are just selling something.
No thanks.
Years ago, a company sent me a poster listing the warning signs of stroke. Although it was still an advertisement, I decided to hang it up in my exam room as a sort of public service announcement. Unfortunately, I soon discovered that any patient left staring at it for more than 1-2 minutes would start to complain of at least two of the symptoms listed. It got taken down after a few days.
I have nothing against advertising. It pays for websites, television shows, sporting events, newspapers, and magazines.
But my exam room isn’t the place for it. Patients are bombarded with direct-to-consumer advertising for many drugs in every media outlet. The doctor’s discussion room shouldn’t be one of the them.
The meeting between me and a patient should be frank, honest assessments about what should be done and what, specifically, is best for their individual case. I don’t need marketing for a drug that may or may not be appropriate, or easily covered by insurance, staring back at them.
It’s a thin line. Obviously, magazines out in my lobby are full of pharmaceutical ads, and that doesn’t bother me. But once a patient crosses the line into my consultation area it should just be between me and them.
Dr. Block has a solo neurology practice in Scottsdale, Ariz.
In the last few months, I’ve received several posters. They’re always delivered by UPS, and come in a solid cardboard box to keep them from being crushed.
The boxes get opened, and once I know what they are, the whole thing gets tossed in the office recycling.
I know they’re presented as helpful patient information, with some bullet lists and glossy graphics showing brains, nerve transmitters, or patients. But the basic reality is that they’re just advertisements. Like infomercials on TV, they come across as professional and interesting, but at their heart and soul are just selling something.
No thanks.
Years ago, a company sent me a poster listing the warning signs of stroke. Although it was still an advertisement, I decided to hang it up in my exam room as a sort of public service announcement. Unfortunately, I soon discovered that any patient left staring at it for more than 1-2 minutes would start to complain of at least two of the symptoms listed. It got taken down after a few days.
I have nothing against advertising. It pays for websites, television shows, sporting events, newspapers, and magazines.
But my exam room isn’t the place for it. Patients are bombarded with direct-to-consumer advertising for many drugs in every media outlet. The doctor’s discussion room shouldn’t be one of the them.
The meeting between me and a patient should be frank, honest assessments about what should be done and what, specifically, is best for their individual case. I don’t need marketing for a drug that may or may not be appropriate, or easily covered by insurance, staring back at them.
It’s a thin line. Obviously, magazines out in my lobby are full of pharmaceutical ads, and that doesn’t bother me. But once a patient crosses the line into my consultation area it should just be between me and them.
Dr. Block has a solo neurology practice in Scottsdale, Ariz.
In defense of hospital administrators
Improving relationships between leaders and clinicians
In the March 2019 issue of The Hospitalist, I wrote about some key findings from a 2018 survey of U.S. physicians by The Physicians Foundation. It’s no surprise to anyone working in health care today that the survey found alarming levels of professional dissatisfaction, burnout, and pessimism about the future of medicine among respondent physicians. Sadly, it appears that much of that pessimism is directed toward hospitals and their leaders: 46% of survey respondents viewed the relationships between physicians and hospitals as somewhat or mostly negative and adversarial.
Several physicians posted comments online, and they deeply saddened me. My heart hurt for those doctors who wrote, “I loved medicine. It was good for my soul, but medicine left me. Doctors gave up most of their power and large corporations without an ethical foundation and no god, but money took over.” Or “They are waiting so all the senior physicians will retire. Nurses will become leaders who will follow administration’s lead and control physicians. Money and cost cutting is the major driver. Physicians are not valuable anymore because they have different opinions which cost a lot. There is a lot of window dressing, but they actually don’t care. They just want to run a business.” I also read “I was tossed out like dirty laundry water at age 59.” And “On a personal basis, I will try to reason with management exactly once before I bail.” Sigh.
These commenters are well-meaning physicians who had bad experiences with hospital leaders they saw as uncaring and unresponsive to their concerns as clinicians. Their experiences left them demoralized and embittered. I’m truly sorry for that.
I’m a recovering hospital administrator myself. My business partner John Nelson, MD, MHM, likes to tell people that he has successfully deprogrammed me from the way most administrators think about doctors, but he’s mostly joking (at least I think he is). I can tell you that most of the hospital leaders I have met – both when I was still an administrator and now in my consulting work – are well-intentioned people who care deeply about patients and their fellow health care professionals and are trying hard to do the right thing. Many of them could have earned more and had better career opportunities doing similar work in a field other than health care, but they chose health care out of a sincere desire to do good and help people.
A big part of the problem is that doctors and administrators come to health care from very different starting points, and so have very different perspectives. They generally function in separate silos, each paying attention to their own comfortable little part of that monster we call a health care delivery system. Often, neither administrators nor doctors have made enough effort to cross over and understand the issues and perspectives of people in other silos. As a result, it’s easy for assumptions and biases to creep in and poison our interactions.
When we interpret the behavior of others, we humans tend to overemphasize dispositional factors, such as personality or motives, and to discount situational factors, such as external stressors. Psychologists call this the fundamental attribution error or correspondence bias, and the result is usually heightened conflict as a result of presumed negative intentions on the part of others (“All she cares about is making a profit”) and discounting circumstantial factors that might be influencing others’ behavior (“She is facing reduced market share and a funding shortfall, and she’s fearful for the future of the institution”).
Add in another phenomenon known as the actor-observer bias, in which we tend to attribute others’ behavior to their dispositions but attribute our own behavior to the circumstances (“That administrator lost his temper because he’s a demanding jerk, but I only lost my temper because he pushed me over the edge”).
Is it possible that hospital leaders and doctors are reading each other inaccurately and that they’re making assumptions about each other’s intentions that get in the way of having constructive dialogue? How can we get to a place of greater trust? I don’t know the whole answer, of course, but I have a few ideas to offer.
Read the full post at hospitalleader.org.
Improving relationships between leaders and clinicians
Improving relationships between leaders and clinicians
In the March 2019 issue of The Hospitalist, I wrote about some key findings from a 2018 survey of U.S. physicians by The Physicians Foundation. It’s no surprise to anyone working in health care today that the survey found alarming levels of professional dissatisfaction, burnout, and pessimism about the future of medicine among respondent physicians. Sadly, it appears that much of that pessimism is directed toward hospitals and their leaders: 46% of survey respondents viewed the relationships between physicians and hospitals as somewhat or mostly negative and adversarial.
Several physicians posted comments online, and they deeply saddened me. My heart hurt for those doctors who wrote, “I loved medicine. It was good for my soul, but medicine left me. Doctors gave up most of their power and large corporations without an ethical foundation and no god, but money took over.” Or “They are waiting so all the senior physicians will retire. Nurses will become leaders who will follow administration’s lead and control physicians. Money and cost cutting is the major driver. Physicians are not valuable anymore because they have different opinions which cost a lot. There is a lot of window dressing, but they actually don’t care. They just want to run a business.” I also read “I was tossed out like dirty laundry water at age 59.” And “On a personal basis, I will try to reason with management exactly once before I bail.” Sigh.
These commenters are well-meaning physicians who had bad experiences with hospital leaders they saw as uncaring and unresponsive to their concerns as clinicians. Their experiences left them demoralized and embittered. I’m truly sorry for that.
I’m a recovering hospital administrator myself. My business partner John Nelson, MD, MHM, likes to tell people that he has successfully deprogrammed me from the way most administrators think about doctors, but he’s mostly joking (at least I think he is). I can tell you that most of the hospital leaders I have met – both when I was still an administrator and now in my consulting work – are well-intentioned people who care deeply about patients and their fellow health care professionals and are trying hard to do the right thing. Many of them could have earned more and had better career opportunities doing similar work in a field other than health care, but they chose health care out of a sincere desire to do good and help people.
A big part of the problem is that doctors and administrators come to health care from very different starting points, and so have very different perspectives. They generally function in separate silos, each paying attention to their own comfortable little part of that monster we call a health care delivery system. Often, neither administrators nor doctors have made enough effort to cross over and understand the issues and perspectives of people in other silos. As a result, it’s easy for assumptions and biases to creep in and poison our interactions.
When we interpret the behavior of others, we humans tend to overemphasize dispositional factors, such as personality or motives, and to discount situational factors, such as external stressors. Psychologists call this the fundamental attribution error or correspondence bias, and the result is usually heightened conflict as a result of presumed negative intentions on the part of others (“All she cares about is making a profit”) and discounting circumstantial factors that might be influencing others’ behavior (“She is facing reduced market share and a funding shortfall, and she’s fearful for the future of the institution”).
Add in another phenomenon known as the actor-observer bias, in which we tend to attribute others’ behavior to their dispositions but attribute our own behavior to the circumstances (“That administrator lost his temper because he’s a demanding jerk, but I only lost my temper because he pushed me over the edge”).
Is it possible that hospital leaders and doctors are reading each other inaccurately and that they’re making assumptions about each other’s intentions that get in the way of having constructive dialogue? How can we get to a place of greater trust? I don’t know the whole answer, of course, but I have a few ideas to offer.
Read the full post at hospitalleader.org.
In the March 2019 issue of The Hospitalist, I wrote about some key findings from a 2018 survey of U.S. physicians by The Physicians Foundation. It’s no surprise to anyone working in health care today that the survey found alarming levels of professional dissatisfaction, burnout, and pessimism about the future of medicine among respondent physicians. Sadly, it appears that much of that pessimism is directed toward hospitals and their leaders: 46% of survey respondents viewed the relationships between physicians and hospitals as somewhat or mostly negative and adversarial.
Several physicians posted comments online, and they deeply saddened me. My heart hurt for those doctors who wrote, “I loved medicine. It was good for my soul, but medicine left me. Doctors gave up most of their power and large corporations without an ethical foundation and no god, but money took over.” Or “They are waiting so all the senior physicians will retire. Nurses will become leaders who will follow administration’s lead and control physicians. Money and cost cutting is the major driver. Physicians are not valuable anymore because they have different opinions which cost a lot. There is a lot of window dressing, but they actually don’t care. They just want to run a business.” I also read “I was tossed out like dirty laundry water at age 59.” And “On a personal basis, I will try to reason with management exactly once before I bail.” Sigh.
These commenters are well-meaning physicians who had bad experiences with hospital leaders they saw as uncaring and unresponsive to their concerns as clinicians. Their experiences left them demoralized and embittered. I’m truly sorry for that.
I’m a recovering hospital administrator myself. My business partner John Nelson, MD, MHM, likes to tell people that he has successfully deprogrammed me from the way most administrators think about doctors, but he’s mostly joking (at least I think he is). I can tell you that most of the hospital leaders I have met – both when I was still an administrator and now in my consulting work – are well-intentioned people who care deeply about patients and their fellow health care professionals and are trying hard to do the right thing. Many of them could have earned more and had better career opportunities doing similar work in a field other than health care, but they chose health care out of a sincere desire to do good and help people.
A big part of the problem is that doctors and administrators come to health care from very different starting points, and so have very different perspectives. They generally function in separate silos, each paying attention to their own comfortable little part of that monster we call a health care delivery system. Often, neither administrators nor doctors have made enough effort to cross over and understand the issues and perspectives of people in other silos. As a result, it’s easy for assumptions and biases to creep in and poison our interactions.
When we interpret the behavior of others, we humans tend to overemphasize dispositional factors, such as personality or motives, and to discount situational factors, such as external stressors. Psychologists call this the fundamental attribution error or correspondence bias, and the result is usually heightened conflict as a result of presumed negative intentions on the part of others (“All she cares about is making a profit”) and discounting circumstantial factors that might be influencing others’ behavior (“She is facing reduced market share and a funding shortfall, and she’s fearful for the future of the institution”).
Add in another phenomenon known as the actor-observer bias, in which we tend to attribute others’ behavior to their dispositions but attribute our own behavior to the circumstances (“That administrator lost his temper because he’s a demanding jerk, but I only lost my temper because he pushed me over the edge”).
Is it possible that hospital leaders and doctors are reading each other inaccurately and that they’re making assumptions about each other’s intentions that get in the way of having constructive dialogue? How can we get to a place of greater trust? I don’t know the whole answer, of course, but I have a few ideas to offer.
Read the full post at hospitalleader.org.
The hospital outpatient facility may soon lose its secret sauce
If it’s happening in Cincinnati, it is happening everywhere. All the young doctors are being hired by hospital systems at better pay than private practices can afford. When I asked the CEO at one Cincinnati hospital about the trend, he explained: “We like to have referrals available for our primary care physicians.” Sounds nice, but I don’t believe it.
Hospital outpatient facilities have been reaping the benefits of site-of-service differential payments for years. Under the current Centers for Medicare/Medicaid Services payment scales, identical services are reimbursed at extraordinarily higher rates – differentials amounting to, on average, approximately 360% of Medicare’s payment for the same mix of services when they are performed in a physician’s office – if they are delivered at off-campus hospital outpatient departments rather than independent doctors’ offices. Technically, these outpatient departments can be an office that has been bought by the hospital and proximity is not an issue. Many off-campus hospital outpatient departments in my area are as far away as 35 miles, some in strip malls no less!
That situation may soon change, though. The CMS has proposed eliminating the site-of-service differentials for hospital outpatient services. The proposal is being aggressively opposed by hospital lobbyists and has even inspired lawsuits because it would blow the lid off the extraordinary payment differential available to hospital outpatient departments (“Proposed site-neutral payment policy sets the stage for battle royale between CMS, hospitals,” Modern Healthcare, July 26, 2018).
It’s a change that’s long overdue.
In the period from 2001 to 2017, Medicare Part B payments to physicians increased only 6%, while Medicare’s index of inflation measuring the cost of running a medical practice increased 30%. After adjustment for inflation in practice costs, physician pay has declined 19%, thus failing to match increases in office overhead costs. In that same 17-year period, Medicare hospital payments increased roughly 50%, including average annual increases of 2.6% for inpatient services and 2.5% per year for outpatient services. Hospitals have thus received payment increases more than eightfold greater than payment adjustments to physicians in the period from 2001 to 2017!
I think we have found the secret sauce!
Obviously, some of this largesse was spread over the recruitment of physicians, buying offices, and creating of secret sauce clinics. Hospital purchases of private offices and physician employment at hospitals soared to nearly 33%.
But much went to the hospital’s bottom line.
Hospitals have enjoyed 28 annual year-over-year increases in payments for services rendered in hospital outpatient facilities.
Many of these hospital systems claim to make no extra money using the hospital outpatient system. If so, eliminating the site-of-service differential will not affect them. We will see.
I think the elimination of the site-of-service differential will have profound impacts on office medicine. While the AMA is asking that the savings (several billion over 10 years) be funneled back into the office setting to correct past underpayments, just the correction of the distortion will benefit office practice. The recruitment of new physicians by hospitals, and the practice-buying binge, appear to have subsided. Expect many of these satellites to close, and their employed physicians, young and old, to be coming back into the job market. Expect Medicare beneficiaries to pay lower copays and deductibles.
Corrections of distortions like the site-of-service differential empower patients and independent physicians. Thank the AMA for exposing the unfairness and allowing the CMS to act. You may not know it, but the American Medical Association puts together a tremendous – some would say overwhelming – amount of research together on topics of importance to physicians. Some of this is fascinating. I direct you to the AMA’s Report 4 of the Council on Medical Service (I-18)
This report lays it all out, and explains what has happened.
Dr. Coldiron is in private practice but maintains a clinical assistant professorship at the University of Cincinnati. He cares for patients, teaches medical students and residents, and has several active clinical research projects. Dr. Coldiron is the author of more than 80 scientific letters, papers, and several book chapters, and he speaks frequently on a variety of topics. He is a past president of the American Academy of Dermatology. Write to him at [email protected].
If it’s happening in Cincinnati, it is happening everywhere. All the young doctors are being hired by hospital systems at better pay than private practices can afford. When I asked the CEO at one Cincinnati hospital about the trend, he explained: “We like to have referrals available for our primary care physicians.” Sounds nice, but I don’t believe it.
Hospital outpatient facilities have been reaping the benefits of site-of-service differential payments for years. Under the current Centers for Medicare/Medicaid Services payment scales, identical services are reimbursed at extraordinarily higher rates – differentials amounting to, on average, approximately 360% of Medicare’s payment for the same mix of services when they are performed in a physician’s office – if they are delivered at off-campus hospital outpatient departments rather than independent doctors’ offices. Technically, these outpatient departments can be an office that has been bought by the hospital and proximity is not an issue. Many off-campus hospital outpatient departments in my area are as far away as 35 miles, some in strip malls no less!
That situation may soon change, though. The CMS has proposed eliminating the site-of-service differentials for hospital outpatient services. The proposal is being aggressively opposed by hospital lobbyists and has even inspired lawsuits because it would blow the lid off the extraordinary payment differential available to hospital outpatient departments (“Proposed site-neutral payment policy sets the stage for battle royale between CMS, hospitals,” Modern Healthcare, July 26, 2018).
It’s a change that’s long overdue.
In the period from 2001 to 2017, Medicare Part B payments to physicians increased only 6%, while Medicare’s index of inflation measuring the cost of running a medical practice increased 30%. After adjustment for inflation in practice costs, physician pay has declined 19%, thus failing to match increases in office overhead costs. In that same 17-year period, Medicare hospital payments increased roughly 50%, including average annual increases of 2.6% for inpatient services and 2.5% per year for outpatient services. Hospitals have thus received payment increases more than eightfold greater than payment adjustments to physicians in the period from 2001 to 2017!
I think we have found the secret sauce!
Obviously, some of this largesse was spread over the recruitment of physicians, buying offices, and creating of secret sauce clinics. Hospital purchases of private offices and physician employment at hospitals soared to nearly 33%.
But much went to the hospital’s bottom line.
Hospitals have enjoyed 28 annual year-over-year increases in payments for services rendered in hospital outpatient facilities.
Many of these hospital systems claim to make no extra money using the hospital outpatient system. If so, eliminating the site-of-service differential will not affect them. We will see.
I think the elimination of the site-of-service differential will have profound impacts on office medicine. While the AMA is asking that the savings (several billion over 10 years) be funneled back into the office setting to correct past underpayments, just the correction of the distortion will benefit office practice. The recruitment of new physicians by hospitals, and the practice-buying binge, appear to have subsided. Expect many of these satellites to close, and their employed physicians, young and old, to be coming back into the job market. Expect Medicare beneficiaries to pay lower copays and deductibles.
Corrections of distortions like the site-of-service differential empower patients and independent physicians. Thank the AMA for exposing the unfairness and allowing the CMS to act. You may not know it, but the American Medical Association puts together a tremendous – some would say overwhelming – amount of research together on topics of importance to physicians. Some of this is fascinating. I direct you to the AMA’s Report 4 of the Council on Medical Service (I-18)
This report lays it all out, and explains what has happened.
Dr. Coldiron is in private practice but maintains a clinical assistant professorship at the University of Cincinnati. He cares for patients, teaches medical students and residents, and has several active clinical research projects. Dr. Coldiron is the author of more than 80 scientific letters, papers, and several book chapters, and he speaks frequently on a variety of topics. He is a past president of the American Academy of Dermatology. Write to him at [email protected].
If it’s happening in Cincinnati, it is happening everywhere. All the young doctors are being hired by hospital systems at better pay than private practices can afford. When I asked the CEO at one Cincinnati hospital about the trend, he explained: “We like to have referrals available for our primary care physicians.” Sounds nice, but I don’t believe it.
Hospital outpatient facilities have been reaping the benefits of site-of-service differential payments for years. Under the current Centers for Medicare/Medicaid Services payment scales, identical services are reimbursed at extraordinarily higher rates – differentials amounting to, on average, approximately 360% of Medicare’s payment for the same mix of services when they are performed in a physician’s office – if they are delivered at off-campus hospital outpatient departments rather than independent doctors’ offices. Technically, these outpatient departments can be an office that has been bought by the hospital and proximity is not an issue. Many off-campus hospital outpatient departments in my area are as far away as 35 miles, some in strip malls no less!
That situation may soon change, though. The CMS has proposed eliminating the site-of-service differentials for hospital outpatient services. The proposal is being aggressively opposed by hospital lobbyists and has even inspired lawsuits because it would blow the lid off the extraordinary payment differential available to hospital outpatient departments (“Proposed site-neutral payment policy sets the stage for battle royale between CMS, hospitals,” Modern Healthcare, July 26, 2018).
It’s a change that’s long overdue.
In the period from 2001 to 2017, Medicare Part B payments to physicians increased only 6%, while Medicare’s index of inflation measuring the cost of running a medical practice increased 30%. After adjustment for inflation in practice costs, physician pay has declined 19%, thus failing to match increases in office overhead costs. In that same 17-year period, Medicare hospital payments increased roughly 50%, including average annual increases of 2.6% for inpatient services and 2.5% per year for outpatient services. Hospitals have thus received payment increases more than eightfold greater than payment adjustments to physicians in the period from 2001 to 2017!
I think we have found the secret sauce!
Obviously, some of this largesse was spread over the recruitment of physicians, buying offices, and creating of secret sauce clinics. Hospital purchases of private offices and physician employment at hospitals soared to nearly 33%.
But much went to the hospital’s bottom line.
Hospitals have enjoyed 28 annual year-over-year increases in payments for services rendered in hospital outpatient facilities.
Many of these hospital systems claim to make no extra money using the hospital outpatient system. If so, eliminating the site-of-service differential will not affect them. We will see.
I think the elimination of the site-of-service differential will have profound impacts on office medicine. While the AMA is asking that the savings (several billion over 10 years) be funneled back into the office setting to correct past underpayments, just the correction of the distortion will benefit office practice. The recruitment of new physicians by hospitals, and the practice-buying binge, appear to have subsided. Expect many of these satellites to close, and their employed physicians, young and old, to be coming back into the job market. Expect Medicare beneficiaries to pay lower copays and deductibles.
Corrections of distortions like the site-of-service differential empower patients and independent physicians. Thank the AMA for exposing the unfairness and allowing the CMS to act. You may not know it, but the American Medical Association puts together a tremendous – some would say overwhelming – amount of research together on topics of importance to physicians. Some of this is fascinating. I direct you to the AMA’s Report 4 of the Council on Medical Service (I-18)
This report lays it all out, and explains what has happened.
Dr. Coldiron is in private practice but maintains a clinical assistant professorship at the University of Cincinnati. He cares for patients, teaches medical students and residents, and has several active clinical research projects. Dr. Coldiron is the author of more than 80 scientific letters, papers, and several book chapters, and he speaks frequently on a variety of topics. He is a past president of the American Academy of Dermatology. Write to him at [email protected].
One percent better
Hurray! . Of course, I might be overplaying my excitement here: EMR updates are emotionally closest to a trip to the dentist – usually turn out fine, but hardly worth circling on the calendar.
Like a good dental cleaning however, these updates can be beneficial. Although uncomfortable, EMR redesigned menus and shortcuts can help – once you’re used to them. It typically doesn’t take long for most of us to learn the “improvements” so we’re at least not worse off. It is also a good time to update customized features. I try to use updates as an opportunity to refresh SmartPhrases, update order preferences, or rearrange my desktop to be more efficient.
Given how much my quality of life depends upon my EMR skills, it’s a shame I don’t make an effort to work on it more often. Really, why wait to make improvements just once a year? Why not get better every day?
This idea of continuous improvement is a popular meme in the self-improvement community right now. Instead of working on goals or adjusting your routine episodically, set an intention to get better, just a little, daily. Sometimes it’s described as the 1% model. The idea is that improving your habits or work flow by 1% each day will yield compound benefits with time. It is an aggregation of marginal gains with a surprising payout. For example, daily 1% improvements would mean you are 37 times more effective by the end of a year. Now, I don’t believe this mathematical model is necessarily accurate or even necessary. But the concept that a little development done daily yields lasting improvement seems to be true.
The corollary, that if you got a little worse each day, you’d be much worse off at the end of a year, is also reasonable. That’s how most health problems set in: continuous and insidious aggregation of bad choices. Why then not use that same principle for good instead?
The Japanese thought of this idea a generation ago. Applied to manufacturing, they called it Kaizen, “continuous improvement.” It was a managerial principle that reminded people to look for opportunities to improve, just a little, wherever they were in the process and to do so each day. It led to remarkable reductions in waste and became a key to their economic success.
Opportunities for relentless improvement abound in our work too. For example, when you write an order or work up a diagnosis, rather than just enter it, you might save it as a panel. When you find yourself using the same word or phrase, save it to your dictionary to pull it up with minimal keystrokes. When you research a difficult disease you’ve not seen lately, save the diagnostic questions as a template so you can pull it up in real time the next time it walks in. When you set up your procedure tray, place items so they can be picked up efficiently and moved out of the way quickly. No matter how good your setup or template is today, you can find a tiny improvement that would make it a little better tomorrow. And you’ll reap gains from that day forward.
I don’t expect this EMR update will have much impact on my quality of life. It will however be a reminder that like flossing, improvements are best done daily. You and your dentist will thank me someday.
Dr. Benabio is director of Healthcare Transformation and chief of dermatology at Kaiser Permanente San Diego. The opinions expressed in this column are his own and do not represent those of Kaiser Permanente. Dr. Benabio is @Dermdoc on Twitter. Write to him at [email protected].
Hurray! . Of course, I might be overplaying my excitement here: EMR updates are emotionally closest to a trip to the dentist – usually turn out fine, but hardly worth circling on the calendar.
Like a good dental cleaning however, these updates can be beneficial. Although uncomfortable, EMR redesigned menus and shortcuts can help – once you’re used to them. It typically doesn’t take long for most of us to learn the “improvements” so we’re at least not worse off. It is also a good time to update customized features. I try to use updates as an opportunity to refresh SmartPhrases, update order preferences, or rearrange my desktop to be more efficient.
Given how much my quality of life depends upon my EMR skills, it’s a shame I don’t make an effort to work on it more often. Really, why wait to make improvements just once a year? Why not get better every day?
This idea of continuous improvement is a popular meme in the self-improvement community right now. Instead of working on goals or adjusting your routine episodically, set an intention to get better, just a little, daily. Sometimes it’s described as the 1% model. The idea is that improving your habits or work flow by 1% each day will yield compound benefits with time. It is an aggregation of marginal gains with a surprising payout. For example, daily 1% improvements would mean you are 37 times more effective by the end of a year. Now, I don’t believe this mathematical model is necessarily accurate or even necessary. But the concept that a little development done daily yields lasting improvement seems to be true.
The corollary, that if you got a little worse each day, you’d be much worse off at the end of a year, is also reasonable. That’s how most health problems set in: continuous and insidious aggregation of bad choices. Why then not use that same principle for good instead?
The Japanese thought of this idea a generation ago. Applied to manufacturing, they called it Kaizen, “continuous improvement.” It was a managerial principle that reminded people to look for opportunities to improve, just a little, wherever they were in the process and to do so each day. It led to remarkable reductions in waste and became a key to their economic success.
Opportunities for relentless improvement abound in our work too. For example, when you write an order or work up a diagnosis, rather than just enter it, you might save it as a panel. When you find yourself using the same word or phrase, save it to your dictionary to pull it up with minimal keystrokes. When you research a difficult disease you’ve not seen lately, save the diagnostic questions as a template so you can pull it up in real time the next time it walks in. When you set up your procedure tray, place items so they can be picked up efficiently and moved out of the way quickly. No matter how good your setup or template is today, you can find a tiny improvement that would make it a little better tomorrow. And you’ll reap gains from that day forward.
I don’t expect this EMR update will have much impact on my quality of life. It will however be a reminder that like flossing, improvements are best done daily. You and your dentist will thank me someday.
Dr. Benabio is director of Healthcare Transformation and chief of dermatology at Kaiser Permanente San Diego. The opinions expressed in this column are his own and do not represent those of Kaiser Permanente. Dr. Benabio is @Dermdoc on Twitter. Write to him at [email protected].
Hurray! . Of course, I might be overplaying my excitement here: EMR updates are emotionally closest to a trip to the dentist – usually turn out fine, but hardly worth circling on the calendar.
Like a good dental cleaning however, these updates can be beneficial. Although uncomfortable, EMR redesigned menus and shortcuts can help – once you’re used to them. It typically doesn’t take long for most of us to learn the “improvements” so we’re at least not worse off. It is also a good time to update customized features. I try to use updates as an opportunity to refresh SmartPhrases, update order preferences, or rearrange my desktop to be more efficient.
Given how much my quality of life depends upon my EMR skills, it’s a shame I don’t make an effort to work on it more often. Really, why wait to make improvements just once a year? Why not get better every day?
This idea of continuous improvement is a popular meme in the self-improvement community right now. Instead of working on goals or adjusting your routine episodically, set an intention to get better, just a little, daily. Sometimes it’s described as the 1% model. The idea is that improving your habits or work flow by 1% each day will yield compound benefits with time. It is an aggregation of marginal gains with a surprising payout. For example, daily 1% improvements would mean you are 37 times more effective by the end of a year. Now, I don’t believe this mathematical model is necessarily accurate or even necessary. But the concept that a little development done daily yields lasting improvement seems to be true.
The corollary, that if you got a little worse each day, you’d be much worse off at the end of a year, is also reasonable. That’s how most health problems set in: continuous and insidious aggregation of bad choices. Why then not use that same principle for good instead?
The Japanese thought of this idea a generation ago. Applied to manufacturing, they called it Kaizen, “continuous improvement.” It was a managerial principle that reminded people to look for opportunities to improve, just a little, wherever they were in the process and to do so each day. It led to remarkable reductions in waste and became a key to their economic success.
Opportunities for relentless improvement abound in our work too. For example, when you write an order or work up a diagnosis, rather than just enter it, you might save it as a panel. When you find yourself using the same word or phrase, save it to your dictionary to pull it up with minimal keystrokes. When you research a difficult disease you’ve not seen lately, save the diagnostic questions as a template so you can pull it up in real time the next time it walks in. When you set up your procedure tray, place items so they can be picked up efficiently and moved out of the way quickly. No matter how good your setup or template is today, you can find a tiny improvement that would make it a little better tomorrow. And you’ll reap gains from that day forward.
I don’t expect this EMR update will have much impact on my quality of life. It will however be a reminder that like flossing, improvements are best done daily. You and your dentist will thank me someday.
Dr. Benabio is director of Healthcare Transformation and chief of dermatology at Kaiser Permanente San Diego. The opinions expressed in this column are his own and do not represent those of Kaiser Permanente. Dr. Benabio is @Dermdoc on Twitter. Write to him at [email protected].
Nitrous oxide in dermatology
. When used properly, with meticulous patient monitoring, it is safe and effective. In my practice, I have used it for procedures as simple as a skin biopsy. While we have excellent topical numbing options for pain control, nitrous oxide works well as an anxiolytic and can help calm the patient who is nervous or has a fear of needles.
Nitrous oxide is a tasteless gas synthesized and released by cells. Inhalational nitrous oxide is absorbed from the lungs and diffuses into plasma, where it acts on the central nervous system as an anxiolytic and analgesic by blocking the NMDA receptor. It has a quick onset of action and short duration, is easily titrated, and has a low side effect profile.
Initially used to provide pain relief during labor in the late 1800s, nitrous oxide is now rarely used in the United States as inhalational analgesia during surgery or labor; however, use in dentistry and pediatrics is common. In a recent review of PubMed and Cochrane databases by Brotzman et al., eight studies on the use of nitrous oxide in dermatology were identified. Studies reported favorable safety and efficacy of nitrous oxide in providing analgesia during dermatologic procedures, which included facial rejuvenation, hair transplantation, and pediatric procedures. Several other studies also discussed the use of nitrous oxide in combination with tumescent anesthesia for venous ablation and liposuction. All adverse effects were limited to the time of inhalation and included euphoria, laughter, nausea, dizziness, and vertigo. There are no studies reviewing the risk of nitrous oxide used during CO2 resurfacing procedures.
In five of the eight studies, vital signs and oxygen saturation were recorded during the period of inhalation. Almost all patients maintained adequate oxygen saturation and vitals also remained stable in these five studies, except for a slight increase in systolic and diastolic arterial pressure after ulcer debridement. In four of the eight studies, a 50% nitrous oxide/50% oxygen mixture delivered through an on-demand valve activated by a patient’s inspired breaths was used to minimize the risk of oversedation and to prevent hypoxia.
Contraindications for using nitrous oxide are pregnancy (in patients, health care providers, and assistants). Relative contraindications include nasal obstruction, chronic obstructive pulmonary disease, active cystic fibrosis, recent tympanic membrane surgery, and claustrophobia. According to the National Institute for Occupational Safety and Health, occupational exposure to nitrous oxide can lead to adverse effects that include reduced fertility and spontaneous abortion, as well as neurologic, renal, and hepatic diseases. The consensus of the majority of the studies in the PubMed/Cochrane review is that nitrous oxide provided a significant reduction in pain during dermatologic procedures, with mild and transient adverse effects. The effects dissipated quickly and thus patients could drive themselves home. But studies remain limited, and more well designed, randomized clinical trials are needed to provide clinical guidelines, safety monitoring protocols, and evidence for the use of nitrous oxide in dermatology. In my opinion, when more data are available, it will become one of the mainstays of analgesia in dermatologic procedures, particularly for pediatric, Mohs, and facial rejuvenation procedures.
Dr. Talakoub Dr. Wesley and are cocontributors to this column. Dr. Talakoub is in private practice in McLean, Va. Dr. Wesley practices dermatology in Beverly Hills, Calif. This month’s column is by Dr. Talakoub. Write to them at [email protected]. They had no relevant disclosures.
Sources
Brotzman EA et al. Dermatol Surg. 2018 May;44(5):661-9.
“Controlling Exposures to Nitrous Oxide During Anesthetic Administration,” National Institute for Occupational Safety and Health (https://www.cdc.gov/niosh/docs/94-100/default.html).
. When used properly, with meticulous patient monitoring, it is safe and effective. In my practice, I have used it for procedures as simple as a skin biopsy. While we have excellent topical numbing options for pain control, nitrous oxide works well as an anxiolytic and can help calm the patient who is nervous or has a fear of needles.
Nitrous oxide is a tasteless gas synthesized and released by cells. Inhalational nitrous oxide is absorbed from the lungs and diffuses into plasma, where it acts on the central nervous system as an anxiolytic and analgesic by blocking the NMDA receptor. It has a quick onset of action and short duration, is easily titrated, and has a low side effect profile.
Initially used to provide pain relief during labor in the late 1800s, nitrous oxide is now rarely used in the United States as inhalational analgesia during surgery or labor; however, use in dentistry and pediatrics is common. In a recent review of PubMed and Cochrane databases by Brotzman et al., eight studies on the use of nitrous oxide in dermatology were identified. Studies reported favorable safety and efficacy of nitrous oxide in providing analgesia during dermatologic procedures, which included facial rejuvenation, hair transplantation, and pediatric procedures. Several other studies also discussed the use of nitrous oxide in combination with tumescent anesthesia for venous ablation and liposuction. All adverse effects were limited to the time of inhalation and included euphoria, laughter, nausea, dizziness, and vertigo. There are no studies reviewing the risk of nitrous oxide used during CO2 resurfacing procedures.
In five of the eight studies, vital signs and oxygen saturation were recorded during the period of inhalation. Almost all patients maintained adequate oxygen saturation and vitals also remained stable in these five studies, except for a slight increase in systolic and diastolic arterial pressure after ulcer debridement. In four of the eight studies, a 50% nitrous oxide/50% oxygen mixture delivered through an on-demand valve activated by a patient’s inspired breaths was used to minimize the risk of oversedation and to prevent hypoxia.
Contraindications for using nitrous oxide are pregnancy (in patients, health care providers, and assistants). Relative contraindications include nasal obstruction, chronic obstructive pulmonary disease, active cystic fibrosis, recent tympanic membrane surgery, and claustrophobia. According to the National Institute for Occupational Safety and Health, occupational exposure to nitrous oxide can lead to adverse effects that include reduced fertility and spontaneous abortion, as well as neurologic, renal, and hepatic diseases. The consensus of the majority of the studies in the PubMed/Cochrane review is that nitrous oxide provided a significant reduction in pain during dermatologic procedures, with mild and transient adverse effects. The effects dissipated quickly and thus patients could drive themselves home. But studies remain limited, and more well designed, randomized clinical trials are needed to provide clinical guidelines, safety monitoring protocols, and evidence for the use of nitrous oxide in dermatology. In my opinion, when more data are available, it will become one of the mainstays of analgesia in dermatologic procedures, particularly for pediatric, Mohs, and facial rejuvenation procedures.
Dr. Talakoub Dr. Wesley and are cocontributors to this column. Dr. Talakoub is in private practice in McLean, Va. Dr. Wesley practices dermatology in Beverly Hills, Calif. This month’s column is by Dr. Talakoub. Write to them at [email protected]. They had no relevant disclosures.
Sources
Brotzman EA et al. Dermatol Surg. 2018 May;44(5):661-9.
“Controlling Exposures to Nitrous Oxide During Anesthetic Administration,” National Institute for Occupational Safety and Health (https://www.cdc.gov/niosh/docs/94-100/default.html).
. When used properly, with meticulous patient monitoring, it is safe and effective. In my practice, I have used it for procedures as simple as a skin biopsy. While we have excellent topical numbing options for pain control, nitrous oxide works well as an anxiolytic and can help calm the patient who is nervous or has a fear of needles.
Nitrous oxide is a tasteless gas synthesized and released by cells. Inhalational nitrous oxide is absorbed from the lungs and diffuses into plasma, where it acts on the central nervous system as an anxiolytic and analgesic by blocking the NMDA receptor. It has a quick onset of action and short duration, is easily titrated, and has a low side effect profile.
Initially used to provide pain relief during labor in the late 1800s, nitrous oxide is now rarely used in the United States as inhalational analgesia during surgery or labor; however, use in dentistry and pediatrics is common. In a recent review of PubMed and Cochrane databases by Brotzman et al., eight studies on the use of nitrous oxide in dermatology were identified. Studies reported favorable safety and efficacy of nitrous oxide in providing analgesia during dermatologic procedures, which included facial rejuvenation, hair transplantation, and pediatric procedures. Several other studies also discussed the use of nitrous oxide in combination with tumescent anesthesia for venous ablation and liposuction. All adverse effects were limited to the time of inhalation and included euphoria, laughter, nausea, dizziness, and vertigo. There are no studies reviewing the risk of nitrous oxide used during CO2 resurfacing procedures.
In five of the eight studies, vital signs and oxygen saturation were recorded during the period of inhalation. Almost all patients maintained adequate oxygen saturation and vitals also remained stable in these five studies, except for a slight increase in systolic and diastolic arterial pressure after ulcer debridement. In four of the eight studies, a 50% nitrous oxide/50% oxygen mixture delivered through an on-demand valve activated by a patient’s inspired breaths was used to minimize the risk of oversedation and to prevent hypoxia.
Contraindications for using nitrous oxide are pregnancy (in patients, health care providers, and assistants). Relative contraindications include nasal obstruction, chronic obstructive pulmonary disease, active cystic fibrosis, recent tympanic membrane surgery, and claustrophobia. According to the National Institute for Occupational Safety and Health, occupational exposure to nitrous oxide can lead to adverse effects that include reduced fertility and spontaneous abortion, as well as neurologic, renal, and hepatic diseases. The consensus of the majority of the studies in the PubMed/Cochrane review is that nitrous oxide provided a significant reduction in pain during dermatologic procedures, with mild and transient adverse effects. The effects dissipated quickly and thus patients could drive themselves home. But studies remain limited, and more well designed, randomized clinical trials are needed to provide clinical guidelines, safety monitoring protocols, and evidence for the use of nitrous oxide in dermatology. In my opinion, when more data are available, it will become one of the mainstays of analgesia in dermatologic procedures, particularly for pediatric, Mohs, and facial rejuvenation procedures.
Dr. Talakoub Dr. Wesley and are cocontributors to this column. Dr. Talakoub is in private practice in McLean, Va. Dr. Wesley practices dermatology in Beverly Hills, Calif. This month’s column is by Dr. Talakoub. Write to them at [email protected]. They had no relevant disclosures.
Sources
Brotzman EA et al. Dermatol Surg. 2018 May;44(5):661-9.
“Controlling Exposures to Nitrous Oxide During Anesthetic Administration,” National Institute for Occupational Safety and Health (https://www.cdc.gov/niosh/docs/94-100/default.html).
Acute psychosis: Is it schizophrenia or bipolar disorder?
Patients’ functional outcome assessment results are critical
I have been amazed at psychiatrists who could see a patient who was obviously acutely psychotic and tell whether they had schizophrenia or bipolar disorder while the patient was acutely psychotic. I am amazed because I cannot do it, although I used to think I could.
Earlier in my career, I would see patients who were floridly psychotic who would have all the symptoms of schizophrenia, and I would think “Yep, they have schizophrenia, all right.” After all, when I was starting out in psychiatry, I thought that Schneiderian first-rank symptoms were pathognomonic of schizophrenia, but research later showed that these first-rank symptoms could also be characteristic of dissociative disorder.
I quickly learned that some of the patients I thought had schizophrenia would recover and return to their premorbid level of functioning after the psychotic episode. Accordingly, by definition – for example, there was not a deterioration of psychosocial functioning after their psychotic episode – I would have to revise their diagnosis to bipolar disorder.
Finally, I got hip and realized that I could not determine patients’ diagnoses when they were acutely psychotic, and I started diagnosing patients as having a psychosis not otherwise specified (NOS).
Of course, using the NOS designation made many of my academic colleagues scoff at my diagnostic skills, but then I read the DSM-IV Guidebook by Frances, First, and Pincus (1995), and it was explained the NOS designation was wrongly maligned. Apparently, it was learned that there was extensive comorbidity between various diagnostic categories, and, it was explicated, approximately 50% of patients could not fit neatly into any specific diagnostic category. In fact, regarding psychotic and affective disorders, depending on how good a history patients and/or their family could deliver, it would sometimes take the resolution of the patients’ psychosis before it became clear that they were or were not going to return to premorbid functioning or continue to show significant psychosocial deterioration.
Since psychiatrists do not yet have objective diagnostic tests to determine whether a psychotic patient has some form of schizophrenia or bipolar disorder, because I do not think we can tell the patients’ post psychotic outcomes.
I recently had one patient who had been hospitalized for 39 days, and, who was so acutely floridly psychotic, I did not think she was going to recover. She was on antipsychotic medication at bedtime and other mood stabilizers during the day, but she had to be in soft restraints for a significant period of time and was getting several antipsychotic medication injections daily because she was extremely rambunctious and dangerously disruptive on the medical-surgical/psychiatric floor. Finally, when I reluctantly added lithium to her treatment regimen (I was unenthusiastic about putting her on lithium, which had worked for her in the past, because her kidneys were not functioning well and she had arrived at the hospital with lithium toxicity), she recovered. The transformation was remarkable.
So, it seems to me that a functional outcome assessment should determine the difference between patients who have bipolar disorder and schizophrenia as, by definition, if you do not have a deterioration in your psychosocial functioning you probably have bipolar disorder, and if you do have a deterioration in your psychosocial functioning you probably have schizophrenia. From a practical standpoint, post psychotic functioning is a major distinction between these two diagnoses by definition, and, since we don’t have objective measures to delineate bipolar disorder from schizophrenia (some studies have shown there is remarkable overlap between these two disorders), it seems to me we should give more consideration to post psychotic functioning, instead of trying to nail the patients’ diagnoses when they are acutely psychotic.
Dr. Bell is a staff psychiatrist at Jackson Park Hospital’s medical/surgical-psychiatry inpatient unit in Chicago, clinical psychiatrist emeritus in the department of psychiatry at the University of Illinois at Chicago, former president/CEO of Community Mental Health Council, and former director of the Institute for Juvenile Research (birthplace of child psychiatry), also in Chicago. Be sure to check out Dr. Bell’s new book Fetal Alcohol Exposure in the African-American Community.
Patients’ functional outcome assessment results are critical
Patients’ functional outcome assessment results are critical
I have been amazed at psychiatrists who could see a patient who was obviously acutely psychotic and tell whether they had schizophrenia or bipolar disorder while the patient was acutely psychotic. I am amazed because I cannot do it, although I used to think I could.
Earlier in my career, I would see patients who were floridly psychotic who would have all the symptoms of schizophrenia, and I would think “Yep, they have schizophrenia, all right.” After all, when I was starting out in psychiatry, I thought that Schneiderian first-rank symptoms were pathognomonic of schizophrenia, but research later showed that these first-rank symptoms could also be characteristic of dissociative disorder.
I quickly learned that some of the patients I thought had schizophrenia would recover and return to their premorbid level of functioning after the psychotic episode. Accordingly, by definition – for example, there was not a deterioration of psychosocial functioning after their psychotic episode – I would have to revise their diagnosis to bipolar disorder.
Finally, I got hip and realized that I could not determine patients’ diagnoses when they were acutely psychotic, and I started diagnosing patients as having a psychosis not otherwise specified (NOS).
Of course, using the NOS designation made many of my academic colleagues scoff at my diagnostic skills, but then I read the DSM-IV Guidebook by Frances, First, and Pincus (1995), and it was explained the NOS designation was wrongly maligned. Apparently, it was learned that there was extensive comorbidity between various diagnostic categories, and, it was explicated, approximately 50% of patients could not fit neatly into any specific diagnostic category. In fact, regarding psychotic and affective disorders, depending on how good a history patients and/or their family could deliver, it would sometimes take the resolution of the patients’ psychosis before it became clear that they were or were not going to return to premorbid functioning or continue to show significant psychosocial deterioration.
Since psychiatrists do not yet have objective diagnostic tests to determine whether a psychotic patient has some form of schizophrenia or bipolar disorder, because I do not think we can tell the patients’ post psychotic outcomes.
I recently had one patient who had been hospitalized for 39 days, and, who was so acutely floridly psychotic, I did not think she was going to recover. She was on antipsychotic medication at bedtime and other mood stabilizers during the day, but she had to be in soft restraints for a significant period of time and was getting several antipsychotic medication injections daily because she was extremely rambunctious and dangerously disruptive on the medical-surgical/psychiatric floor. Finally, when I reluctantly added lithium to her treatment regimen (I was unenthusiastic about putting her on lithium, which had worked for her in the past, because her kidneys were not functioning well and she had arrived at the hospital with lithium toxicity), she recovered. The transformation was remarkable.
So, it seems to me that a functional outcome assessment should determine the difference between patients who have bipolar disorder and schizophrenia as, by definition, if you do not have a deterioration in your psychosocial functioning you probably have bipolar disorder, and if you do have a deterioration in your psychosocial functioning you probably have schizophrenia. From a practical standpoint, post psychotic functioning is a major distinction between these two diagnoses by definition, and, since we don’t have objective measures to delineate bipolar disorder from schizophrenia (some studies have shown there is remarkable overlap between these two disorders), it seems to me we should give more consideration to post psychotic functioning, instead of trying to nail the patients’ diagnoses when they are acutely psychotic.
Dr. Bell is a staff psychiatrist at Jackson Park Hospital’s medical/surgical-psychiatry inpatient unit in Chicago, clinical psychiatrist emeritus in the department of psychiatry at the University of Illinois at Chicago, former president/CEO of Community Mental Health Council, and former director of the Institute for Juvenile Research (birthplace of child psychiatry), also in Chicago. Be sure to check out Dr. Bell’s new book Fetal Alcohol Exposure in the African-American Community.
I have been amazed at psychiatrists who could see a patient who was obviously acutely psychotic and tell whether they had schizophrenia or bipolar disorder while the patient was acutely psychotic. I am amazed because I cannot do it, although I used to think I could.
Earlier in my career, I would see patients who were floridly psychotic who would have all the symptoms of schizophrenia, and I would think “Yep, they have schizophrenia, all right.” After all, when I was starting out in psychiatry, I thought that Schneiderian first-rank symptoms were pathognomonic of schizophrenia, but research later showed that these first-rank symptoms could also be characteristic of dissociative disorder.
I quickly learned that some of the patients I thought had schizophrenia would recover and return to their premorbid level of functioning after the psychotic episode. Accordingly, by definition – for example, there was not a deterioration of psychosocial functioning after their psychotic episode – I would have to revise their diagnosis to bipolar disorder.
Finally, I got hip and realized that I could not determine patients’ diagnoses when they were acutely psychotic, and I started diagnosing patients as having a psychosis not otherwise specified (NOS).
Of course, using the NOS designation made many of my academic colleagues scoff at my diagnostic skills, but then I read the DSM-IV Guidebook by Frances, First, and Pincus (1995), and it was explained the NOS designation was wrongly maligned. Apparently, it was learned that there was extensive comorbidity between various diagnostic categories, and, it was explicated, approximately 50% of patients could not fit neatly into any specific diagnostic category. In fact, regarding psychotic and affective disorders, depending on how good a history patients and/or their family could deliver, it would sometimes take the resolution of the patients’ psychosis before it became clear that they were or were not going to return to premorbid functioning or continue to show significant psychosocial deterioration.
Since psychiatrists do not yet have objective diagnostic tests to determine whether a psychotic patient has some form of schizophrenia or bipolar disorder, because I do not think we can tell the patients’ post psychotic outcomes.
I recently had one patient who had been hospitalized for 39 days, and, who was so acutely floridly psychotic, I did not think she was going to recover. She was on antipsychotic medication at bedtime and other mood stabilizers during the day, but she had to be in soft restraints for a significant period of time and was getting several antipsychotic medication injections daily because she was extremely rambunctious and dangerously disruptive on the medical-surgical/psychiatric floor. Finally, when I reluctantly added lithium to her treatment regimen (I was unenthusiastic about putting her on lithium, which had worked for her in the past, because her kidneys were not functioning well and she had arrived at the hospital with lithium toxicity), she recovered. The transformation was remarkable.
So, it seems to me that a functional outcome assessment should determine the difference between patients who have bipolar disorder and schizophrenia as, by definition, if you do not have a deterioration in your psychosocial functioning you probably have bipolar disorder, and if you do have a deterioration in your psychosocial functioning you probably have schizophrenia. From a practical standpoint, post psychotic functioning is a major distinction between these two diagnoses by definition, and, since we don’t have objective measures to delineate bipolar disorder from schizophrenia (some studies have shown there is remarkable overlap between these two disorders), it seems to me we should give more consideration to post psychotic functioning, instead of trying to nail the patients’ diagnoses when they are acutely psychotic.
Dr. Bell is a staff psychiatrist at Jackson Park Hospital’s medical/surgical-psychiatry inpatient unit in Chicago, clinical psychiatrist emeritus in the department of psychiatry at the University of Illinois at Chicago, former president/CEO of Community Mental Health Council, and former director of the Institute for Juvenile Research (birthplace of child psychiatry), also in Chicago. Be sure to check out Dr. Bell’s new book Fetal Alcohol Exposure in the African-American Community.
The type II error and black holes
An international group of scientists have announced they have an image of a black hole. This feat of scientific achievement and teamwork is another giant step in humankind’s understanding of the universe. It isn’t easy to find something that isn’t there. Black holes exist and this one is about 6.5 billion times more massive than Earth’s sun. That is a lot of “there.”
In medical research, most articles are about discovering something new. Lately, it is also common to publish studies that claim that something doesn’t exist. No difference is found between treatment A and treatment B. Two decades ago those negative studies rarely were published, but there was merit in the idea that more of them should be published. However, that merit presupposed that the negative studies worthy of publication would be well designed, robust, and, most importantly, contain a power calculation showing that the methodology would have detected the phenomenon if the phenomenon were large enough to be clinically important. Alas, the literature has been flooded with negative studies finding no effect because the studies were hopelessly underpowered and never had a realistic chance of detecting anything. This fake news pollutes our medical knowledge.
To clarify, let me provide a simple example. With my myopia, at 100 yards and without my glasses, I can’t detect the difference between Lebron James and Megan Rapinoe, although I know Megan is better at corner kicks.
Now let me give a second, more complex example that obfuscates the same detection issue. Are there moons circling Jupiter? I go out each night, find Jupiter, take a picture with my trusty cell phone, and examine the picture for any evidence of an object(s) circling the planet. I do this many times. How many? Well, if I only do it three times, people will doubt my science, but doing it 1,000 times would take too long. In my experience, most negative studies seem to involve about 30-50 patients. So one picture a week for a year will produce 52 observations. That is a lot of cold nights under the stars. I will use my scientific knowledge and ability to read sky charts to locate Jupiter. (There is an app for that.) I will use my experience to distinguish Jupiter from Venus and Mars. There will be cloudy days, so maybe only 30 clear pictures will be obtained. I will have a second observer examine the photos. We will calculate a kappa statistic for inter-rater agreement. There will be pictures and tables of numbers. When I’m done, I will publish an article saying that Jupiter doesn’t have moons because I didn’t find any. Trust me, I’m a doctor.
Science doesn’t work that way. Science doesn’t care how smart I am, how dedicated I am, how expensive my cell phone is, or how much work I put into the project, science wants empiric proof. My failure to find moons does not refute their existence. A claim that something does NOT exist cannot be correctly made by simply showing that the P value is greater than .05. A statistically insignificant P value also might also mean that my experiment, despite all my time, effort, commitment, and data collection, is simply inadequate to detect the phenomenon. My cell phone has enough pixels to see Jupiter but not its moons. The phone isn’t powerful enough. My claim is a type II error.
One needs to specify the threshold size of a clinically important effect and then show that your methods and results were powerful enough to have detected something that small. Only then may you correctly publish a conclusion that there is nothing there, a donut hole in the black void of space.
I invite you to do your own survey. As you read journal articles, identify the next 10 times you read a conclusion that claims no effect was found. Scour that article carefully for any indication of the size of effect that those methods and results would have been able to detect. Look for a power calculation. Grade the article with a simple pass/fail on that point. Did the authors provide that information in a way you can understand, or do you just have to trust them? Take President Reagan’s advice, “Trust, but verify.” Most of the 10 articles will lack the calculation and many negative claims are type II errors.
Dr. Powell is a pediatric hospitalist and clinical ethics consultant living in St. Louis. Email him at [email protected].
An international group of scientists have announced they have an image of a black hole. This feat of scientific achievement and teamwork is another giant step in humankind’s understanding of the universe. It isn’t easy to find something that isn’t there. Black holes exist and this one is about 6.5 billion times more massive than Earth’s sun. That is a lot of “there.”
In medical research, most articles are about discovering something new. Lately, it is also common to publish studies that claim that something doesn’t exist. No difference is found between treatment A and treatment B. Two decades ago those negative studies rarely were published, but there was merit in the idea that more of them should be published. However, that merit presupposed that the negative studies worthy of publication would be well designed, robust, and, most importantly, contain a power calculation showing that the methodology would have detected the phenomenon if the phenomenon were large enough to be clinically important. Alas, the literature has been flooded with negative studies finding no effect because the studies were hopelessly underpowered and never had a realistic chance of detecting anything. This fake news pollutes our medical knowledge.
To clarify, let me provide a simple example. With my myopia, at 100 yards and without my glasses, I can’t detect the difference between Lebron James and Megan Rapinoe, although I know Megan is better at corner kicks.
Now let me give a second, more complex example that obfuscates the same detection issue. Are there moons circling Jupiter? I go out each night, find Jupiter, take a picture with my trusty cell phone, and examine the picture for any evidence of an object(s) circling the planet. I do this many times. How many? Well, if I only do it three times, people will doubt my science, but doing it 1,000 times would take too long. In my experience, most negative studies seem to involve about 30-50 patients. So one picture a week for a year will produce 52 observations. That is a lot of cold nights under the stars. I will use my scientific knowledge and ability to read sky charts to locate Jupiter. (There is an app for that.) I will use my experience to distinguish Jupiter from Venus and Mars. There will be cloudy days, so maybe only 30 clear pictures will be obtained. I will have a second observer examine the photos. We will calculate a kappa statistic for inter-rater agreement. There will be pictures and tables of numbers. When I’m done, I will publish an article saying that Jupiter doesn’t have moons because I didn’t find any. Trust me, I’m a doctor.
Science doesn’t work that way. Science doesn’t care how smart I am, how dedicated I am, how expensive my cell phone is, or how much work I put into the project, science wants empiric proof. My failure to find moons does not refute their existence. A claim that something does NOT exist cannot be correctly made by simply showing that the P value is greater than .05. A statistically insignificant P value also might also mean that my experiment, despite all my time, effort, commitment, and data collection, is simply inadequate to detect the phenomenon. My cell phone has enough pixels to see Jupiter but not its moons. The phone isn’t powerful enough. My claim is a type II error.
One needs to specify the threshold size of a clinically important effect and then show that your methods and results were powerful enough to have detected something that small. Only then may you correctly publish a conclusion that there is nothing there, a donut hole in the black void of space.
I invite you to do your own survey. As you read journal articles, identify the next 10 times you read a conclusion that claims no effect was found. Scour that article carefully for any indication of the size of effect that those methods and results would have been able to detect. Look for a power calculation. Grade the article with a simple pass/fail on that point. Did the authors provide that information in a way you can understand, or do you just have to trust them? Take President Reagan’s advice, “Trust, but verify.” Most of the 10 articles will lack the calculation and many negative claims are type II errors.
Dr. Powell is a pediatric hospitalist and clinical ethics consultant living in St. Louis. Email him at [email protected].
An international group of scientists have announced they have an image of a black hole. This feat of scientific achievement and teamwork is another giant step in humankind’s understanding of the universe. It isn’t easy to find something that isn’t there. Black holes exist and this one is about 6.5 billion times more massive than Earth’s sun. That is a lot of “there.”
In medical research, most articles are about discovering something new. Lately, it is also common to publish studies that claim that something doesn’t exist. No difference is found between treatment A and treatment B. Two decades ago those negative studies rarely were published, but there was merit in the idea that more of them should be published. However, that merit presupposed that the negative studies worthy of publication would be well designed, robust, and, most importantly, contain a power calculation showing that the methodology would have detected the phenomenon if the phenomenon were large enough to be clinically important. Alas, the literature has been flooded with negative studies finding no effect because the studies were hopelessly underpowered and never had a realistic chance of detecting anything. This fake news pollutes our medical knowledge.
To clarify, let me provide a simple example. With my myopia, at 100 yards and without my glasses, I can’t detect the difference between Lebron James and Megan Rapinoe, although I know Megan is better at corner kicks.
Now let me give a second, more complex example that obfuscates the same detection issue. Are there moons circling Jupiter? I go out each night, find Jupiter, take a picture with my trusty cell phone, and examine the picture for any evidence of an object(s) circling the planet. I do this many times. How many? Well, if I only do it three times, people will doubt my science, but doing it 1,000 times would take too long. In my experience, most negative studies seem to involve about 30-50 patients. So one picture a week for a year will produce 52 observations. That is a lot of cold nights under the stars. I will use my scientific knowledge and ability to read sky charts to locate Jupiter. (There is an app for that.) I will use my experience to distinguish Jupiter from Venus and Mars. There will be cloudy days, so maybe only 30 clear pictures will be obtained. I will have a second observer examine the photos. We will calculate a kappa statistic for inter-rater agreement. There will be pictures and tables of numbers. When I’m done, I will publish an article saying that Jupiter doesn’t have moons because I didn’t find any. Trust me, I’m a doctor.
Science doesn’t work that way. Science doesn’t care how smart I am, how dedicated I am, how expensive my cell phone is, or how much work I put into the project, science wants empiric proof. My failure to find moons does not refute their existence. A claim that something does NOT exist cannot be correctly made by simply showing that the P value is greater than .05. A statistically insignificant P value also might also mean that my experiment, despite all my time, effort, commitment, and data collection, is simply inadequate to detect the phenomenon. My cell phone has enough pixels to see Jupiter but not its moons. The phone isn’t powerful enough. My claim is a type II error.
One needs to specify the threshold size of a clinically important effect and then show that your methods and results were powerful enough to have detected something that small. Only then may you correctly publish a conclusion that there is nothing there, a donut hole in the black void of space.
I invite you to do your own survey. As you read journal articles, identify the next 10 times you read a conclusion that claims no effect was found. Scour that article carefully for any indication of the size of effect that those methods and results would have been able to detect. Look for a power calculation. Grade the article with a simple pass/fail on that point. Did the authors provide that information in a way you can understand, or do you just have to trust them? Take President Reagan’s advice, “Trust, but verify.” Most of the 10 articles will lack the calculation and many negative claims are type II errors.
Dr. Powell is a pediatric hospitalist and clinical ethics consultant living in St. Louis. Email him at [email protected].