Commentary

I suspect that most members of the SVS are aware of the recent New York Times article entitled “Medicare payments surge for stents to unblock blood vessels in limbs” and which was the subject of our front page news article last month (http://vswebn.org/NYTstents). In that article Dr. Peter Lawrence, the President of the SVS, described steps that the SVS has taken to address the appropriateness of vascular interventions. It was his inspired leadership that led to his devoting the Stanley Crawford symposium at last year’s Vascular Annual Meeting specifically to the problem of unnecessary procedures. Those of you who have read my editorials over the last year will recognize that I also have been on a campaign against the indiscriminate use of both venous and endovascular procedures, especially by non–vascular physicians. However, we must acknowledge that even some of our own are abusing the system for financial gain.

One of the major points made by the New York Times article is that many of these unnecessary procedures are being performed by cardiologists in outpatient centers with little or no oversight. In full disclosure I must admit that my group does lease space in an outpatient center. I have also published on the benefits of such a center and the mechanism for its installation (J. Vasc. Surg. 2009; 49:1073-6).

The reimbursement for a procedure performed in a physician-owned or -leased outpatient facility is far greater than can be achieved in a hospital-owned facility. However, since the physician is responsible for the expenses incurred in such outpatient facilities, there is a financial incentive to do more with inexpensive devices that may be less effective. However, most vascular surgeons who utilize such centers will nevertheless do what is best for the patient in spite of higher costs. Further, patients may benefit from these centers because of convenience and for the provision of a more personable environment than can be found in a hospital inpatient or outpatient facility. Additionally, since the risk of complications from complex interventions, which can be difficult to manage in an outpatient facility, most ethical physicians will ensure that only the safest procedures are undertaken. Personally, I have performed more than 500 procedures in our facility over the last 7 years and have never encountered a pseudoaneurysm, retroperitoneal hematoma, or other complication needing hospitalization.

It is my belief that the excessive procedures delineated in the New York Times article are probably not representative of the majority of such centers. It is, however, quite true that there is no oversight or ombudsman to protect the patient in these outpatient facilities. Hospital-employed or university vascular surgeons may correctly imply that there is more oversight of procedures performed in hospital facilities and that this should limit unnecessary procedures. Needless to say, that is not the case in all institutions.

In our 600-bed municipal hospital, there is limited peer review and the few times when it has been applied it has, on occasion, resulted in legal suits against the reviewing medical staff. Additionally, institutions that reward practitioners based on relative value units may also induce a perverse incentive to overuse procedures.

As Dr. Lawrence describes in his article, site of service may not be the only driving force behind unnecessary interventions. In fact the Clinical Council of the SVS has seized upon appropriate care in office-based centers and is working on constructive suggestions to ensure not only that site of service is convenient for patients, but also that it provides appropriate high quality care. For the time being the SVS recognizes that we need improved oversight and peer review in these physician-owned centers, and that we should not simply abandon them because of the abusive behavior of a few unethical practitioners.

The New York Times article and Dr. Lawrence’s article and letter to the New York Times struck a chord with our membership. It has provoked an outpouring of comments and suggestions from our membership. Some of these are to be found in this edition as letters to the editor. It is apparent that many of us are horrified by what we are seeing, not only in outpatient facilities but also in hospitals.

I believe this is such an important issue that I have requested our associate editors to write a brief comment on their views on the matter and to specifically identify methods of rectifying the current overuse of vascular procedures (see the following 2 pages).

I am hopeful that the NY Times article and the responses we publish will instigate vascular surgeons to stand up for our profession and the well-being of our patients. For if we do not, we will continue to be marginalized by newspaper reporters and government agencies. They will continue to lump us together with interventionalists who may not follow the same ethical road that most of us travel.

I suspect that most members of the SVS are aware of the recent New York Times article entitled “Medicare payments surge for stents to unblock blood vessels in limbs” and which was the subject of our front page news article last month (http://vswebn.org/NYTstents). In that article Dr. Peter Lawrence, the President of the SVS, described steps that the SVS has taken to address the appropriateness of vascular interventions. It was his inspired leadership that led to his devoting the Stanley Crawford symposium at last year’s Vascular Annual Meeting specifically to the problem of unnecessary procedures. Those of you who have read my editorials over the last year will recognize that I also have been on a campaign against the indiscriminate use of both venous and endovascular procedures, especially by non–vascular physicians. However, we must acknowledge that even some of our own are abusing the system for financial gain.

One of the major points made by the New York Times article is that many of these unnecessary procedures are being performed by cardiologists in outpatient centers with little or no oversight. In full disclosure I must admit that my group does lease space in an outpatient center. I have also published on the benefits of such a center and the mechanism for its installation (J. Vasc. Surg. 2009; 49:1073-6).

The reimbursement for a procedure performed in a physician-owned or -leased outpatient facility is far greater than can be achieved in a hospital-owned facility. However, since the physician is responsible for the expenses incurred in such outpatient facilities, there is a financial incentive to do more with inexpensive devices that may be less effective. However, most vascular surgeons who utilize such centers will nevertheless do what is best for the patient in spite of higher costs. Further, patients may benefit from these centers because of convenience and for the provision of a more personable environment than can be found in a hospital inpatient or outpatient facility. Additionally, since the risk of complications from complex interventions, which can be difficult to manage in an outpatient facility, most ethical physicians will ensure that only the safest procedures are undertaken. Personally, I have performed more than 500 procedures in our facility over the last 7 years and have never encountered a pseudoaneurysm, retroperitoneal hematoma, or other complication needing hospitalization.

It is my belief that the excessive procedures delineated in the New York Times article are probably not representative of the majority of such centers. It is, however, quite true that there is no oversight or ombudsman to protect the patient in these outpatient facilities. Hospital-employed or university vascular surgeons may correctly imply that there is more oversight of procedures performed in hospital facilities and that this should limit unnecessary procedures. Needless to say, that is not the case in all institutions.

In our 600-bed municipal hospital, there is limited peer review and the few times when it has been applied it has, on occasion, resulted in legal suits against the reviewing medical staff. Additionally, institutions that reward practitioners based on relative value units may also induce a perverse incentive to overuse procedures.

As Dr. Lawrence describes in his article, site of service may not be the only driving force behind unnecessary interventions. In fact the Clinical Council of the SVS has seized upon appropriate care in office-based centers and is working on constructive suggestions to ensure not only that site of service is convenient for patients, but also that it provides appropriate high quality care. For the time being the SVS recognizes that we need improved oversight and peer review in these physician-owned centers, and that we should not simply abandon them because of the abusive behavior of a few unethical practitioners.

The New York Times article and Dr. Lawrence’s article and letter to the New York Times struck a chord with our membership. It has provoked an outpouring of comments and suggestions from our membership. Some of these are to be found in this edition as letters to the editor. It is apparent that many of us are horrified by what we are seeing, not only in outpatient facilities but also in hospitals.

I believe this is such an important issue that I have requested our associate editors to write a brief comment on their views on the matter and to specifically identify methods of rectifying the current overuse of vascular procedures (see the following 2 pages).

I am hopeful that the NY Times article and the responses we publish will instigate vascular surgeons to stand up for our profession and the well-being of our patients. For if we do not, we will continue to be marginalized by newspaper reporters and government agencies. They will continue to lump us together with interventionalists who may not follow the same ethical road that most of us travel.

I suspect that most members of the SVS are aware of the recent New York Times article entitled “Medicare payments surge for stents to unblock blood vessels in limbs” and which was the subject of our front page news article last month (http://vswebn.org/NYTstents). In that article Dr. Peter Lawrence, the President of the SVS, described steps that the SVS has taken to address the appropriateness of vascular interventions. It was his inspired leadership that led to his devoting the Stanley Crawford symposium at last year’s Vascular Annual Meeting specifically to the problem of unnecessary procedures. Those of you who have read my editorials over the last year will recognize that I also have been on a campaign against the indiscriminate use of both venous and endovascular procedures, especially by non–vascular physicians. However, we must acknowledge that even some of our own are abusing the system for financial gain.

One of the major points made by the New York Times article is that many of these unnecessary procedures are being performed by cardiologists in outpatient centers with little or no oversight. In full disclosure I must admit that my group does lease space in an outpatient center. I have also published on the benefits of such a center and the mechanism for its installation (J. Vasc. Surg. 2009; 49:1073-6).

The reimbursement for a procedure performed in a physician-owned or -leased outpatient facility is far greater than can be achieved in a hospital-owned facility. However, since the physician is responsible for the expenses incurred in such outpatient facilities, there is a financial incentive to do more with inexpensive devices that may be less effective. However, most vascular surgeons who utilize such centers will nevertheless do what is best for the patient in spite of higher costs. Further, patients may benefit from these centers because of convenience and for the provision of a more personable environment than can be found in a hospital inpatient or outpatient facility. Additionally, since the risk of complications from complex interventions, which can be difficult to manage in an outpatient facility, most ethical physicians will ensure that only the safest procedures are undertaken. Personally, I have performed more than 500 procedures in our facility over the last 7 years and have never encountered a pseudoaneurysm, retroperitoneal hematoma, or other complication needing hospitalization.

It is my belief that the excessive procedures delineated in the New York Times article are probably not representative of the majority of such centers. It is, however, quite true that there is no oversight or ombudsman to protect the patient in these outpatient facilities. Hospital-employed or university vascular surgeons may correctly imply that there is more oversight of procedures performed in hospital facilities and that this should limit unnecessary procedures. Needless to say, that is not the case in all institutions.

In our 600-bed municipal hospital, there is limited peer review and the few times when it has been applied it has, on occasion, resulted in legal suits against the reviewing medical staff. Additionally, institutions that reward practitioners based on relative value units may also induce a perverse incentive to overuse procedures.

As Dr. Lawrence describes in his article, site of service may not be the only driving force behind unnecessary interventions. In fact the Clinical Council of the SVS has seized upon appropriate care in office-based centers and is working on constructive suggestions to ensure not only that site of service is convenient for patients, but also that it provides appropriate high quality care. For the time being the SVS recognizes that we need improved oversight and peer review in these physician-owned centers, and that we should not simply abandon them because of the abusive behavior of a few unethical practitioners.

The New York Times article and Dr. Lawrence’s article and letter to the New York Times struck a chord with our membership. It has provoked an outpouring of comments and suggestions from our membership. Some of these are to be found in this edition as letters to the editor. It is apparent that many of us are horrified by what we are seeing, not only in outpatient facilities but also in hospitals.

I believe this is such an important issue that I have requested our associate editors to write a brief comment on their views on the matter and to specifically identify methods of rectifying the current overuse of vascular procedures (see the following 2 pages).

I am hopeful that the NY Times article and the responses we publish will instigate vascular surgeons to stand up for our profession and the well-being of our patients. For if we do not, we will continue to be marginalized by newspaper reporters and government agencies. They will continue to lump us together with interventionalists who may not follow the same ethical road that most of us travel.

Is it possible to give the best critical care while spending less money and resources doing it? Can we reduce waste while improving quality in a so-called lean approach to critical care? I believe that we have too many critical care beds, and we fill some of those beds with patients who can be taken care of at less intense levels of care—which are also less expensive.

Most work that is done to improve critical care looks at the quality of care. This is an area where a lot of data are accumulating. Take septic shock, for example. In the recently published ProCESS trial (The ProCESS Investigators. N Engl J Med. 2014. 370[18]:1683), the 60-day in-hospital mortality for septic shock was 18.2% to 21.0%. A lot of institutions (including mine) are struggling to get their septic shock mortality rate under 30%. Although some people critique the ProCESS trial mortality rate on patient selection, most of us try to figure out how to duplicate that lower rate. We do this in areas other than septic shock. If we are comparable in whatever quality statistic, we applaud our success. If we aren’t comparable, we look at ways to improve, often based on what was done in that particular study.

How big of a financial burden is our critical care spending? According to an analysis of critical care beds by Halpern and colleagues (Crit Care Med. 2004;32[6]:1254), the number of hospital beds decreased 26.4% between 1985 and 2000, and the absolute number of critical care beds increased 26.2% (quantitated at 67,357 adult beds in 2007 per SCCM.org, www.sccm.org/Communications/Pages/CriticalCareStats.aspx). Critical care beds cost $2,674 per day in 2000, up from $1,185 (our CFOs tell us it is more like $3,500 to $4,000 per day now). They represented 13.3% of hospital costs, 4.2% of national health expenditures (NHE), and 0.56% of gross domestic product (GDP). There are 55,000 critically ill patients cared for each day in the United States, representing 5 million ICU patients per year. This is an enormous expenditure of money and it is growing.

Another interesting observation by Halpern and colleagues (Crit Care Med. 2004;32:1254) was that critical care beds were only at 65% occupancy. This reflects my own experience where we operate at a 70% average ICU bed occupancy. We have created a larger financial burden with the fixed costs of one-third more ICU beds than we actually use. Some bed availability is desirable, but how much is too much? Are we doing the best job to give quality care and spend money wisely? Can we be more efficient in the throughput of patients and in their care? Admission criteria should be part of any unit, designed to place all patients who need ICU care appropriately in the ICU and exclude those whose care can be managed at a lesser level of intensity and cost. Discharge criteria, care protocols (e.g., wake up and wean), checklists, and daily attention to the usual parameters (e.g., DVT prophylaxis) are essential for high-quality but efficient care. Done 24/7, we can maximize efficiency and quality with a minimum of ICU readmissions. Throughput is part of every physician’s job description. The physician who wants one more day for his or her patient in the ICU simply because the nurse has fewer patients misses a number of points. Why would anyone want more exposure to resistant organisms, more noise, more awakenings, and less sleep, just to name a few? Keeping that non-ICU patient in the ICU bed might even delay the transfer of another patient coming from the ED, where we know they often don’t get good ICU care.

Are the beds filled only with what we intensivists would consider legitimate ICU patients, defined by both generally accepted (endotracheal tube in place) and individually specified criteria (unit specific related to other unit capabilities)? That would impact cost. An interesting article by Gooch and Kahn (JAMA. 2014; 311[6]:567) discussed the demand elasticity of the ICU. They considered the changes in case mix of patients between days of high and low bed availability. They contended that when ICU beds were available, there was an increase in patients who were unlikely to benefit from ICU admission. This group included a population of patients likely to survive and whose illness severity was low and a population of patients who were unlikely to survive and had a high illness severity. In other words, admissions expand to fill the staff-able beds. If this is true, it is another area where better management could lower costs without reducing the quality of care.

What if bed availability truly is reduced, often by a lack of critical care nursing staff if not physical beds? Here the answer is unclear. Town (Crit Care Med. 2014;42[9]:2037) looked at ICU readmission rates and the odds of having a cardiac arrest on the ward related to bed availability. Five ICUs with 63 beds total were examined. As ICU bed availability decreased, the odds of patients who were discharged from the ICU being readmitted to the ICU went up. Also, the odds of patients having a cardiac arrest on the ward increased when medical (not total) ICU beds were less available. In 2013, Wagner and colleagues (Ann Intern Med. 2013;159[7]:447) looked at 155 ICUs with 200,730 patients discharged from ICUs to hospital floors from 2001 to 2008. They examined what they call the strain metrics. These included the standardized ICU census, the proportion of new admissions, and the average predicted probability of death of the other patients in the ICU on the days of ICU discharge. When the strain metrics increased, ICU patients had shorter ICU length of stay and ICU readmission odds went up. They didn’t, however, see an increased odds of death, a reduced odds of being discharged home, or a longer total hospital LOS. In a third study reported in 2008 in the Annals of Internal Medicine by Howell and colleagues (Ann Intern Med. 2008;149[11]:804), an innovative method of bed management was described. Because of an overcrowded ED and a high ambulance diversion rate, hospitalists implemented a system of bed control that was based on knowledge of ICU beds and ED congestion and flow. Bed assignments were better controlled by twice-daily ICU rounds and regular visits to the ED: throughput for admitted patients decreased by 98 minutes and time on diversion decreased significantly.

Mery and Kahn reported in 2013 (Crit Care. 2013;17[3]:315) that when ICU bed availability was reduced, there was a reduction in the likelihood of ICU admission within 2 hours of a medical emergency team (MET) activation. What is interesting about this study done in three hospitals in Calgary, Alberta, Canada, is that there was an increased likelihood that the patient goals of care changed to comfort care when there was no bed availability, compared with two ICU beds being available. Even more interesting is that hospital mortality did not vary significantly by ICU bed availability: More patients were moved to palliative care yet no more people died. Perhaps a lack of ICU beds expedited appropriateness of care.

To summarize, we have more patients in critical care beds where we spend ever-increasing amounts of our health-care dollars, but we seem to have more critical care beds than we need. We still have patients in our ICUs who would be better cared for elsewhere in our institutions. We can perform more cost-effective throughput when we are pressed to do so and usually we can do it safely.

I contend that the next improvement in lean ICU medicine will be better management tools. Comprehensive checklists have helped me where computer solutions have yet to be developed. I am working to create hardware/software management solutions that will make my job more cost-effective and provide a sustainable process for what comes after me.

Dr. Waxman is associate professor of medicine, KU School of Medicine, Kansas City, Kan.; medical director, Medical Surgical ICU/PCU, Research Medical Center; and adjunct professor, Rockhurst University, Helzberg School of Management, Kansas City, Mo.

Is it possible to give the best critical care while spending less money and resources doing it? Can we reduce waste while improving quality in a so-called lean approach to critical care? I believe that we have too many critical care beds, and we fill some of those beds with patients who can be taken care of at less intense levels of care—which are also less expensive.

Most work that is done to improve critical care looks at the quality of care. This is an area where a lot of data are accumulating. Take septic shock, for example. In the recently published ProCESS trial (The ProCESS Investigators. N Engl J Med. 2014. 370[18]:1683), the 60-day in-hospital mortality for septic shock was 18.2% to 21.0%. A lot of institutions (including mine) are struggling to get their septic shock mortality rate under 30%. Although some people critique the ProCESS trial mortality rate on patient selection, most of us try to figure out how to duplicate that lower rate. We do this in areas other than septic shock. If we are comparable in whatever quality statistic, we applaud our success. If we aren’t comparable, we look at ways to improve, often based on what was done in that particular study.

How big of a financial burden is our critical care spending? According to an analysis of critical care beds by Halpern and colleagues (Crit Care Med. 2004;32[6]:1254), the number of hospital beds decreased 26.4% between 1985 and 2000, and the absolute number of critical care beds increased 26.2% (quantitated at 67,357 adult beds in 2007 per SCCM.org, www.sccm.org/Communications/Pages/CriticalCareStats.aspx). Critical care beds cost $2,674 per day in 2000, up from $1,185 (our CFOs tell us it is more like $3,500 to $4,000 per day now). They represented 13.3% of hospital costs, 4.2% of national health expenditures (NHE), and 0.56% of gross domestic product (GDP). There are 55,000 critically ill patients cared for each day in the United States, representing 5 million ICU patients per year. This is an enormous expenditure of money and it is growing.

Another interesting observation by Halpern and colleagues (Crit Care Med. 2004;32:1254) was that critical care beds were only at 65% occupancy. This reflects my own experience where we operate at a 70% average ICU bed occupancy. We have created a larger financial burden with the fixed costs of one-third more ICU beds than we actually use. Some bed availability is desirable, but how much is too much? Are we doing the best job to give quality care and spend money wisely? Can we be more efficient in the throughput of patients and in their care? Admission criteria should be part of any unit, designed to place all patients who need ICU care appropriately in the ICU and exclude those whose care can be managed at a lesser level of intensity and cost. Discharge criteria, care protocols (e.g., wake up and wean), checklists, and daily attention to the usual parameters (e.g., DVT prophylaxis) are essential for high-quality but efficient care. Done 24/7, we can maximize efficiency and quality with a minimum of ICU readmissions. Throughput is part of every physician’s job description. The physician who wants one more day for his or her patient in the ICU simply because the nurse has fewer patients misses a number of points. Why would anyone want more exposure to resistant organisms, more noise, more awakenings, and less sleep, just to name a few? Keeping that non-ICU patient in the ICU bed might even delay the transfer of another patient coming from the ED, where we know they often don’t get good ICU care.

Are the beds filled only with what we intensivists would consider legitimate ICU patients, defined by both generally accepted (endotracheal tube in place) and individually specified criteria (unit specific related to other unit capabilities)? That would impact cost. An interesting article by Gooch and Kahn (JAMA. 2014; 311[6]:567) discussed the demand elasticity of the ICU. They considered the changes in case mix of patients between days of high and low bed availability. They contended that when ICU beds were available, there was an increase in patients who were unlikely to benefit from ICU admission. This group included a population of patients likely to survive and whose illness severity was low and a population of patients who were unlikely to survive and had a high illness severity. In other words, admissions expand to fill the staff-able beds. If this is true, it is another area where better management could lower costs without reducing the quality of care.

What if bed availability truly is reduced, often by a lack of critical care nursing staff if not physical beds? Here the answer is unclear. Town (Crit Care Med. 2014;42[9]:2037) looked at ICU readmission rates and the odds of having a cardiac arrest on the ward related to bed availability. Five ICUs with 63 beds total were examined. As ICU bed availability decreased, the odds of patients who were discharged from the ICU being readmitted to the ICU went up. Also, the odds of patients having a cardiac arrest on the ward increased when medical (not total) ICU beds were less available. In 2013, Wagner and colleagues (Ann Intern Med. 2013;159[7]:447) looked at 155 ICUs with 200,730 patients discharged from ICUs to hospital floors from 2001 to 2008. They examined what they call the strain metrics. These included the standardized ICU census, the proportion of new admissions, and the average predicted probability of death of the other patients in the ICU on the days of ICU discharge. When the strain metrics increased, ICU patients had shorter ICU length of stay and ICU readmission odds went up. They didn’t, however, see an increased odds of death, a reduced odds of being discharged home, or a longer total hospital LOS. In a third study reported in 2008 in the Annals of Internal Medicine by Howell and colleagues (Ann Intern Med. 2008;149[11]:804), an innovative method of bed management was described. Because of an overcrowded ED and a high ambulance diversion rate, hospitalists implemented a system of bed control that was based on knowledge of ICU beds and ED congestion and flow. Bed assignments were better controlled by twice-daily ICU rounds and regular visits to the ED: throughput for admitted patients decreased by 98 minutes and time on diversion decreased significantly.

Mery and Kahn reported in 2013 (Crit Care. 2013;17[3]:315) that when ICU bed availability was reduced, there was a reduction in the likelihood of ICU admission within 2 hours of a medical emergency team (MET) activation. What is interesting about this study done in three hospitals in Calgary, Alberta, Canada, is that there was an increased likelihood that the patient goals of care changed to comfort care when there was no bed availability, compared with two ICU beds being available. Even more interesting is that hospital mortality did not vary significantly by ICU bed availability: More patients were moved to palliative care yet no more people died. Perhaps a lack of ICU beds expedited appropriateness of care.

To summarize, we have more patients in critical care beds where we spend ever-increasing amounts of our health-care dollars, but we seem to have more critical care beds than we need. We still have patients in our ICUs who would be better cared for elsewhere in our institutions. We can perform more cost-effective throughput when we are pressed to do so and usually we can do it safely.

I contend that the next improvement in lean ICU medicine will be better management tools. Comprehensive checklists have helped me where computer solutions have yet to be developed. I am working to create hardware/software management solutions that will make my job more cost-effective and provide a sustainable process for what comes after me.

Dr. Waxman is associate professor of medicine, KU School of Medicine, Kansas City, Kan.; medical director, Medical Surgical ICU/PCU, Research Medical Center; and adjunct professor, Rockhurst University, Helzberg School of Management, Kansas City, Mo.

Is it possible to give the best critical care while spending less money and resources doing it? Can we reduce waste while improving quality in a so-called lean approach to critical care? I believe that we have too many critical care beds, and we fill some of those beds with patients who can be taken care of at less intense levels of care—which are also less expensive.

Most work that is done to improve critical care looks at the quality of care. This is an area where a lot of data are accumulating. Take septic shock, for example. In the recently published ProCESS trial (The ProCESS Investigators. N Engl J Med. 2014. 370[18]:1683), the 60-day in-hospital mortality for septic shock was 18.2% to 21.0%. A lot of institutions (including mine) are struggling to get their septic shock mortality rate under 30%. Although some people critique the ProCESS trial mortality rate on patient selection, most of us try to figure out how to duplicate that lower rate. We do this in areas other than septic shock. If we are comparable in whatever quality statistic, we applaud our success. If we aren’t comparable, we look at ways to improve, often based on what was done in that particular study.

How big of a financial burden is our critical care spending? According to an analysis of critical care beds by Halpern and colleagues (Crit Care Med. 2004;32[6]:1254), the number of hospital beds decreased 26.4% between 1985 and 2000, and the absolute number of critical care beds increased 26.2% (quantitated at 67,357 adult beds in 2007 per SCCM.org, www.sccm.org/Communications/Pages/CriticalCareStats.aspx). Critical care beds cost $2,674 per day in 2000, up from $1,185 (our CFOs tell us it is more like $3,500 to $4,000 per day now). They represented 13.3% of hospital costs, 4.2% of national health expenditures (NHE), and 0.56% of gross domestic product (GDP). There are 55,000 critically ill patients cared for each day in the United States, representing 5 million ICU patients per year. This is an enormous expenditure of money and it is growing.

Another interesting observation by Halpern and colleagues (Crit Care Med. 2004;32:1254) was that critical care beds were only at 65% occupancy. This reflects my own experience where we operate at a 70% average ICU bed occupancy. We have created a larger financial burden with the fixed costs of one-third more ICU beds than we actually use. Some bed availability is desirable, but how much is too much? Are we doing the best job to give quality care and spend money wisely? Can we be more efficient in the throughput of patients and in their care? Admission criteria should be part of any unit, designed to place all patients who need ICU care appropriately in the ICU and exclude those whose care can be managed at a lesser level of intensity and cost. Discharge criteria, care protocols (e.g., wake up and wean), checklists, and daily attention to the usual parameters (e.g., DVT prophylaxis) are essential for high-quality but efficient care. Done 24/7, we can maximize efficiency and quality with a minimum of ICU readmissions. Throughput is part of every physician’s job description. The physician who wants one more day for his or her patient in the ICU simply because the nurse has fewer patients misses a number of points. Why would anyone want more exposure to resistant organisms, more noise, more awakenings, and less sleep, just to name a few? Keeping that non-ICU patient in the ICU bed might even delay the transfer of another patient coming from the ED, where we know they often don’t get good ICU care.

Are the beds filled only with what we intensivists would consider legitimate ICU patients, defined by both generally accepted (endotracheal tube in place) and individually specified criteria (unit specific related to other unit capabilities)? That would impact cost. An interesting article by Gooch and Kahn (JAMA. 2014; 311[6]:567) discussed the demand elasticity of the ICU. They considered the changes in case mix of patients between days of high and low bed availability. They contended that when ICU beds were available, there was an increase in patients who were unlikely to benefit from ICU admission. This group included a population of patients likely to survive and whose illness severity was low and a population of patients who were unlikely to survive and had a high illness severity. In other words, admissions expand to fill the staff-able beds. If this is true, it is another area where better management could lower costs without reducing the quality of care.

What if bed availability truly is reduced, often by a lack of critical care nursing staff if not physical beds? Here the answer is unclear. Town (Crit Care Med. 2014;42[9]:2037) looked at ICU readmission rates and the odds of having a cardiac arrest on the ward related to bed availability. Five ICUs with 63 beds total were examined. As ICU bed availability decreased, the odds of patients who were discharged from the ICU being readmitted to the ICU went up. Also, the odds of patients having a cardiac arrest on the ward increased when medical (not total) ICU beds were less available. In 2013, Wagner and colleagues (Ann Intern Med. 2013;159[7]:447) looked at 155 ICUs with 200,730 patients discharged from ICUs to hospital floors from 2001 to 2008. They examined what they call the strain metrics. These included the standardized ICU census, the proportion of new admissions, and the average predicted probability of death of the other patients in the ICU on the days of ICU discharge. When the strain metrics increased, ICU patients had shorter ICU length of stay and ICU readmission odds went up. They didn’t, however, see an increased odds of death, a reduced odds of being discharged home, or a longer total hospital LOS. In a third study reported in 2008 in the Annals of Internal Medicine by Howell and colleagues (Ann Intern Med. 2008;149[11]:804), an innovative method of bed management was described. Because of an overcrowded ED and a high ambulance diversion rate, hospitalists implemented a system of bed control that was based on knowledge of ICU beds and ED congestion and flow. Bed assignments were better controlled by twice-daily ICU rounds and regular visits to the ED: throughput for admitted patients decreased by 98 minutes and time on diversion decreased significantly.

Mery and Kahn reported in 2013 (Crit Care. 2013;17[3]:315) that when ICU bed availability was reduced, there was a reduction in the likelihood of ICU admission within 2 hours of a medical emergency team (MET) activation. What is interesting about this study done in three hospitals in Calgary, Alberta, Canada, is that there was an increased likelihood that the patient goals of care changed to comfort care when there was no bed availability, compared with two ICU beds being available. Even more interesting is that hospital mortality did not vary significantly by ICU bed availability: More patients were moved to palliative care yet no more people died. Perhaps a lack of ICU beds expedited appropriateness of care.

To summarize, we have more patients in critical care beds where we spend ever-increasing amounts of our health-care dollars, but we seem to have more critical care beds than we need. We still have patients in our ICUs who would be better cared for elsewhere in our institutions. We can perform more cost-effective throughput when we are pressed to do so and usually we can do it safely.

I contend that the next improvement in lean ICU medicine will be better management tools. Comprehensive checklists have helped me where computer solutions have yet to be developed. I am working to create hardware/software management solutions that will make my job more cost-effective and provide a sustainable process for what comes after me.

Dr. Waxman is associate professor of medicine, KU School of Medicine, Kansas City, Kan.; medical director, Medical Surgical ICU/PCU, Research Medical Center; and adjunct professor, Rockhurst University, Helzberg School of Management, Kansas City, Mo.

The Centers for Disease Control and Prevention’s recent report updating the estimated number of neural tube defects prevented by folic acid fortification of enriched cereal grain products clearly shows the huge impact of fortification: From 1999 through 2011, fortification prevented neural tube defects in about 1,300 births a year in the United States (MMWR 2015;64:1-5).

This is a dramatic example of how a relatively simple public health intervention – in this case, the mandatory addition of an inexpensive B vitamin to a portion of the food supply – is having a dramatic impact on a major birth defect.

Unfortunately, though, people may develop similar expectations that other micronutrients during pregnancy may prevent other birth defects or improve developmental outcomes, without adequate supportive evidence. For example, experimental animal studies have suggested that supplements of polyunsaturated fatty acids (PUFAs) during pregnancy improve brain development in the offspring (J. Perinat. Med. 2008;36;5-14). While there is no evidence that this is true in humans, there are prenatal vitamins that include PUFAs on the market.

Based on a review of nine randomized controlled studies that compared long chain PUFA supplementation to a placebo or no supplement in pregnant women, my colleagues and I concluded that the available research “regarding the maternal supplementation of PUFAs in retinal and neurocognitive development of the infant is not consistent in showing a benefit to supplementation” (Obstet.Gynecol. Int. 2012 [doi:10.1155/2012/591531]).

In a somewhat similar manner, an increasing number of women are taking megavitamins as part of their lifestyle, with the belief that “more is better.”

©Juanmonino/iStockphoto

Megavitamins may not necessarily be harmless. There is evidence from randomized trials that evaluated vitamin E or vitamin C for preeclampsia that vitamin E supplementation during pregnancy may cause intrauterine growth restriction (IUGR). This was confirmed by a study of 82 women who had been exposed to high doses of vitamin E supplements ranging from 400 IU to 1,200 IU a day during the first trimester. At Motherisk, we found that the mean birth weight among the babies of the women who had been exposed to high doses of vitamin E was significantly lower than the mean birth weight of the babies of the controls. But we did not find a significant difference in the rates of live births, preterm delivery, miscarriages, or stillbirths (Reprod. Toxicol. 2005;20:85-8). These women were on vitamin E as part of their lifestyle and not for any particular medical reason.

The medical community needs to keep in mind that while the folic acid fortification of flour and other products has shown dramatic effects in the overall population, as the CDC report shows, it may not meet the needs of specific populations of women who are at a greater risk of having a baby with a neural tube defect. As pointed out in the Morbidity and Mortality Weekly Report, these groups include Hispanic women, who may not consume as much folic acid or are at a greater risk of having a genetic polymorphism that makes them more susceptible to a folate insufficiency.

Flour fortification provides relatively small amounts of folic acid, possibly 200 mcg more a day, at best. But it has been shown that a woman who has had a previous child with a neural tube defect, a high-risk group, needs 5 mg per day to have an impact on prevention (Lancet 1991;338:131-7).

It is therefore important to keep in mind that there are high-risk groups who may need more than the amount provided by flour fortification. These groups include women on antiepileptic drugs or drugs that have antifolate activity, such as sulfonamide and methotrexate; as well as those with some genetic polymorphisms in the folate cycle.

Courtesy of the National Cancer Institute (NCI)

Women who smoke also tend to have lower folate levels, as do women with diabetes or who are obese. Women with celiac disease may have lower folate levels because they do not eat bread or flour-based products. Low-income women who may not eat sufficient green leafy vegetables, which are expensive and contain high levels of folic acid, may also be at greater risk.

A question that is still not resolved is whether folic acid can prevent other malformations, not just neural tube defects. There is some evidence that folic acid supplementation may also reduce the risk of cardiovascular defects and oral clefts. A randomized trial comparing folic acid to no folic acid to address these questions would be unethical. Instead, observational studies could evaluate the rate of these malformations after the fortification program began. Despite this major public health advance, we should always try to do even better and prevent more cases of neural tube defects and other malformations.

Dr. Koren is professor of pediatrics, pharmacology, pharmacy, and medical genetics at the University of Toronto. He is director of the Motherisk Program. He received grant support to conduct studies on folic acid from Duchesnay Inc., Canada. E-mail him at [email protected].

The Centers for Disease Control and Prevention’s recent report updating the estimated number of neural tube defects prevented by folic acid fortification of enriched cereal grain products clearly shows the huge impact of fortification: From 1999 through 2011, fortification prevented neural tube defects in about 1,300 births a year in the United States (MMWR 2015;64:1-5).

This is a dramatic example of how a relatively simple public health intervention – in this case, the mandatory addition of an inexpensive B vitamin to a portion of the food supply – is having a dramatic impact on a major birth defect.

Unfortunately, though, people may develop similar expectations that other micronutrients during pregnancy may prevent other birth defects or improve developmental outcomes, without adequate supportive evidence. For example, experimental animal studies have suggested that supplements of polyunsaturated fatty acids (PUFAs) during pregnancy improve brain development in the offspring (J. Perinat. Med. 2008;36;5-14). While there is no evidence that this is true in humans, there are prenatal vitamins that include PUFAs on the market.

Based on a review of nine randomized controlled studies that compared long chain PUFA supplementation to a placebo or no supplement in pregnant women, my colleagues and I concluded that the available research “regarding the maternal supplementation of PUFAs in retinal and neurocognitive development of the infant is not consistent in showing a benefit to supplementation” (Obstet.Gynecol. Int. 2012 [doi:10.1155/2012/591531]).

In a somewhat similar manner, an increasing number of women are taking megavitamins as part of their lifestyle, with the belief that “more is better.”

©Juanmonino/iStockphoto

Megavitamins may not necessarily be harmless. There is evidence from randomized trials that evaluated vitamin E or vitamin C for preeclampsia that vitamin E supplementation during pregnancy may cause intrauterine growth restriction (IUGR). This was confirmed by a study of 82 women who had been exposed to high doses of vitamin E supplements ranging from 400 IU to 1,200 IU a day during the first trimester. At Motherisk, we found that the mean birth weight among the babies of the women who had been exposed to high doses of vitamin E was significantly lower than the mean birth weight of the babies of the controls. But we did not find a significant difference in the rates of live births, preterm delivery, miscarriages, or stillbirths (Reprod. Toxicol. 2005;20:85-8). These women were on vitamin E as part of their lifestyle and not for any particular medical reason.

The medical community needs to keep in mind that while the folic acid fortification of flour and other products has shown dramatic effects in the overall population, as the CDC report shows, it may not meet the needs of specific populations of women who are at a greater risk of having a baby with a neural tube defect. As pointed out in the Morbidity and Mortality Weekly Report, these groups include Hispanic women, who may not consume as much folic acid or are at a greater risk of having a genetic polymorphism that makes them more susceptible to a folate insufficiency.

Flour fortification provides relatively small amounts of folic acid, possibly 200 mcg more a day, at best. But it has been shown that a woman who has had a previous child with a neural tube defect, a high-risk group, needs 5 mg per day to have an impact on prevention (Lancet 1991;338:131-7).

It is therefore important to keep in mind that there are high-risk groups who may need more than the amount provided by flour fortification. These groups include women on antiepileptic drugs or drugs that have antifolate activity, such as sulfonamide and methotrexate; as well as those with some genetic polymorphisms in the folate cycle.

Courtesy of the National Cancer Institute (NCI)

Women who smoke also tend to have lower folate levels, as do women with diabetes or who are obese. Women with celiac disease may have lower folate levels because they do not eat bread or flour-based products. Low-income women who may not eat sufficient green leafy vegetables, which are expensive and contain high levels of folic acid, may also be at greater risk.

A question that is still not resolved is whether folic acid can prevent other malformations, not just neural tube defects. There is some evidence that folic acid supplementation may also reduce the risk of cardiovascular defects and oral clefts. A randomized trial comparing folic acid to no folic acid to address these questions would be unethical. Instead, observational studies could evaluate the rate of these malformations after the fortification program began. Despite this major public health advance, we should always try to do even better and prevent more cases of neural tube defects and other malformations.

Dr. Koren is professor of pediatrics, pharmacology, pharmacy, and medical genetics at the University of Toronto. He is director of the Motherisk Program. He received grant support to conduct studies on folic acid from Duchesnay Inc., Canada. E-mail him at [email protected].

The Centers for Disease Control and Prevention’s recent report updating the estimated number of neural tube defects prevented by folic acid fortification of enriched cereal grain products clearly shows the huge impact of fortification: From 1999 through 2011, fortification prevented neural tube defects in about 1,300 births a year in the United States (MMWR 2015;64:1-5).

This is a dramatic example of how a relatively simple public health intervention – in this case, the mandatory addition of an inexpensive B vitamin to a portion of the food supply – is having a dramatic impact on a major birth defect.

Unfortunately, though, people may develop similar expectations that other micronutrients during pregnancy may prevent other birth defects or improve developmental outcomes, without adequate supportive evidence. For example, experimental animal studies have suggested that supplements of polyunsaturated fatty acids (PUFAs) during pregnancy improve brain development in the offspring (J. Perinat. Med. 2008;36;5-14). While there is no evidence that this is true in humans, there are prenatal vitamins that include PUFAs on the market.

Based on a review of nine randomized controlled studies that compared long chain PUFA supplementation to a placebo or no supplement in pregnant women, my colleagues and I concluded that the available research “regarding the maternal supplementation of PUFAs in retinal and neurocognitive development of the infant is not consistent in showing a benefit to supplementation” (Obstet.Gynecol. Int. 2012 [doi:10.1155/2012/591531]).

In a somewhat similar manner, an increasing number of women are taking megavitamins as part of their lifestyle, with the belief that “more is better.”

©Juanmonino/iStockphoto

Megavitamins may not necessarily be harmless. There is evidence from randomized trials that evaluated vitamin E or vitamin C for preeclampsia that vitamin E supplementation during pregnancy may cause intrauterine growth restriction (IUGR). This was confirmed by a study of 82 women who had been exposed to high doses of vitamin E supplements ranging from 400 IU to 1,200 IU a day during the first trimester. At Motherisk, we found that the mean birth weight among the babies of the women who had been exposed to high doses of vitamin E was significantly lower than the mean birth weight of the babies of the controls. But we did not find a significant difference in the rates of live births, preterm delivery, miscarriages, or stillbirths (Reprod. Toxicol. 2005;20:85-8). These women were on vitamin E as part of their lifestyle and not for any particular medical reason.

The medical community needs to keep in mind that while the folic acid fortification of flour and other products has shown dramatic effects in the overall population, as the CDC report shows, it may not meet the needs of specific populations of women who are at a greater risk of having a baby with a neural tube defect. As pointed out in the Morbidity and Mortality Weekly Report, these groups include Hispanic women, who may not consume as much folic acid or are at a greater risk of having a genetic polymorphism that makes them more susceptible to a folate insufficiency.

Flour fortification provides relatively small amounts of folic acid, possibly 200 mcg more a day, at best. But it has been shown that a woman who has had a previous child with a neural tube defect, a high-risk group, needs 5 mg per day to have an impact on prevention (Lancet 1991;338:131-7).

It is therefore important to keep in mind that there are high-risk groups who may need more than the amount provided by flour fortification. These groups include women on antiepileptic drugs or drugs that have antifolate activity, such as sulfonamide and methotrexate; as well as those with some genetic polymorphisms in the folate cycle.

Courtesy of the National Cancer Institute (NCI)

Women who smoke also tend to have lower folate levels, as do women with diabetes or who are obese. Women with celiac disease may have lower folate levels because they do not eat bread or flour-based products. Low-income women who may not eat sufficient green leafy vegetables, which are expensive and contain high levels of folic acid, may also be at greater risk.

A question that is still not resolved is whether folic acid can prevent other malformations, not just neural tube defects. There is some evidence that folic acid supplementation may also reduce the risk of cardiovascular defects and oral clefts. A randomized trial comparing folic acid to no folic acid to address these questions would be unethical. Instead, observational studies could evaluate the rate of these malformations after the fortification program began. Despite this major public health advance, we should always try to do even better and prevent more cases of neural tube defects and other malformations.

Dr. Koren is professor of pediatrics, pharmacology, pharmacy, and medical genetics at the University of Toronto. He is director of the Motherisk Program. He received grant support to conduct studies on folic acid from Duchesnay Inc., Canada. E-mail him at [email protected].

In these days of struggles over obesity, it may be hard to remember that being too thin may be a bigger health threat than being too fat. Anorexia nervosa is a very serious but hidden disorder in which the person has a relentless pursuit of thinness, is unwilling to maintain a healthy weight, has distorted body image and intense fear of gaining weight, disturbed eating behavior, and, in girls, amenorrhea.

Anorexia nervosa is actually the third-leading chronic illness in adolescent females and has a mortality rate as high as 20% – one-third by suicide. Boys are not only not immune, but also are even more difficult to suspect and detect. While most affected children improve with behavioral treatment, anorexia nervosa severe enough to warrant hospitalization can result in permanent damage to bones, heart, and brain.

I refer to these patients as “children” here, but you may rightly associate anorexia with adolescents: 43% of those affected had onset at 16-20 years and 86% by 20 years. But listen to this disturbing statistic: 42% of 1st-3rd grade girls report that they want to be thinner and 81% of 10-year-olds are “afraid” of being fat. Over half of teen girls and one-third of boys skip meals, fast, smoke cigarettes, vomit, or take laxatives to control weight – ineffective practices that can lead to eating disorders. Healthy foods and exercise may seem too slow or difficult ways to control weight.

Even with a prevalence of 0.5% you may be wondering, “Gee, I haven’t seen anyone with that for years!” But you probably have been seeing children with the most common presentations of anorexia, which are concerns over complications rather than a request for help with excess weight loss. These are usually complaints about abdominal pain, bloating, or constipation, but may be about headaches, amenorrhea, or feeling faint. You may see them for the first time after an intercurrent illness such as viral gastroenteritis or mononucleosis that sends their emaciated bodies over the edge. Do those patients sound more familiar?

Anorexia nervosa works its damage from starvation and purging behaviors. Any system of the body can be affected from starvation, ranging from suppression of bone marrow with anemia, low white count, and low platelets; endocrine suppression with low TSH and T4 and amenorrhea; cardiomyopathy with resulting mitral valve prolapse, arrhythmias, and syncope; or even seizures and brain atrophy. Depression and anxiety are pretty inevitable when one is starving but, while comorbid, their primacy or severity really can’t be assessed until the starvation state is resolved.

Why aren’t the affected children worried about these serious complications? Actually, they may be worried when they find out about them, but their first fear is about getting fat. Characteristic of anorexia is a distorted body image that nags at them incessantly to lose weight. In U.S. culture, weight loss and fitness ads are all around us, making this concern seem quite normal or even more urgent. They may even panic and get angry if their excessive exercise routine is interrupted. The missing link is that they can’t see that they are not overweight, instead fearing being fat.

Many children with anorexia have tried to stop their dieting but failed. They may be ashamed, embarrassed, or worried about being stigmatized if they are found out. But they often feel that they are on the right path for themselves. At best they are ambivalent about being detected and pushed into treatment. So they get really good at hiding their condition, sometimes getting new ideas online. Common strategies to evade detection include eating apart from the family, saying they are “not hungry now” or even cooking for others but not eating themselves. They wear baggy clothes to hide their emaciation. They often exercise to an extreme, in any weather, whether sick or well. When it is time to be weighed they may drink quarts of water and fill pockets with stones so their true weight loss is not evident.

Actions children take for weight control or loss create much of the morbidity. Most common are use of laxatives and diuretics that can result in fatal electrolyte imbalances and arrhythmias. Purging in anorexia and also in bulimia nervosa can result in gastroesophageal reflux disease, esophageal tears, and bleeding. Self-induced vomiting also destroys tooth enamel, fosters cavities, and can cause scars of palate or knuckles from forcing their hand down their throat. Hypoglycemia from severe restriction can even result in seizures.

When your patients have those metabolic and physical signs, you are not likely to be tricked into thinking all is well. But those athletes in your practice, of whom you and the parents are so proud, can sneak up on you. Those participating in individual “aesthetic” sports such as dance, figure skating, and gymnastics are especially vulnerable to (and rewarded by) extreme thinness. They have been coached to be slim. But to make it worse, the most elite athletes also often have personalities that make extreme weight control possible including perfectionism, competitiveness, compulsiveness, drive, and high activity level.

Parents of children with anorexia may be ambivalent, also, as they see their child eating healthy foods and exercising as they have encouraged them to do. It is not so clear when they have gone too far. But 35% of “normal dieters” go on to pathological dieting and, of those, 20%-25% develop eating disorders of varying degree.

As with most disorders, earlier detection of anorexia symptoms can allow for an easier treatment course and fewer long-term complications. So, when should you be thinking and asking about abnormal eating? Certainly, it is time to ask questions when a child is not gaining weight appropriately, is losing weight to below 15% of appropriate weight for height, or has 3 or more months of amenorrhea. But also consider it when you hear complaints of abdominal pain, headache, or feeling faint that you can’t explain. Ask directly “What would you like to weigh?” A desired weight that would give a body mass index (BMI) of <19 kg/m² is nearly diagnostic. Also ask them to, “Tell me what you eat at each meal on a typical day,” looking for extremely low-calorie bizarre choices such as all lettuce, and “How much exercise do you do daily?” Be specific in collecting information about dieting, binging, self-induced vomiting, and use of laxatives, diuretics, or diet pills for weight control. Asking family members what they have observed about the child’s exercise, dieting, and statements about body image gives even more objective information that the child may try to obscure.

Specific screening self report tools such as the SCOFF questionnaire and Patient Health Questionnaire – Adolescents (PHQ-A) used for all teens or those with signs of weight loss are both a way to get more accurate information and a valuable point of conversation.

When you detect signs and symptoms, the initial work up should include complete blood count, electrolytes, liver function, thyroid-stimulating hormone, and urinalysis, but most importantly an accurate height, weight, and BMI measured in underwear in a gown. Amenorrhea may require endocrine tests as well. While malignancy, endocrine and gastrointestinal disorders are in the differential, characteristic history, physical exam, and lab results will point to the diagnosis. If there is bradycardia or low potassium, chloride, or sodium, an electrocardiogram and hospitalization are urgent as these are the harbingers of life-threatening arrhythmias that are the most common cause of death.

So when you suspect anorexia, you may be facing a difficult-to-detect, life-threatening condition with resistant patients and even reluctant parents. While you may be able to make a contract for biweekly weigh-ins and coaching for subclinical anorexia not otherwise specified, a team will be needed in most full-blown cases. Eating disorder programs are often part of departments of psychiatry, but adolescent specialists also may have assembled needed teams.

Dr. Howard is assistant professor of pediatrics at the Johns Hopkins University School of Medicine, Baltimore, and creator of CHADIS. She has no other relevant disclosures. Dr. Howard’s contribution to this publication was as a paid expert to Frontline. E-mail her at [email protected].

In these days of struggles over obesity, it may be hard to remember that being too thin may be a bigger health threat than being too fat. Anorexia nervosa is a very serious but hidden disorder in which the person has a relentless pursuit of thinness, is unwilling to maintain a healthy weight, has distorted body image and intense fear of gaining weight, disturbed eating behavior, and, in girls, amenorrhea.

Anorexia nervosa is actually the third-leading chronic illness in adolescent females and has a mortality rate as high as 20% – one-third by suicide. Boys are not only not immune, but also are even more difficult to suspect and detect. While most affected children improve with behavioral treatment, anorexia nervosa severe enough to warrant hospitalization can result in permanent damage to bones, heart, and brain.

I refer to these patients as “children” here, but you may rightly associate anorexia with adolescents: 43% of those affected had onset at 16-20 years and 86% by 20 years. But listen to this disturbing statistic: 42% of 1st-3rd grade girls report that they want to be thinner and 81% of 10-year-olds are “afraid” of being fat. Over half of teen girls and one-third of boys skip meals, fast, smoke cigarettes, vomit, or take laxatives to control weight – ineffective practices that can lead to eating disorders. Healthy foods and exercise may seem too slow or difficult ways to control weight.

Even with a prevalence of 0.5% you may be wondering, “Gee, I haven’t seen anyone with that for years!” But you probably have been seeing children with the most common presentations of anorexia, which are concerns over complications rather than a request for help with excess weight loss. These are usually complaints about abdominal pain, bloating, or constipation, but may be about headaches, amenorrhea, or feeling faint. You may see them for the first time after an intercurrent illness such as viral gastroenteritis or mononucleosis that sends their emaciated bodies over the edge. Do those patients sound more familiar?

Anorexia nervosa works its damage from starvation and purging behaviors. Any system of the body can be affected from starvation, ranging from suppression of bone marrow with anemia, low white count, and low platelets; endocrine suppression with low TSH and T4 and amenorrhea; cardiomyopathy with resulting mitral valve prolapse, arrhythmias, and syncope; or even seizures and brain atrophy. Depression and anxiety are pretty inevitable when one is starving but, while comorbid, their primacy or severity really can’t be assessed until the starvation state is resolved.

Why aren’t the affected children worried about these serious complications? Actually, they may be worried when they find out about them, but their first fear is about getting fat. Characteristic of anorexia is a distorted body image that nags at them incessantly to lose weight. In U.S. culture, weight loss and fitness ads are all around us, making this concern seem quite normal or even more urgent. They may even panic and get angry if their excessive exercise routine is interrupted. The missing link is that they can’t see that they are not overweight, instead fearing being fat.

Many children with anorexia have tried to stop their dieting but failed. They may be ashamed, embarrassed, or worried about being stigmatized if they are found out. But they often feel that they are on the right path for themselves. At best they are ambivalent about being detected and pushed into treatment. So they get really good at hiding their condition, sometimes getting new ideas online. Common strategies to evade detection include eating apart from the family, saying they are “not hungry now” or even cooking for others but not eating themselves. They wear baggy clothes to hide their emaciation. They often exercise to an extreme, in any weather, whether sick or well. When it is time to be weighed they may drink quarts of water and fill pockets with stones so their true weight loss is not evident.

Actions children take for weight control or loss create much of the morbidity. Most common are use of laxatives and diuretics that can result in fatal electrolyte imbalances and arrhythmias. Purging in anorexia and also in bulimia nervosa can result in gastroesophageal reflux disease, esophageal tears, and bleeding. Self-induced vomiting also destroys tooth enamel, fosters cavities, and can cause scars of palate or knuckles from forcing their hand down their throat. Hypoglycemia from severe restriction can even result in seizures.

When your patients have those metabolic and physical signs, you are not likely to be tricked into thinking all is well. But those athletes in your practice, of whom you and the parents are so proud, can sneak up on you. Those participating in individual “aesthetic” sports such as dance, figure skating, and gymnastics are especially vulnerable to (and rewarded by) extreme thinness. They have been coached to be slim. But to make it worse, the most elite athletes also often have personalities that make extreme weight control possible including perfectionism, competitiveness, compulsiveness, drive, and high activity level.

Parents of children with anorexia may be ambivalent, also, as they see their child eating healthy foods and exercising as they have encouraged them to do. It is not so clear when they have gone too far. But 35% of “normal dieters” go on to pathological dieting and, of those, 20%-25% develop eating disorders of varying degree.

As with most disorders, earlier detection of anorexia symptoms can allow for an easier treatment course and fewer long-term complications. So, when should you be thinking and asking about abnormal eating? Certainly, it is time to ask questions when a child is not gaining weight appropriately, is losing weight to below 15% of appropriate weight for height, or has 3 or more months of amenorrhea. But also consider it when you hear complaints of abdominal pain, headache, or feeling faint that you can’t explain. Ask directly “What would you like to weigh?” A desired weight that would give a body mass index (BMI) of <19 kg/m² is nearly diagnostic. Also ask them to, “Tell me what you eat at each meal on a typical day,” looking for extremely low-calorie bizarre choices such as all lettuce, and “How much exercise do you do daily?” Be specific in collecting information about dieting, binging, self-induced vomiting, and use of laxatives, diuretics, or diet pills for weight control. Asking family members what they have observed about the child’s exercise, dieting, and statements about body image gives even more objective information that the child may try to obscure.

Specific screening self report tools such as the SCOFF questionnaire and Patient Health Questionnaire – Adolescents (PHQ-A) used for all teens or those with signs of weight loss are both a way to get more accurate information and a valuable point of conversation.

When you detect signs and symptoms, the initial work up should include complete blood count, electrolytes, liver function, thyroid-stimulating hormone, and urinalysis, but most importantly an accurate height, weight, and BMI measured in underwear in a gown. Amenorrhea may require endocrine tests as well. While malignancy, endocrine and gastrointestinal disorders are in the differential, characteristic history, physical exam, and lab results will point to the diagnosis. If there is bradycardia or low potassium, chloride, or sodium, an electrocardiogram and hospitalization are urgent as these are the harbingers of life-threatening arrhythmias that are the most common cause of death.

So when you suspect anorexia, you may be facing a difficult-to-detect, life-threatening condition with resistant patients and even reluctant parents. While you may be able to make a contract for biweekly weigh-ins and coaching for subclinical anorexia not otherwise specified, a team will be needed in most full-blown cases. Eating disorder programs are often part of departments of psychiatry, but adolescent specialists also may have assembled needed teams.

Dr. Howard is assistant professor of pediatrics at the Johns Hopkins University School of Medicine, Baltimore, and creator of CHADIS. She has no other relevant disclosures. Dr. Howard’s contribution to this publication was as a paid expert to Frontline. E-mail her at [email protected].

In these days of struggles over obesity, it may be hard to remember that being too thin may be a bigger health threat than being too fat. Anorexia nervosa is a very serious but hidden disorder in which the person has a relentless pursuit of thinness, is unwilling to maintain a healthy weight, has distorted body image and intense fear of gaining weight, disturbed eating behavior, and, in girls, amenorrhea.

Anorexia nervosa is actually the third-leading chronic illness in adolescent females and has a mortality rate as high as 20% – one-third by suicide. Boys are not only not immune, but also are even more difficult to suspect and detect. While most affected children improve with behavioral treatment, anorexia nervosa severe enough to warrant hospitalization can result in permanent damage to bones, heart, and brain.

I refer to these patients as “children” here, but you may rightly associate anorexia with adolescents: 43% of those affected had onset at 16-20 years and 86% by 20 years. But listen to this disturbing statistic: 42% of 1st-3rd grade girls report that they want to be thinner and 81% of 10-year-olds are “afraid” of being fat. Over half of teen girls and one-third of boys skip meals, fast, smoke cigarettes, vomit, or take laxatives to control weight – ineffective practices that can lead to eating disorders. Healthy foods and exercise may seem too slow or difficult ways to control weight.

Even with a prevalence of 0.5% you may be wondering, “Gee, I haven’t seen anyone with that for years!” But you probably have been seeing children with the most common presentations of anorexia, which are concerns over complications rather than a request for help with excess weight loss. These are usually complaints about abdominal pain, bloating, or constipation, but may be about headaches, amenorrhea, or feeling faint. You may see them for the first time after an intercurrent illness such as viral gastroenteritis or mononucleosis that sends their emaciated bodies over the edge. Do those patients sound more familiar?

Anorexia nervosa works its damage from starvation and purging behaviors. Any system of the body can be affected from starvation, ranging from suppression of bone marrow with anemia, low white count, and low platelets; endocrine suppression with low TSH and T4 and amenorrhea; cardiomyopathy with resulting mitral valve prolapse, arrhythmias, and syncope; or even seizures and brain atrophy. Depression and anxiety are pretty inevitable when one is starving but, while comorbid, their primacy or severity really can’t be assessed until the starvation state is resolved.

Why aren’t the affected children worried about these serious complications? Actually, they may be worried when they find out about them, but their first fear is about getting fat. Characteristic of anorexia is a distorted body image that nags at them incessantly to lose weight. In U.S. culture, weight loss and fitness ads are all around us, making this concern seem quite normal or even more urgent. They may even panic and get angry if their excessive exercise routine is interrupted. The missing link is that they can’t see that they are not overweight, instead fearing being fat.

Many children with anorexia have tried to stop their dieting but failed. They may be ashamed, embarrassed, or worried about being stigmatized if they are found out. But they often feel that they are on the right path for themselves. At best they are ambivalent about being detected and pushed into treatment. So they get really good at hiding their condition, sometimes getting new ideas online. Common strategies to evade detection include eating apart from the family, saying they are “not hungry now” or even cooking for others but not eating themselves. They wear baggy clothes to hide their emaciation. They often exercise to an extreme, in any weather, whether sick or well. When it is time to be weighed they may drink quarts of water and fill pockets with stones so their true weight loss is not evident.

Actions children take for weight control or loss create much of the morbidity. Most common are use of laxatives and diuretics that can result in fatal electrolyte imbalances and arrhythmias. Purging in anorexia and also in bulimia nervosa can result in gastroesophageal reflux disease, esophageal tears, and bleeding. Self-induced vomiting also destroys tooth enamel, fosters cavities, and can cause scars of palate or knuckles from forcing their hand down their throat. Hypoglycemia from severe restriction can even result in seizures.

When your patients have those metabolic and physical signs, you are not likely to be tricked into thinking all is well. But those athletes in your practice, of whom you and the parents are so proud, can sneak up on you. Those participating in individual “aesthetic” sports such as dance, figure skating, and gymnastics are especially vulnerable to (and rewarded by) extreme thinness. They have been coached to be slim. But to make it worse, the most elite athletes also often have personalities that make extreme weight control possible including perfectionism, competitiveness, compulsiveness, drive, and high activity level.

Parents of children with anorexia may be ambivalent, also, as they see their child eating healthy foods and exercising as they have encouraged them to do. It is not so clear when they have gone too far. But 35% of “normal dieters” go on to pathological dieting and, of those, 20%-25% develop eating disorders of varying degree.

As with most disorders, earlier detection of anorexia symptoms can allow for an easier treatment course and fewer long-term complications. So, when should you be thinking and asking about abnormal eating? Certainly, it is time to ask questions when a child is not gaining weight appropriately, is losing weight to below 15% of appropriate weight for height, or has 3 or more months of amenorrhea. But also consider it when you hear complaints of abdominal pain, headache, or feeling faint that you can’t explain. Ask directly “What would you like to weigh?” A desired weight that would give a body mass index (BMI) of <19 kg/m² is nearly diagnostic. Also ask them to, “Tell me what you eat at each meal on a typical day,” looking for extremely low-calorie bizarre choices such as all lettuce, and “How much exercise do you do daily?” Be specific in collecting information about dieting, binging, self-induced vomiting, and use of laxatives, diuretics, or diet pills for weight control. Asking family members what they have observed about the child’s exercise, dieting, and statements about body image gives even more objective information that the child may try to obscure.

Specific screening self report tools such as the SCOFF questionnaire and Patient Health Questionnaire – Adolescents (PHQ-A) used for all teens or those with signs of weight loss are both a way to get more accurate information and a valuable point of conversation.

When you detect signs and symptoms, the initial work up should include complete blood count, electrolytes, liver function, thyroid-stimulating hormone, and urinalysis, but most importantly an accurate height, weight, and BMI measured in underwear in a gown. Amenorrhea may require endocrine tests as well. While malignancy, endocrine and gastrointestinal disorders are in the differential, characteristic history, physical exam, and lab results will point to the diagnosis. If there is bradycardia or low potassium, chloride, or sodium, an electrocardiogram and hospitalization are urgent as these are the harbingers of life-threatening arrhythmias that are the most common cause of death.

So when you suspect anorexia, you may be facing a difficult-to-detect, life-threatening condition with resistant patients and even reluctant parents. While you may be able to make a contract for biweekly weigh-ins and coaching for subclinical anorexia not otherwise specified, a team will be needed in most full-blown cases. Eating disorder programs are often part of departments of psychiatry, but adolescent specialists also may have assembled needed teams.

Dr. Howard is assistant professor of pediatrics at the Johns Hopkins University School of Medicine, Baltimore, and creator of CHADIS. She has no other relevant disclosures. Dr. Howard’s contribution to this publication was as a paid expert to Frontline. E-mail her at [email protected].

Why are American cardiologists so far behind the worldwide curve in performing percutaneous coronary interventions by the radial-artery route?

The degree to which ACS patients suffer needlessly when they undergo percutaneous coronary intervention (PCI) via their femoral artery and not with transradial access was finally, definitively demonstrated in results from the MATRIX Access trial, presented earlier this week at the annual meeting of the American College of Cardiology. The MATRIX results showed in more than 8,000 patients that using a transradial approach for PCI was linked with a statistically significant improvement in 30-day patient survival, a 0.6% absolute difference. For every 167 patients treated by the transradial route, an additional patient lived, compared with similar patients treated with transfemoral access.

The radial approach also cut serious access-site bleeding episodes by an absolute 0.7%, and it was this difference that appeared to mainly drive the difference in patient survival. As study discussant Dr. Roxana Mehran declared from the dais following the MATRIX report, “Bleeding matters! Here is where it’s been proven.”

Results from a second, unrelated trial reported at the meeting, TOTAL, showed that during 2010-2014, in more than 10,000 patients with ST-elevation myocardial infarction treated by PCI in 20 different countries, 68% of patients underwent their procedure via a transradial route.

In contrast, cardiologists I spoke with at the meeting said that recent estimates of PCI use by U.S. interventionalists indicated that they perform roughly 20% of PCIs transradially. That level substantially jumped over the past decade; 10 years ago U.S. transradial use stood at about 3% of all PCIs, my sources said. But 20% still lags woefully behind a worldwide rate of 68%, especially when access site can make a life-or-death difference.

Interventionalists at the meeting also told me some reasons why transfemoral access remains favored. First, it’s the approach many operators first trained in, so they are more familiar and comfortable with it. Second, transradial PCI can take longer, result in higher radiation exposure, and in some patients it’s simply impossible, which means crossover to transfemoral anyway. Finally, transfemoral PCI is just plain easier, they said.

Courtesy Wikipedia Commons/Henry Gray/Public Domain

Most of these reasons fall flat when contrasted with causing significantly fewer serious bleeds and improved survival. Of course, when transradial proves impossible there is no choice other than going with transfemoral, but as proponents of transradial said at the meeting, it is a matter of making transradial the initial, default strategy and only resorting to transfemoral when absolutely necessary.

The MATRIX results had another very important finding: To get the best outcomes, centers that offer PCI to acute coronary syndrome patients can’t simply dabble with the transradial approach; they need to be all in. A subanalysis of the MATRIX mortality benefit for transradial procedures showed a striking and statistically significant link between operator commitment to the transradial approach and the ability to give patients a mortality benefit by using the transradial approach. This analysis subdivided the patients into three categories depending on the frequency at which the center where they were treated performed transradial PCI. The three subgroups were centers that did 64% or fewer of their cases transradially, centers that did 65%-79% of their patients transradially, and centers that did 80% or more of their cases via the radial artery.

The data showed that patients treated at centers that used the transradial approach in no more than 64% of their cases actually had a small trend toward better 30-day survival rates when they underwent a transfemoral procedure, although it was not a statistically significant difference. Among the subgroup of patients treated at centers that fell into the middle range of transradial use in everyday practice there was a trend toward better survival with transradial treatment, compared with transfemoral, but again not a statistically significant difference.

It was only among the patients treated at centers that used transradial access nearly all the time, for 80% or more of cases, where transradial use made a statistically significant difference in survival. In this subgroup, patients treated transradially had a 52% relative survival advantage compared with similar patients treated at the same center but via a transfemoral approach.

In other words, when a center in the MATRIX trial did at least 80% of cases with the transradial approach, the patients treated there that way had less than half the 30-day mortality rate, compared with similar patients treated at the same center but by PCI that used a transfemoral approach.

Choosing the PCI access site has moved beyond physician preference and convenience. It’s a matter of patient well-being.

[email protected]

On Twitter @mitchelzoler

Why are American cardiologists so far behind the worldwide curve in performing percutaneous coronary interventions by the radial-artery route?

The degree to which ACS patients suffer needlessly when they undergo percutaneous coronary intervention (PCI) via their femoral artery and not with transradial access was finally, definitively demonstrated in results from the MATRIX Access trial, presented earlier this week at the annual meeting of the American College of Cardiology. The MATRIX results showed in more than 8,000 patients that using a transradial approach for PCI was linked with a statistically significant improvement in 30-day patient survival, a 0.6% absolute difference. For every 167 patients treated by the transradial route, an additional patient lived, compared with similar patients treated with transfemoral access.

The radial approach also cut serious access-site bleeding episodes by an absolute 0.7%, and it was this difference that appeared to mainly drive the difference in patient survival. As study discussant Dr. Roxana Mehran declared from the dais following the MATRIX report, “Bleeding matters! Here is where it’s been proven.”

Results from a second, unrelated trial reported at the meeting, TOTAL, showed that during 2010-2014, in more than 10,000 patients with ST-elevation myocardial infarction treated by PCI in 20 different countries, 68% of patients underwent their procedure via a transradial route.

In contrast, cardiologists I spoke with at the meeting said that recent estimates of PCI use by U.S. interventionalists indicated that they perform roughly 20% of PCIs transradially. That level substantially jumped over the past decade; 10 years ago U.S. transradial use stood at about 3% of all PCIs, my sources said. But 20% still lags woefully behind a worldwide rate of 68%, especially when access site can make a life-or-death difference.

Interventionalists at the meeting also told me some reasons why transfemoral access remains favored. First, it’s the approach many operators first trained in, so they are more familiar and comfortable with it. Second, transradial PCI can take longer, result in higher radiation exposure, and in some patients it’s simply impossible, which means crossover to transfemoral anyway. Finally, transfemoral PCI is just plain easier, they said.

Courtesy Wikipedia Commons/Henry Gray/Public Domain

Most of these reasons fall flat when contrasted with causing significantly fewer serious bleeds and improved survival. Of course, when transradial proves impossible there is no choice other than going with transfemoral, but as proponents of transradial said at the meeting, it is a matter of making transradial the initial, default strategy and only resorting to transfemoral when absolutely necessary.

The MATRIX results had another very important finding: To get the best outcomes, centers that offer PCI to acute coronary syndrome patients can’t simply dabble with the transradial approach; they need to be all in. A subanalysis of the MATRIX mortality benefit for transradial procedures showed a striking and statistically significant link between operator commitment to the transradial approach and the ability to give patients a mortality benefit by using the transradial approach. This analysis subdivided the patients into three categories depending on the frequency at which the center where they were treated performed transradial PCI. The three subgroups were centers that did 64% or fewer of their cases transradially, centers that did 65%-79% of their patients transradially, and centers that did 80% or more of their cases via the radial artery.

The data showed that patients treated at centers that used the transradial approach in no more than 64% of their cases actually had a small trend toward better 30-day survival rates when they underwent a transfemoral procedure, although it was not a statistically significant difference. Among the subgroup of patients treated at centers that fell into the middle range of transradial use in everyday practice there was a trend toward better survival with transradial treatment, compared with transfemoral, but again not a statistically significant difference.

It was only among the patients treated at centers that used transradial access nearly all the time, for 80% or more of cases, where transradial use made a statistically significant difference in survival. In this subgroup, patients treated transradially had a 52% relative survival advantage compared with similar patients treated at the same center but via a transfemoral approach.

In other words, when a center in the MATRIX trial did at least 80% of cases with the transradial approach, the patients treated there that way had less than half the 30-day mortality rate, compared with similar patients treated at the same center but by PCI that used a transfemoral approach.

Choosing the PCI access site has moved beyond physician preference and convenience. It’s a matter of patient well-being.

[email protected]

On Twitter @mitchelzoler

Why are American cardiologists so far behind the worldwide curve in performing percutaneous coronary interventions by the radial-artery route?

The degree to which ACS patients suffer needlessly when they undergo percutaneous coronary intervention (PCI) via their femoral artery and not with transradial access was finally, definitively demonstrated in results from the MATRIX Access trial, presented earlier this week at the annual meeting of the American College of Cardiology. The MATRIX results showed in more than 8,000 patients that using a transradial approach for PCI was linked with a statistically significant improvement in 30-day patient survival, a 0.6% absolute difference. For every 167 patients treated by the transradial route, an additional patient lived, compared with similar patients treated with transfemoral access.

The radial approach also cut serious access-site bleeding episodes by an absolute 0.7%, and it was this difference that appeared to mainly drive the difference in patient survival. As study discussant Dr. Roxana Mehran declared from the dais following the MATRIX report, “Bleeding matters! Here is where it’s been proven.”

Results from a second, unrelated trial reported at the meeting, TOTAL, showed that during 2010-2014, in more than 10,000 patients with ST-elevation myocardial infarction treated by PCI in 20 different countries, 68% of patients underwent their procedure via a transradial route.

In contrast, cardiologists I spoke with at the meeting said that recent estimates of PCI use by U.S. interventionalists indicated that they perform roughly 20% of PCIs transradially. That level substantially jumped over the past decade; 10 years ago U.S. transradial use stood at about 3% of all PCIs, my sources said. But 20% still lags woefully behind a worldwide rate of 68%, especially when access site can make a life-or-death difference.

Interventionalists at the meeting also told me some reasons why transfemoral access remains favored. First, it’s the approach many operators first trained in, so they are more familiar and comfortable with it. Second, transradial PCI can take longer, result in higher radiation exposure, and in some patients it’s simply impossible, which means crossover to transfemoral anyway. Finally, transfemoral PCI is just plain easier, they said.

Courtesy Wikipedia Commons/Henry Gray/Public Domain

Most of these reasons fall flat when contrasted with causing significantly fewer serious bleeds and improved survival. Of course, when transradial proves impossible there is no choice other than going with transfemoral, but as proponents of transradial said at the meeting, it is a matter of making transradial the initial, default strategy and only resorting to transfemoral when absolutely necessary.

The MATRIX results had another very important finding: To get the best outcomes, centers that offer PCI to acute coronary syndrome patients can’t simply dabble with the transradial approach; they need to be all in. A subanalysis of the MATRIX mortality benefit for transradial procedures showed a striking and statistically significant link between operator commitment to the transradial approach and the ability to give patients a mortality benefit by using the transradial approach. This analysis subdivided the patients into three categories depending on the frequency at which the center where they were treated performed transradial PCI. The three subgroups were centers that did 64% or fewer of their cases transradially, centers that did 65%-79% of their patients transradially, and centers that did 80% or more of their cases via the radial artery.

The data showed that patients treated at centers that used the transradial approach in no more than 64% of their cases actually had a small trend toward better 30-day survival rates when they underwent a transfemoral procedure, although it was not a statistically significant difference. Among the subgroup of patients treated at centers that fell into the middle range of transradial use in everyday practice there was a trend toward better survival with transradial treatment, compared with transfemoral, but again not a statistically significant difference.

It was only among the patients treated at centers that used transradial access nearly all the time, for 80% or more of cases, where transradial use made a statistically significant difference in survival. In this subgroup, patients treated transradially had a 52% relative survival advantage compared with similar patients treated at the same center but via a transfemoral approach.

In other words, when a center in the MATRIX trial did at least 80% of cases with the transradial approach, the patients treated there that way had less than half the 30-day mortality rate, compared with similar patients treated at the same center but by PCI that used a transfemoral approach.

Choosing the PCI access site has moved beyond physician preference and convenience. It’s a matter of patient well-being.

[email protected]

On Twitter @mitchelzoler