This chapter looks at work generated by the surveyed hospitalists. Overall, the median charges per year for physician hospitalists are $288,242 and the median collections are $160,000 (a 56% collection rate). The typical surveyed physician had a median of 2,259 encounters, 468 admissions and consultations, and 3,000 RVUs. The analyses below examine these measures from the following perspectives: region, employment model, specialty/provider type, and compensation model.

• Consistent with the compensation and productivity input measures, academic hospitalists have low median collections ($110,000 vs. $160,000 overall), low encounters (1,600 vs. 2,259 overall), low admissions and consults (371 vs. 468). However, academic hospitalists generate an equivalent number of RVUs (3,000) indicating that they are delivering more complex services. NOTE: At 40% ($110,000/$278,122), the median collection rate for academic groups is the lowest of all employment categories. This may be explained by the payer mix at academic medical centers.



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• Hospitalist-only groups, both local and multi-state, generate the most work output. With regard to median charges generated, local groups are 21% higher ($350,000 vs. $288,242) and multi-state groups are 4% higher ($300,988 vs. $288,242). Hospitalists in multi-state groups have remarkable performance with regard to collections, achieving a 95% collection rate compared to a overall average of 56%. These hospitalist-only groups also have much higher encounters, admissions/consults, and RVUs.
• As in the Productivity Inputs, Eastern hospitalists have the lowest measures of Productivity Outputs. Hospitalists in the Southern region generate the most work in all five categories of outputs.
• Compared with adult medicine hospitalists, pediatricians generate fewer charges ($203,554 vs. $290,000), collections ($111,000 vs. $160,100), encounters (1,300 vs. 2,340), admissions/consults (441 vs. 470), and RVUs (1,990 vs. 3,000).
• Non-physicians generate about half the charges, collections, admissions/consults, and RVUs of physician hospitalists.
• Productivity–based compensation appears to have a positive impact on Productivity Output (the incentives appear to work).
• Compared with hospitalists with a 100% salary model, hospitalists that have a 100% productivity model have median charges 65% higher ($385,200 vs. $233,251), median collections that are 56% higher ($200,000 vs. $128,063), encounters that are 64% higher (3,000 vs. 1,831), admissions/consults that are 44% higher (575 vs. 400), and more than twice the median number of RVUs (4,967 vs. 2,395). In all cases hospitalists with a mixed compensation model fall in the middle of the two medians.

This chapter looks at work generated by the surveyed hospitalists. Overall, the median charges per year for physician hospitalists are $288,242 and the median collections are $160,000 (a 56% collection rate). The typical surveyed physician had a median of 2,259 encounters, 468 admissions and consultations, and 3,000 RVUs. The analyses below examine these measures from the following perspectives: region, employment model, specialty/provider type, and compensation model.

• Consistent with the compensation and productivity input measures, academic hospitalists have low median collections ($110,000 vs. $160,000 overall), low encounters (1,600 vs. 2,259 overall), low admissions and consults (371 vs. 468). However, academic hospitalists generate an equivalent number of RVUs (3,000) indicating that they are delivering more complex services. NOTE: At 40% ($110,000/$278,122), the median collection rate for academic groups is the lowest of all employment categories. This may be explained by the payer mix at academic medical centers.



click for large version



click for large version



click for large version



click for large version

• Hospitalist-only groups, both local and multi-state, generate the most work output. With regard to median charges generated, local groups are 21% higher ($350,000 vs. $288,242) and multi-state groups are 4% higher ($300,988 vs. $288,242). Hospitalists in multi-state groups have remarkable performance with regard to collections, achieving a 95% collection rate compared to a overall average of 56%. These hospitalist-only groups also have much higher encounters, admissions/consults, and RVUs.
• As in the Productivity Inputs, Eastern hospitalists have the lowest measures of Productivity Outputs. Hospitalists in the Southern region generate the most work in all five categories of outputs.
• Compared with adult medicine hospitalists, pediatricians generate fewer charges ($203,554 vs. $290,000), collections ($111,000 vs. $160,100), encounters (1,300 vs. 2,340), admissions/consults (441 vs. 470), and RVUs (1,990 vs. 3,000).
• Non-physicians generate about half the charges, collections, admissions/consults, and RVUs of physician hospitalists.
• Productivity–based compensation appears to have a positive impact on Productivity Output (the incentives appear to work).
• Compared with hospitalists with a 100% salary model, hospitalists that have a 100% productivity model have median charges 65% higher ($385,200 vs. $233,251), median collections that are 56% higher ($200,000 vs. $128,063), encounters that are 64% higher (3,000 vs. 1,831), admissions/consults that are 44% higher (575 vs. 400), and more than twice the median number of RVUs (4,967 vs. 2,395). In all cases hospitalists with a mixed compensation model fall in the middle of the two medians.

This chapter looks at work generated by the surveyed hospitalists. Overall, the median charges per year for physician hospitalists are $288,242 and the median collections are $160,000 (a 56% collection rate). The typical surveyed physician had a median of 2,259 encounters, 468 admissions and consultations, and 3,000 RVUs. The analyses below examine these measures from the following perspectives: region, employment model, specialty/provider type, and compensation model.

• Consistent with the compensation and productivity input measures, academic hospitalists have low median collections ($110,000 vs. $160,000 overall), low encounters (1,600 vs. 2,259 overall), low admissions and consults (371 vs. 468). However, academic hospitalists generate an equivalent number of RVUs (3,000) indicating that they are delivering more complex services. NOTE: At 40% ($110,000/$278,122), the median collection rate for academic groups is the lowest of all employment categories. This may be explained by the payer mix at academic medical centers.



click for large version



click for large version



click for large version



click for large version

• Hospitalist-only groups, both local and multi-state, generate the most work output. With regard to median charges generated, local groups are 21% higher ($350,000 vs. $288,242) and multi-state groups are 4% higher ($300,988 vs. $288,242). Hospitalists in multi-state groups have remarkable performance with regard to collections, achieving a 95% collection rate compared to a overall average of 56%. These hospitalist-only groups also have much higher encounters, admissions/consults, and RVUs.
• As in the Productivity Inputs, Eastern hospitalists have the lowest measures of Productivity Outputs. Hospitalists in the Southern region generate the most work in all five categories of outputs.
• Compared with adult medicine hospitalists, pediatricians generate fewer charges ($203,554 vs. $290,000), collections ($111,000 vs. $160,100), encounters (1,300 vs. 2,340), admissions/consults (441 vs. 470), and RVUs (1,990 vs. 3,000).
• Non-physicians generate about half the charges, collections, admissions/consults, and RVUs of physician hospitalists.
• Productivity–based compensation appears to have a positive impact on Productivity Output (the incentives appear to work).
• Compared with hospitalists with a 100% salary model, hospitalists that have a 100% productivity model have median charges 65% higher ($385,200 vs. $233,251), median collections that are 56% higher ($200,000 vs. $128,063), encounters that are 64% higher (3,000 vs. 1,831), admissions/consults that are 44% higher (575 vs. 400), and more than twice the median number of RVUs (4,967 vs. 2,395). In all cases hospitalists with a mixed compensation model fall in the middle of the two medians.

The next Annual Meeting is near. This means that the year, serving as your President, has nearly come to an end. As a result, this will be my last column. It is a good time for reflection.

First, I must thank the thousands of hospitalists who have joined SHM, filled out surveys, and attended meetings (either nationally or locally). You see, SHM’s data on hospitalists—where they are, what they do, and numbers in practice—is the source of information people outside the profession are using to understand and make decisions about our growing specialty. There is strength in numbers and your participation at every level infuses the energy necessary for us to continue the journey of becoming a legitimate specialty. Thank you.

As an organization, we have made significant progress toward our mission of making quality and safety core to what it means to practice hospital medicine. We have joined a number of other organizations, associations, and foundations to create various initiatives aimed at improving the quality and safety of care delivered in our hospitals. Specific areas of focus to date have been in the care of geriatric, diabetic, cardiac, and critically ill patients. We have also begun to address key preventative strategies such as antibiotic resistance and thromboembolic disease prophylaxis. These national partnerships SHM has formed with such organizations as the American College of Chest Physicians, American Association of Critical Care Nurses, American Hospital Association, Hartford Foundation, American College of Cardiology, Institute of Health Care Improvement, Joint Commission, and many others, demonstrate the breadth of teamwork that is necessary to care for patients across the continuum. Hospitalists are a crucial part of that team as more and more of our nation’s patients are cared for by hospitalists during their acute illnesses.

It has been an amazing year of watching this organization grow and mature. But what do I worry about as I leave my post? What is the kernel of concern that I must ensure is passed on with this next “transition of care” of our organization? It is that which defines us. I mentioned in my speech at lunch last year that we (the Society of Hospital Medicine) would fail if what hospitalists became known as were simply those pediatricians or internists who spent more time than their peers in the hospital. I don’t know about you, but at least once each month someone will approach me and say “I spend 25% of my time seeing patients in the hospital—So I must be a hospitalist!” (Quoting the original work of Drs. Robert Wachter and Lee Goldman in their 1996 New England Journal of Medicine article.) Well, as time has passed and the field has clearly evolved with more than 10,000 hospitalists practicing, the definition has clearly evolved.

But is our defi nition of what we do still based on time in the hospital? Or is it a more substantial definition? Is it about one’s professional focus? Is it about where one’s passion for medicine lies? What one wakes up in the middle of the night worrying about? What is a hospitalist?

The definition set forth by the Society of Hospital Medicine (adopted in the spring of 2000) is the following: Hospitalists are doctors whose primary professional focus is the general medical care of hospitalized patients. Their activities may include patient care, teaching, research, and leadership related to hospital care. Hospital medicine is a specialty organized around a site of care (the hospital) rather than an organ (like cardiology), a disease (like oncology), or a patient’s age (like pediatrics).

It seems silly to be asking this question of what defines us after writing about the burgeoning specialty. But as was pointed out in February’s JGIM issue, “varied employment relationships create diverse practice structures, priorities and roles.” Our practices have each grown so quickly out of local market pressures and individual hospital needs that we have evolved in slightly different directions. This is a natural consequence of such rapid growth. Just like any other specialty, practice structures and employment models will differ across the country. But I would challenge us to ensure that our higher priorities do not differ.

 

The American health care system needs an entire army of physicians and other providers to give whole heartedly and completely of their professional time, creativity, and energy to the hospital… to fix current system problems. It is no different than the cardiologists of today spending their energy and time discovering at the molecular level what causes ventricular dysfunction and then translating that knowledge to bedside care. Hospitalists, are specialists of in hospital medicine, and must do for the hospital what cardiologists do to the heart. We must study and learn what causes the health care delivered by the hospital to fail. Then we must translate that knowledge to the care of all patients in the hospital by improving the systems of care delivery.

According to Dr. Charles Mayo, “The definition of a specialist as one who ‘knows more and more about less and less. Its truth makes essential that the specialist, to do efficient work, must have some association with others who, taken altogether, represent the whole of which the specialty is only a part.” Our generalist colleagues care about the hospital as much as we do but do not necessarily have the time to concentrate specifically on hospital systems. There are so many other things that require their attention at the same time, but we need them to be there.

So we are only a part of what is needed to deliver the best care to all patients. But we have become a critical part of that team in the hospital. It is the hospitalists who, through their chosen focus on one aspect of medicine, will need to give the energy, creativity, and time to improving our systems of health care delivery in the hospital and across key transitions of care. Regardless of where we practice or how our practice is structured, our higher calling as a specialty is to determine the root causes of what ails the hospitals of this country. Then, as a specialty we must discover new mechanisms that would provide care at the level of quality called for by our patients. If we as hospitalists are truly specialists… If we are experts at delivering hospital based care… Then we have a vested interest in addressing these higher priorities. The improvements in health care that will be achieved, because a group of providers have dedicated their careers to making the hospital a better place for our patients, will ultimately make the definition of a hospitalist quite clear.

The next Annual Meeting is near. This means that the year, serving as your President, has nearly come to an end. As a result, this will be my last column. It is a good time for reflection.

First, I must thank the thousands of hospitalists who have joined SHM, filled out surveys, and attended meetings (either nationally or locally). You see, SHM’s data on hospitalists—where they are, what they do, and numbers in practice—is the source of information people outside the profession are using to understand and make decisions about our growing specialty. There is strength in numbers and your participation at every level infuses the energy necessary for us to continue the journey of becoming a legitimate specialty. Thank you.

As an organization, we have made significant progress toward our mission of making quality and safety core to what it means to practice hospital medicine. We have joined a number of other organizations, associations, and foundations to create various initiatives aimed at improving the quality and safety of care delivered in our hospitals. Specific areas of focus to date have been in the care of geriatric, diabetic, cardiac, and critically ill patients. We have also begun to address key preventative strategies such as antibiotic resistance and thromboembolic disease prophylaxis. These national partnerships SHM has formed with such organizations as the American College of Chest Physicians, American Association of Critical Care Nurses, American Hospital Association, Hartford Foundation, American College of Cardiology, Institute of Health Care Improvement, Joint Commission, and many others, demonstrate the breadth of teamwork that is necessary to care for patients across the continuum. Hospitalists are a crucial part of that team as more and more of our nation’s patients are cared for by hospitalists during their acute illnesses.

It has been an amazing year of watching this organization grow and mature. But what do I worry about as I leave my post? What is the kernel of concern that I must ensure is passed on with this next “transition of care” of our organization? It is that which defines us. I mentioned in my speech at lunch last year that we (the Society of Hospital Medicine) would fail if what hospitalists became known as were simply those pediatricians or internists who spent more time than their peers in the hospital. I don’t know about you, but at least once each month someone will approach me and say “I spend 25% of my time seeing patients in the hospital—So I must be a hospitalist!” (Quoting the original work of Drs. Robert Wachter and Lee Goldman in their 1996 New England Journal of Medicine article.) Well, as time has passed and the field has clearly evolved with more than 10,000 hospitalists practicing, the definition has clearly evolved.

But is our defi nition of what we do still based on time in the hospital? Or is it a more substantial definition? Is it about one’s professional focus? Is it about where one’s passion for medicine lies? What one wakes up in the middle of the night worrying about? What is a hospitalist?

The definition set forth by the Society of Hospital Medicine (adopted in the spring of 2000) is the following: Hospitalists are doctors whose primary professional focus is the general medical care of hospitalized patients. Their activities may include patient care, teaching, research, and leadership related to hospital care. Hospital medicine is a specialty organized around a site of care (the hospital) rather than an organ (like cardiology), a disease (like oncology), or a patient’s age (like pediatrics).

It seems silly to be asking this question of what defines us after writing about the burgeoning specialty. But as was pointed out in February’s JGIM issue, “varied employment relationships create diverse practice structures, priorities and roles.” Our practices have each grown so quickly out of local market pressures and individual hospital needs that we have evolved in slightly different directions. This is a natural consequence of such rapid growth. Just like any other specialty, practice structures and employment models will differ across the country. But I would challenge us to ensure that our higher priorities do not differ.

 

The American health care system needs an entire army of physicians and other providers to give whole heartedly and completely of their professional time, creativity, and energy to the hospital… to fix current system problems. It is no different than the cardiologists of today spending their energy and time discovering at the molecular level what causes ventricular dysfunction and then translating that knowledge to bedside care. Hospitalists, are specialists of in hospital medicine, and must do for the hospital what cardiologists do to the heart. We must study and learn what causes the health care delivered by the hospital to fail. Then we must translate that knowledge to the care of all patients in the hospital by improving the systems of care delivery.

According to Dr. Charles Mayo, “The definition of a specialist as one who ‘knows more and more about less and less. Its truth makes essential that the specialist, to do efficient work, must have some association with others who, taken altogether, represent the whole of which the specialty is only a part.” Our generalist colleagues care about the hospital as much as we do but do not necessarily have the time to concentrate specifically on hospital systems. There are so many other things that require their attention at the same time, but we need them to be there.

So we are only a part of what is needed to deliver the best care to all patients. But we have become a critical part of that team in the hospital. It is the hospitalists who, through their chosen focus on one aspect of medicine, will need to give the energy, creativity, and time to improving our systems of health care delivery in the hospital and across key transitions of care. Regardless of where we practice or how our practice is structured, our higher calling as a specialty is to determine the root causes of what ails the hospitals of this country. Then, as a specialty we must discover new mechanisms that would provide care at the level of quality called for by our patients. If we as hospitalists are truly specialists… If we are experts at delivering hospital based care… Then we have a vested interest in addressing these higher priorities. The improvements in health care that will be achieved, because a group of providers have dedicated their careers to making the hospital a better place for our patients, will ultimately make the definition of a hospitalist quite clear.

The next Annual Meeting is near. This means that the year, serving as your President, has nearly come to an end. As a result, this will be my last column. It is a good time for reflection.

First, I must thank the thousands of hospitalists who have joined SHM, filled out surveys, and attended meetings (either nationally or locally). You see, SHM’s data on hospitalists—where they are, what they do, and numbers in practice—is the source of information people outside the profession are using to understand and make decisions about our growing specialty. There is strength in numbers and your participation at every level infuses the energy necessary for us to continue the journey of becoming a legitimate specialty. Thank you.

As an organization, we have made significant progress toward our mission of making quality and safety core to what it means to practice hospital medicine. We have joined a number of other organizations, associations, and foundations to create various initiatives aimed at improving the quality and safety of care delivered in our hospitals. Specific areas of focus to date have been in the care of geriatric, diabetic, cardiac, and critically ill patients. We have also begun to address key preventative strategies such as antibiotic resistance and thromboembolic disease prophylaxis. These national partnerships SHM has formed with such organizations as the American College of Chest Physicians, American Association of Critical Care Nurses, American Hospital Association, Hartford Foundation, American College of Cardiology, Institute of Health Care Improvement, Joint Commission, and many others, demonstrate the breadth of teamwork that is necessary to care for patients across the continuum. Hospitalists are a crucial part of that team as more and more of our nation’s patients are cared for by hospitalists during their acute illnesses.

It has been an amazing year of watching this organization grow and mature. But what do I worry about as I leave my post? What is the kernel of concern that I must ensure is passed on with this next “transition of care” of our organization? It is that which defines us. I mentioned in my speech at lunch last year that we (the Society of Hospital Medicine) would fail if what hospitalists became known as were simply those pediatricians or internists who spent more time than their peers in the hospital. I don’t know about you, but at least once each month someone will approach me and say “I spend 25% of my time seeing patients in the hospital—So I must be a hospitalist!” (Quoting the original work of Drs. Robert Wachter and Lee Goldman in their 1996 New England Journal of Medicine article.) Well, as time has passed and the field has clearly evolved with more than 10,000 hospitalists practicing, the definition has clearly evolved.

But is our defi nition of what we do still based on time in the hospital? Or is it a more substantial definition? Is it about one’s professional focus? Is it about where one’s passion for medicine lies? What one wakes up in the middle of the night worrying about? What is a hospitalist?

The definition set forth by the Society of Hospital Medicine (adopted in the spring of 2000) is the following: Hospitalists are doctors whose primary professional focus is the general medical care of hospitalized patients. Their activities may include patient care, teaching, research, and leadership related to hospital care. Hospital medicine is a specialty organized around a site of care (the hospital) rather than an organ (like cardiology), a disease (like oncology), or a patient’s age (like pediatrics).

It seems silly to be asking this question of what defines us after writing about the burgeoning specialty. But as was pointed out in February’s JGIM issue, “varied employment relationships create diverse practice structures, priorities and roles.” Our practices have each grown so quickly out of local market pressures and individual hospital needs that we have evolved in slightly different directions. This is a natural consequence of such rapid growth. Just like any other specialty, practice structures and employment models will differ across the country. But I would challenge us to ensure that our higher priorities do not differ.

 

The American health care system needs an entire army of physicians and other providers to give whole heartedly and completely of their professional time, creativity, and energy to the hospital… to fix current system problems. It is no different than the cardiologists of today spending their energy and time discovering at the molecular level what causes ventricular dysfunction and then translating that knowledge to bedside care. Hospitalists, are specialists of in hospital medicine, and must do for the hospital what cardiologists do to the heart. We must study and learn what causes the health care delivered by the hospital to fail. Then we must translate that knowledge to the care of all patients in the hospital by improving the systems of care delivery.

According to Dr. Charles Mayo, “The definition of a specialist as one who ‘knows more and more about less and less. Its truth makes essential that the specialist, to do efficient work, must have some association with others who, taken altogether, represent the whole of which the specialty is only a part.” Our generalist colleagues care about the hospital as much as we do but do not necessarily have the time to concentrate specifically on hospital systems. There are so many other things that require their attention at the same time, but we need them to be there.

So we are only a part of what is needed to deliver the best care to all patients. But we have become a critical part of that team in the hospital. It is the hospitalists who, through their chosen focus on one aspect of medicine, will need to give the energy, creativity, and time to improving our systems of health care delivery in the hospital and across key transitions of care. Regardless of where we practice or how our practice is structured, our higher calling as a specialty is to determine the root causes of what ails the hospitals of this country. Then, as a specialty we must discover new mechanisms that would provide care at the level of quality called for by our patients. If we as hospitalists are truly specialists… If we are experts at delivering hospital based care… Then we have a vested interest in addressing these higher priorities. The improvements in health care that will be achieved, because a group of providers have dedicated their careers to making the hospital a better place for our patients, will ultimately make the definition of a hospitalist quite clear.

When a psychiatrist is sued for negligence, the legal system asks, “Did the doctor depart from the standard of care, and—if so—did that departure proximately cause the harm?” To determine proximate cause, the legal system then asks whether the harm was a “reasonably foreseeable” result of the negligent act.

Inadequate evaluation leads to patient’s suicide, plaintiff alleges

Dallas County (TX) District Court

In 1997, 1 year after suffering a stroke, a 56-year-old man was admitted to a rehabilitation center and seen by a psychiatrist for depression. In February 2000, the patient died after jumping from the center’s fifth-floor window.

The patient’s estate charged that the psychiatrist was negligent and did not adequately evaluate or treat the patient. The defense disputed the charge.

• The jury found for the defense.
  

Dr. Grant’s observations

In this case, the psychiatrist presumably assessed the patient, determined whether he was depressed, and made appropriate treatment interventions. Three years later, the patient killed himself.

Although 3 years passed between the consultation and the suicide, under the law an intervening act that is the reasonably foreseeable result of negligence does not break the causal chain. For example, if the psychiatrist told the patient he needed no treatment and did not need to follow-up with another clinician, the causal chain arguably would still exist. Thus, proper care, not time, will prevent such a suit.

To win a negligence case, the plaintiff must show that the psychiatrist’s actions proximately caused the harm. In order to defend your treatment decisions, document and discuss with the patient:

• the diagnosis and illness severity
  
• possible illness course based on patient history and the illness in question
  
• the need to monitor mood symptoms
  
• basis for treatment recommendations
  
• the possible need for continued treatment and to arrange follow-up care.
  

Plaintiff: Improper treatment caused fatal altercation

Cuyahoga County (OH) Court of Common Pleas

A man in his early 30s was admitted to the hospital’s psychiatric unit for depression, mood disorder, and adjustment disorder secondary to myasthenia gravis. He was estranged from his wife, who was dating another man. The treating psychiatrist discharged the patient after 5 days.

Approximately 40 hours after discharge, the patient went to the other man’s home and confronted him about his relationship with the patient’s wife. The two men then fought, and the other man fatally shot the patient. During the fight, the patient stabbed the other man in the neck with a knife; this man required care and subsequently developed a scar.

The other man and the patient’s estate charged that the psychiatrist did not appropriately evaluate and treat the patient. They claimed that a more thorough evaluation would have resulted in continued hospitalization and prevented the fight.

The defendant argued that the evaluation was thorough, that the discharge met the guidelines of appropriate care, and that the patient posed no risk to himself or others when he was discharged.

• The jury decided for the defense.
  

Dr. Grant’s observations

This case raises the clinically difficult issue of assessing a patient’s danger to self or others and whether this danger is reasonably foreseeable. Although Hughes reports that 17% of psychiatric emergency room patients are homicidal,¹ the American Psychiatric Association notes that 2 of 3 predictions of patient violence are wrong.²

In Tarasoff v Regents of the University of California, the California Supreme Court ruled that clinicians must warn potential victims of, and protect them from, a patient’s intent to harm.³ You should become familiar with the Tarasoff-type legislations in your state. But even if the patient shows no violent intent, the possibility of future violence cannot be ruled out.

During admission, assess and document an inpatient’s risk of violence.⁴ Factors that may increase a depressed patient’s risk of becoming homicidal include:

• past violence
  
• current substance abuse
  
• psychopathy
  
• having suffered physical abuse as a child
  
• violent thoughts.^4-6
  

If sexual infidelity, real or fantasized, precipitated the depression—as it might have in this case—a depressed patient may be at increased risk for homicide.

Check the patient’s records for a history of recurrent violence. Culling this information from the chart is necessary because:

• past violent behavior may predict future violence
  
• patients rarely reveal homicidal thoughts or behavior spontaneously.⁶
  

Knowing a patient’s violent past may aid in treatment. For example, you might order a longer hospitalization or establish more-intensive outpatient services focusing on avoiding aggression and violence. Make sure that follow-up care meets the patient’s needs after discharge.⁷

A psychiatrist may be found negligent after a patient’s violent act if the violence was foreseeable. However, after having seen the patient for 5 days in an inpatient setting, the psychiatrist in this case apparently could clearly document that the patient was not dangerous to himself or others before discharge.

When a psychiatrist is sued for negligence, the legal system asks, “Did the doctor depart from the standard of care, and—if so—did that departure proximately cause the harm?” To determine proximate cause, the legal system then asks whether the harm was a “reasonably foreseeable” result of the negligent act.

Inadequate evaluation leads to patient’s suicide, plaintiff alleges

Dallas County (TX) District Court

In 1997, 1 year after suffering a stroke, a 56-year-old man was admitted to a rehabilitation center and seen by a psychiatrist for depression. In February 2000, the patient died after jumping from the center’s fifth-floor window.

The patient’s estate charged that the psychiatrist was negligent and did not adequately evaluate or treat the patient. The defense disputed the charge.

• The jury found for the defense.
  

Dr. Grant’s observations

In this case, the psychiatrist presumably assessed the patient, determined whether he was depressed, and made appropriate treatment interventions. Three years later, the patient killed himself.

Although 3 years passed between the consultation and the suicide, under the law an intervening act that is the reasonably foreseeable result of negligence does not break the causal chain. For example, if the psychiatrist told the patient he needed no treatment and did not need to follow-up with another clinician, the causal chain arguably would still exist. Thus, proper care, not time, will prevent such a suit.

To win a negligence case, the plaintiff must show that the psychiatrist’s actions proximately caused the harm. In order to defend your treatment decisions, document and discuss with the patient:

• the diagnosis and illness severity
  
• possible illness course based on patient history and the illness in question
  
• the need to monitor mood symptoms
  
• basis for treatment recommendations
  
• the possible need for continued treatment and to arrange follow-up care.
  

Plaintiff: Improper treatment caused fatal altercation

Cuyahoga County (OH) Court of Common Pleas

A man in his early 30s was admitted to the hospital’s psychiatric unit for depression, mood disorder, and adjustment disorder secondary to myasthenia gravis. He was estranged from his wife, who was dating another man. The treating psychiatrist discharged the patient after 5 days.

Approximately 40 hours after discharge, the patient went to the other man’s home and confronted him about his relationship with the patient’s wife. The two men then fought, and the other man fatally shot the patient. During the fight, the patient stabbed the other man in the neck with a knife; this man required care and subsequently developed a scar.

The other man and the patient’s estate charged that the psychiatrist did not appropriately evaluate and treat the patient. They claimed that a more thorough evaluation would have resulted in continued hospitalization and prevented the fight.

The defendant argued that the evaluation was thorough, that the discharge met the guidelines of appropriate care, and that the patient posed no risk to himself or others when he was discharged.

• The jury decided for the defense.
  

Dr. Grant’s observations

This case raises the clinically difficult issue of assessing a patient’s danger to self or others and whether this danger is reasonably foreseeable. Although Hughes reports that 17% of psychiatric emergency room patients are homicidal,¹ the American Psychiatric Association notes that 2 of 3 predictions of patient violence are wrong.²

In Tarasoff v Regents of the University of California, the California Supreme Court ruled that clinicians must warn potential victims of, and protect them from, a patient’s intent to harm.³ You should become familiar with the Tarasoff-type legislations in your state. But even if the patient shows no violent intent, the possibility of future violence cannot be ruled out.

During admission, assess and document an inpatient’s risk of violence.⁴ Factors that may increase a depressed patient’s risk of becoming homicidal include:

• past violence
  
• current substance abuse
  
• psychopathy
  
• having suffered physical abuse as a child
  
• violent thoughts.^4-6
  

If sexual infidelity, real or fantasized, precipitated the depression—as it might have in this case—a depressed patient may be at increased risk for homicide.

Check the patient’s records for a history of recurrent violence. Culling this information from the chart is necessary because:

• past violent behavior may predict future violence
  
• patients rarely reveal homicidal thoughts or behavior spontaneously.⁶
  

Knowing a patient’s violent past may aid in treatment. For example, you might order a longer hospitalization or establish more-intensive outpatient services focusing on avoiding aggression and violence. Make sure that follow-up care meets the patient’s needs after discharge.⁷

A psychiatrist may be found negligent after a patient’s violent act if the violence was foreseeable. However, after having seen the patient for 5 days in an inpatient setting, the psychiatrist in this case apparently could clearly document that the patient was not dangerous to himself or others before discharge.

When a psychiatrist is sued for negligence, the legal system asks, “Did the doctor depart from the standard of care, and—if so—did that departure proximately cause the harm?” To determine proximate cause, the legal system then asks whether the harm was a “reasonably foreseeable” result of the negligent act.

Inadequate evaluation leads to patient’s suicide, plaintiff alleges

Dallas County (TX) District Court

In 1997, 1 year after suffering a stroke, a 56-year-old man was admitted to a rehabilitation center and seen by a psychiatrist for depression. In February 2000, the patient died after jumping from the center’s fifth-floor window.

The patient’s estate charged that the psychiatrist was negligent and did not adequately evaluate or treat the patient. The defense disputed the charge.

• The jury found for the defense.
  

Dr. Grant’s observations

In this case, the psychiatrist presumably assessed the patient, determined whether he was depressed, and made appropriate treatment interventions. Three years later, the patient killed himself.

Although 3 years passed between the consultation and the suicide, under the law an intervening act that is the reasonably foreseeable result of negligence does not break the causal chain. For example, if the psychiatrist told the patient he needed no treatment and did not need to follow-up with another clinician, the causal chain arguably would still exist. Thus, proper care, not time, will prevent such a suit.

To win a negligence case, the plaintiff must show that the psychiatrist’s actions proximately caused the harm. In order to defend your treatment decisions, document and discuss with the patient:

• the diagnosis and illness severity
  
• possible illness course based on patient history and the illness in question
  
• the need to monitor mood symptoms
  
• basis for treatment recommendations
  
• the possible need for continued treatment and to arrange follow-up care.
  

Plaintiff: Improper treatment caused fatal altercation

Cuyahoga County (OH) Court of Common Pleas

A man in his early 30s was admitted to the hospital’s psychiatric unit for depression, mood disorder, and adjustment disorder secondary to myasthenia gravis. He was estranged from his wife, who was dating another man. The treating psychiatrist discharged the patient after 5 days.

Approximately 40 hours after discharge, the patient went to the other man’s home and confronted him about his relationship with the patient’s wife. The two men then fought, and the other man fatally shot the patient. During the fight, the patient stabbed the other man in the neck with a knife; this man required care and subsequently developed a scar.

The other man and the patient’s estate charged that the psychiatrist did not appropriately evaluate and treat the patient. They claimed that a more thorough evaluation would have resulted in continued hospitalization and prevented the fight.

The defendant argued that the evaluation was thorough, that the discharge met the guidelines of appropriate care, and that the patient posed no risk to himself or others when he was discharged.

• The jury decided for the defense.
  

Dr. Grant’s observations

This case raises the clinically difficult issue of assessing a patient’s danger to self or others and whether this danger is reasonably foreseeable. Although Hughes reports that 17% of psychiatric emergency room patients are homicidal,¹ the American Psychiatric Association notes that 2 of 3 predictions of patient violence are wrong.²

In Tarasoff v Regents of the University of California, the California Supreme Court ruled that clinicians must warn potential victims of, and protect them from, a patient’s intent to harm.³ You should become familiar with the Tarasoff-type legislations in your state. But even if the patient shows no violent intent, the possibility of future violence cannot be ruled out.

During admission, assess and document an inpatient’s risk of violence.⁴ Factors that may increase a depressed patient’s risk of becoming homicidal include:

• past violence
  
• current substance abuse
  
• psychopathy
  
• having suffered physical abuse as a child
  
• violent thoughts.^4-6
  

If sexual infidelity, real or fantasized, precipitated the depression—as it might have in this case—a depressed patient may be at increased risk for homicide.

Check the patient’s records for a history of recurrent violence. Culling this information from the chart is necessary because:

• past violent behavior may predict future violence
  
• patients rarely reveal homicidal thoughts or behavior spontaneously.⁶
  

Knowing a patient’s violent past may aid in treatment. For example, you might order a longer hospitalization or establish more-intensive outpatient services focusing on avoiding aggression and violence. Make sure that follow-up care meets the patient’s needs after discharge.⁷

A psychiatrist may be found negligent after a patient’s violent act if the violence was foreseeable. However, after having seen the patient for 5 days in an inpatient setting, the psychiatrist in this case apparently could clearly document that the patient was not dangerous to himself or others before discharge.

A recently described cutaneous fibrosing disorder could be mistaken for scleroderma, but there are some key differences, said Dr. Collier.

Worldwide, there have been only 170 cases of nephrogenic fibrosing dermopathy (NFD) reported since it was first described in 1997, he said. Yet “I think it's far more common than we're led to believe,” he added.

The typical presentation of NFD consists of acute, lumpy, plaquelike indurations involving the lower limbs and occasionally the upper limbs and torso, he said.

Usually, scleroderma starts on the hands and face. But in NFD, these are almost always spared, he said.

The most common distribution of NFD skin presentation is between the ankles and the mid-thighs and between the wrists and mid-upper arms bilaterally, he said. Skin-colored to erythematous papules coalesce into brawny plaques with a peau d'orange appearance. There is a distinctive, irregular edge with amoeboid projections and islands of sparing within the indurated plaque. Eventually, the skin becomes markedly thickened and woody. Pruritis and causalgia are prominent features.

Unlike scleroderma, NFD often causes severe sharp pains in the affected areas, and renal insufficiency is necessary for the diagnosis.

The biopsy will show deposits of collagen and elastin—spindle cells, dendritic cells, and mucin deposits—“which is different from what we see in scleroderma.”

Although NFD was initially thought to be only a cutaneous disease, there now appears to be a severe myopathic component. Joint contractures may develop within days or weeks of onset, likely resulting from facial and muscle fibrosis, Dr. Collier noted.

The abrupt emergence of this disease suggests that toxic exposures, infectious agents, or medical techniques may be involved.

Document

70303_fx1.sml

NFD plaques typically take on a peau d'orange appearence. Courtesy Dr. David H. Collier

A recently described cutaneous fibrosing disorder could be mistaken for scleroderma, but there are some key differences, said Dr. Collier.

Worldwide, there have been only 170 cases of nephrogenic fibrosing dermopathy (NFD) reported since it was first described in 1997, he said. Yet “I think it's far more common than we're led to believe,” he added.

The typical presentation of NFD consists of acute, lumpy, plaquelike indurations involving the lower limbs and occasionally the upper limbs and torso, he said.

Usually, scleroderma starts on the hands and face. But in NFD, these are almost always spared, he said.

The most common distribution of NFD skin presentation is between the ankles and the mid-thighs and between the wrists and mid-upper arms bilaterally, he said. Skin-colored to erythematous papules coalesce into brawny plaques with a peau d'orange appearance. There is a distinctive, irregular edge with amoeboid projections and islands of sparing within the indurated plaque. Eventually, the skin becomes markedly thickened and woody. Pruritis and causalgia are prominent features.

Unlike scleroderma, NFD often causes severe sharp pains in the affected areas, and renal insufficiency is necessary for the diagnosis.

The biopsy will show deposits of collagen and elastin—spindle cells, dendritic cells, and mucin deposits—“which is different from what we see in scleroderma.”

Although NFD was initially thought to be only a cutaneous disease, there now appears to be a severe myopathic component. Joint contractures may develop within days or weeks of onset, likely resulting from facial and muscle fibrosis, Dr. Collier noted.

The abrupt emergence of this disease suggests that toxic exposures, infectious agents, or medical techniques may be involved.

Document

70303_fx1.sml

NFD plaques typically take on a peau d'orange appearence. Courtesy Dr. David H. Collier

A recently described cutaneous fibrosing disorder could be mistaken for scleroderma, but there are some key differences, said Dr. Collier.

Worldwide, there have been only 170 cases of nephrogenic fibrosing dermopathy (NFD) reported since it was first described in 1997, he said. Yet “I think it's far more common than we're led to believe,” he added.

The typical presentation of NFD consists of acute, lumpy, plaquelike indurations involving the lower limbs and occasionally the upper limbs and torso, he said.

Usually, scleroderma starts on the hands and face. But in NFD, these are almost always spared, he said.

The most common distribution of NFD skin presentation is between the ankles and the mid-thighs and between the wrists and mid-upper arms bilaterally, he said. Skin-colored to erythematous papules coalesce into brawny plaques with a peau d'orange appearance. There is a distinctive, irregular edge with amoeboid projections and islands of sparing within the indurated plaque. Eventually, the skin becomes markedly thickened and woody. Pruritis and causalgia are prominent features.

Unlike scleroderma, NFD often causes severe sharp pains in the affected areas, and renal insufficiency is necessary for the diagnosis.

The biopsy will show deposits of collagen and elastin—spindle cells, dendritic cells, and mucin deposits—“which is different from what we see in scleroderma.”

Although NFD was initially thought to be only a cutaneous disease, there now appears to be a severe myopathic component. Joint contractures may develop within days or weeks of onset, likely resulting from facial and muscle fibrosis, Dr. Collier noted.

The abrupt emergence of this disease suggests that toxic exposures, infectious agents, or medical techniques may be involved.

Document

70303_fx1.sml

NFD plaques typically take on a peau d'orange appearence. Courtesy Dr. David H. Collier

SNOWMASS, COLO — The most significant predictor of progression to scleroderma in a patient with new onset Raynaud's phenomenon is the presence of capillary abnormalities at the proximal nail fold, according to David H. Collier, M.D.

Although scleroderma is primarily managed by rheumatologists, it is dermatologists who most commonly identify the early skin manifestations of the disorder, said Dr. Collier of the University of Colorado, Denver, and chief of rheumatology at Denver Health Medical Center.

In addition to Raynaud's, these manifestations include skin thickening, ulceration, telangiectases, calcinosis, and pigmentation changes.

Speaking at a clinical dermatology seminar sponsored by Medicis, Dr. Collier explained that Raynaud's phenomenon is an almost universal component of systemic sclerosis, and yet the vast majority of patients with Raynaud's never progress to scleroderma.

“Up to 10% of adult women can have Raynaud's, and less then 0.1% can go on to develop scleroderma,” he said in an interview, adding that about 77% of Raynaud's patients are female.

By examining the periungual area of the finger, under gel with an opthalmoscope, the physician can easily assess capillary abnormalities at the proximal nail fold, he said.

“Instead of thin little loops of capillaries that you would see in a normal patient, you see capillary dilation and areas that are denuded or dropped out altogether,” he said, explaining that capillary dilation occurs early in the disease, and after about 10 years, only denudation is typically visible.

“A patient with abnormal capilloscopy should be followed every 3-6 months for signs of progression to systemic sclerosis,” he advised, adding that early identification of scleroderma and referral can allow for a prompt pulmonary evaluation and establishment of gastroesophageal reflux prevention/management.

Pitting or ulceration of the fingertips is another indication that a Raynaud's patient has scleroderma, said Dr. Collier.

“Primary Raynaud's disease does not give you pitting. So if you see pits—especially fingertip pits and ulceration—that's a red light [indicating] that you're dealing with an autoimmune disease. It's almost always Raynaud's secondary to scleroderma or mixed connective tissue disease, or occasionally lupus,” he said.

In addition to the evaluation for capillary abnormalities, the scleroderma work-up for patients presenting with Raynaud's should also include autoantibody testing, he said.

“If they also have the antibodies, that's the subgroup that I worry about the most for progressing to scleroderma, but it's not universal. I've certainly followed people with autoantibodies, and they didn't progress.”

Anticentromere antibodies are seen in 20%-30% of scleroderma patients and are the most predictive of risk to progression to limited systemic sclerosis, although they are also commonly seen in primary biliary cirrhosis and, rarely, in other connective tissue diseases, such as rheumatoid arthritis, systemic lupus erythematosus, mixed connective tissue disease, and polymyositis, he said.

Anti-topoisomerase-1 antibodies (e.g., anti-scleroderma [Scl]-70) are present in 9%-20% of scleroderma patients. Anti-RNA polymerase 1-3 antibodies are seen in 20%. Antifibrillarin/anti-U3 ribonucleoprotein (anti-U3 RNP) antibodies are seen in 10%, and anti-neutrophilic cytoplasmic antibodies (ANCA) are seen in about 4%, though mostly in patients with diffuse systemic sclerosis. Finally, antipolymyositis /Scl (anti-PM Scl) and anti-Th/To (which recognizes certain RNA processing enzymes) antibodies are seen in about 2% of scleroderma patients.

SNOWMASS, COLO — The most significant predictor of progression to scleroderma in a patient with new onset Raynaud's phenomenon is the presence of capillary abnormalities at the proximal nail fold, according to David H. Collier, M.D.

Although scleroderma is primarily managed by rheumatologists, it is dermatologists who most commonly identify the early skin manifestations of the disorder, said Dr. Collier of the University of Colorado, Denver, and chief of rheumatology at Denver Health Medical Center.

In addition to Raynaud's, these manifestations include skin thickening, ulceration, telangiectases, calcinosis, and pigmentation changes.

Speaking at a clinical dermatology seminar sponsored by Medicis, Dr. Collier explained that Raynaud's phenomenon is an almost universal component of systemic sclerosis, and yet the vast majority of patients with Raynaud's never progress to scleroderma.

“Up to 10% of adult women can have Raynaud's, and less then 0.1% can go on to develop scleroderma,” he said in an interview, adding that about 77% of Raynaud's patients are female.

By examining the periungual area of the finger, under gel with an opthalmoscope, the physician can easily assess capillary abnormalities at the proximal nail fold, he said.

“Instead of thin little loops of capillaries that you would see in a normal patient, you see capillary dilation and areas that are denuded or dropped out altogether,” he said, explaining that capillary dilation occurs early in the disease, and after about 10 years, only denudation is typically visible.

“A patient with abnormal capilloscopy should be followed every 3-6 months for signs of progression to systemic sclerosis,” he advised, adding that early identification of scleroderma and referral can allow for a prompt pulmonary evaluation and establishment of gastroesophageal reflux prevention/management.

Pitting or ulceration of the fingertips is another indication that a Raynaud's patient has scleroderma, said Dr. Collier.

“Primary Raynaud's disease does not give you pitting. So if you see pits—especially fingertip pits and ulceration—that's a red light [indicating] that you're dealing with an autoimmune disease. It's almost always Raynaud's secondary to scleroderma or mixed connective tissue disease, or occasionally lupus,” he said.

In addition to the evaluation for capillary abnormalities, the scleroderma work-up for patients presenting with Raynaud's should also include autoantibody testing, he said.

“If they also have the antibodies, that's the subgroup that I worry about the most for progressing to scleroderma, but it's not universal. I've certainly followed people with autoantibodies, and they didn't progress.”

Anticentromere antibodies are seen in 20%-30% of scleroderma patients and are the most predictive of risk to progression to limited systemic sclerosis, although they are also commonly seen in primary biliary cirrhosis and, rarely, in other connective tissue diseases, such as rheumatoid arthritis, systemic lupus erythematosus, mixed connective tissue disease, and polymyositis, he said.

Anti-topoisomerase-1 antibodies (e.g., anti-scleroderma [Scl]-70) are present in 9%-20% of scleroderma patients. Anti-RNA polymerase 1-3 antibodies are seen in 20%. Antifibrillarin/anti-U3 ribonucleoprotein (anti-U3 RNP) antibodies are seen in 10%, and anti-neutrophilic cytoplasmic antibodies (ANCA) are seen in about 4%, though mostly in patients with diffuse systemic sclerosis. Finally, antipolymyositis /Scl (anti-PM Scl) and anti-Th/To (which recognizes certain RNA processing enzymes) antibodies are seen in about 2% of scleroderma patients.

SNOWMASS, COLO — The most significant predictor of progression to scleroderma in a patient with new onset Raynaud's phenomenon is the presence of capillary abnormalities at the proximal nail fold, according to David H. Collier, M.D.

Although scleroderma is primarily managed by rheumatologists, it is dermatologists who most commonly identify the early skin manifestations of the disorder, said Dr. Collier of the University of Colorado, Denver, and chief of rheumatology at Denver Health Medical Center.

In addition to Raynaud's, these manifestations include skin thickening, ulceration, telangiectases, calcinosis, and pigmentation changes.

Speaking at a clinical dermatology seminar sponsored by Medicis, Dr. Collier explained that Raynaud's phenomenon is an almost universal component of systemic sclerosis, and yet the vast majority of patients with Raynaud's never progress to scleroderma.

“Up to 10% of adult women can have Raynaud's, and less then 0.1% can go on to develop scleroderma,” he said in an interview, adding that about 77% of Raynaud's patients are female.

By examining the periungual area of the finger, under gel with an opthalmoscope, the physician can easily assess capillary abnormalities at the proximal nail fold, he said.

“Instead of thin little loops of capillaries that you would see in a normal patient, you see capillary dilation and areas that are denuded or dropped out altogether,” he said, explaining that capillary dilation occurs early in the disease, and after about 10 years, only denudation is typically visible.

“A patient with abnormal capilloscopy should be followed every 3-6 months for signs of progression to systemic sclerosis,” he advised, adding that early identification of scleroderma and referral can allow for a prompt pulmonary evaluation and establishment of gastroesophageal reflux prevention/management.

Pitting or ulceration of the fingertips is another indication that a Raynaud's patient has scleroderma, said Dr. Collier.

“Primary Raynaud's disease does not give you pitting. So if you see pits—especially fingertip pits and ulceration—that's a red light [indicating] that you're dealing with an autoimmune disease. It's almost always Raynaud's secondary to scleroderma or mixed connective tissue disease, or occasionally lupus,” he said.

In addition to the evaluation for capillary abnormalities, the scleroderma work-up for patients presenting with Raynaud's should also include autoantibody testing, he said.

“If they also have the antibodies, that's the subgroup that I worry about the most for progressing to scleroderma, but it's not universal. I've certainly followed people with autoantibodies, and they didn't progress.”

Anticentromere antibodies are seen in 20%-30% of scleroderma patients and are the most predictive of risk to progression to limited systemic sclerosis, although they are also commonly seen in primary biliary cirrhosis and, rarely, in other connective tissue diseases, such as rheumatoid arthritis, systemic lupus erythematosus, mixed connective tissue disease, and polymyositis, he said.

Anti-topoisomerase-1 antibodies (e.g., anti-scleroderma [Scl]-70) are present in 9%-20% of scleroderma patients. Anti-RNA polymerase 1-3 antibodies are seen in 20%. Antifibrillarin/anti-U3 ribonucleoprotein (anti-U3 RNP) antibodies are seen in 10%, and anti-neutrophilic cytoplasmic antibodies (ANCA) are seen in about 4%, though mostly in patients with diffuse systemic sclerosis. Finally, antipolymyositis /Scl (anti-PM Scl) and anti-Th/To (which recognizes certain RNA processing enzymes) antibodies are seen in about 2% of scleroderma patients.

Etanercept does not impact maintenance of remission in patients with Wegener's granulomatosis, according to results from a multicenter, randomized, placebo-controlled trial.

“Our results underscore three points,” according to John H. Stone, M.D., of the Johns Hopkins Vasculitis Center, Baltimore. “Standard therapy fails to induce durable remissions in the majority of patients, etanercept does not enhance the effects of standard therapy, and even with the shorter courses of cyclophosphamide, now regarded as the standard of care, adverse events are common and frequently severe, with or without the addition of a specific tumor necrosis factor-? blockade.”

Dr. Stone and other members of the Wegener's Granulomatosis Etanercept Trial Research Group evaluated etanercept for maintenance of remission in 180 patients with Wegener's granulomatosis (N. Engl. J. Med. 2005;352:351-61). Of the total, 89 received 25 mg etanercept twice a week via subcutaneous injection, and 91 received placebo. Each patient received standard therapy that consisted of glucocorticoids plus cyclophosphamide or methotrexate.

During the mean 27-month follow-up period, there were no differences between the etanercept group and the controls in terms of sustained remission (70% vs. 75%, respectively), sustained periods of low-level disease activity (87% vs. 91%, respectively), or the time required to achieve those measures.

In addition, 118 flares occurred in the etanercept group, compared with 134 in the control group, a difference that was not statistically significant.

Etanercept does not impact maintenance of remission in patients with Wegener's granulomatosis, according to results from a multicenter, randomized, placebo-controlled trial.

“Our results underscore three points,” according to John H. Stone, M.D., of the Johns Hopkins Vasculitis Center, Baltimore. “Standard therapy fails to induce durable remissions in the majority of patients, etanercept does not enhance the effects of standard therapy, and even with the shorter courses of cyclophosphamide, now regarded as the standard of care, adverse events are common and frequently severe, with or without the addition of a specific tumor necrosis factor-? blockade.”

Dr. Stone and other members of the Wegener's Granulomatosis Etanercept Trial Research Group evaluated etanercept for maintenance of remission in 180 patients with Wegener's granulomatosis (N. Engl. J. Med. 2005;352:351-61). Of the total, 89 received 25 mg etanercept twice a week via subcutaneous injection, and 91 received placebo. Each patient received standard therapy that consisted of glucocorticoids plus cyclophosphamide or methotrexate.

During the mean 27-month follow-up period, there were no differences between the etanercept group and the controls in terms of sustained remission (70% vs. 75%, respectively), sustained periods of low-level disease activity (87% vs. 91%, respectively), or the time required to achieve those measures.

In addition, 118 flares occurred in the etanercept group, compared with 134 in the control group, a difference that was not statistically significant.

Etanercept does not impact maintenance of remission in patients with Wegener's granulomatosis, according to results from a multicenter, randomized, placebo-controlled trial.

“Our results underscore three points,” according to John H. Stone, M.D., of the Johns Hopkins Vasculitis Center, Baltimore. “Standard therapy fails to induce durable remissions in the majority of patients, etanercept does not enhance the effects of standard therapy, and even with the shorter courses of cyclophosphamide, now regarded as the standard of care, adverse events are common and frequently severe, with or without the addition of a specific tumor necrosis factor-? blockade.”

Dr. Stone and other members of the Wegener's Granulomatosis Etanercept Trial Research Group evaluated etanercept for maintenance of remission in 180 patients with Wegener's granulomatosis (N. Engl. J. Med. 2005;352:351-61). Of the total, 89 received 25 mg etanercept twice a week via subcutaneous injection, and 91 received placebo. Each patient received standard therapy that consisted of glucocorticoids plus cyclophosphamide or methotrexate.

During the mean 27-month follow-up period, there were no differences between the etanercept group and the controls in terms of sustained remission (70% vs. 75%, respectively), sustained periods of low-level disease activity (87% vs. 91%, respectively), or the time required to achieve those measures.

In addition, 118 flares occurred in the etanercept group, compared with 134 in the control group, a difference that was not statistically significant.

SNOWMASS, COLO. — Antimalarials may not only treat active lupus, but also benefit the heart, W. Joseph McCune, M.D., said at a symposium sponsored by the American College of Rheumatology.

Lupus patients have an elevated risk of heart disease, and antimalarials have been shown to have a number of cardioprotective properties, said Dr. McCune, professor of internal medicine at the University of Michigan, Ann Arbor.

Such benefits may help offset the deleterious effects of prednisone, which has been shown to increase cholesterol levels. Each 10-mg titration in prednisone dosage is estimated to increase serum cholesterol by 7.5 mg/dL.

Several studies have shown that antimalarials are associated with lipid profile improvements in lupus patients. Each of those studies has treated patients somewhat differently and has shown slightly different results. “But the body of the studies clearly show that when a benefit is looked for, it is found mostly in lowering LDL cholesterol,” Dr. McCune said.

In one study involving lupus patients not on corticosteroids, antimalarial therapy was associated with a 4% drop in total cholesterol at 3 months and a 1% drop at 6 months, compared with baseline levels. In patients on a corticosteroid, antimalarial therapy was associated with an 11% drop in total cholesterol at 3 months and a 9% drop at 6 months (J. Rheumatol. 1999;26:325-30).

Among diabetes patients, antimalarials have been shown to lower glucose levels in non-insulin-dependent patients. They also reduce insulin requirements in insulin-dependent patients. The dosages used have tended to be much higher than those typically used in rheumatology. However, even at the lower dosages used for treating lupus, it's believed that there is some positive effect on glucose tolerance, Dr. McCune said.

Dehydroepiandrosterone, which can be steroid sparing when it is added to lupus treatment, may produce increases in bone density that could offset steroid-induced osteopenia. But this has not been shown in patients with lupus, and the evidence is not definitive.

Statins clearly have immunomodulatory effects and have been shown to help prevent transplant rejection and to improve rheumatoid arthritis symptoms. However, at present there are no trials of statins used in patients with lupus, Dr. McCune said.

SNOWMASS, COLO. — Antimalarials may not only treat active lupus, but also benefit the heart, W. Joseph McCune, M.D., said at a symposium sponsored by the American College of Rheumatology.

Lupus patients have an elevated risk of heart disease, and antimalarials have been shown to have a number of cardioprotective properties, said Dr. McCune, professor of internal medicine at the University of Michigan, Ann Arbor.

Such benefits may help offset the deleterious effects of prednisone, which has been shown to increase cholesterol levels. Each 10-mg titration in prednisone dosage is estimated to increase serum cholesterol by 7.5 mg/dL.

Several studies have shown that antimalarials are associated with lipid profile improvements in lupus patients. Each of those studies has treated patients somewhat differently and has shown slightly different results. “But the body of the studies clearly show that when a benefit is looked for, it is found mostly in lowering LDL cholesterol,” Dr. McCune said.

In one study involving lupus patients not on corticosteroids, antimalarial therapy was associated with a 4% drop in total cholesterol at 3 months and a 1% drop at 6 months, compared with baseline levels. In patients on a corticosteroid, antimalarial therapy was associated with an 11% drop in total cholesterol at 3 months and a 9% drop at 6 months (J. Rheumatol. 1999;26:325-30).

Among diabetes patients, antimalarials have been shown to lower glucose levels in non-insulin-dependent patients. They also reduce insulin requirements in insulin-dependent patients. The dosages used have tended to be much higher than those typically used in rheumatology. However, even at the lower dosages used for treating lupus, it's believed that there is some positive effect on glucose tolerance, Dr. McCune said.

Dehydroepiandrosterone, which can be steroid sparing when it is added to lupus treatment, may produce increases in bone density that could offset steroid-induced osteopenia. But this has not been shown in patients with lupus, and the evidence is not definitive.

Statins clearly have immunomodulatory effects and have been shown to help prevent transplant rejection and to improve rheumatoid arthritis symptoms. However, at present there are no trials of statins used in patients with lupus, Dr. McCune said.

SNOWMASS, COLO. — Antimalarials may not only treat active lupus, but also benefit the heart, W. Joseph McCune, M.D., said at a symposium sponsored by the American College of Rheumatology.

Lupus patients have an elevated risk of heart disease, and antimalarials have been shown to have a number of cardioprotective properties, said Dr. McCune, professor of internal medicine at the University of Michigan, Ann Arbor.

Such benefits may help offset the deleterious effects of prednisone, which has been shown to increase cholesterol levels. Each 10-mg titration in prednisone dosage is estimated to increase serum cholesterol by 7.5 mg/dL.

Several studies have shown that antimalarials are associated with lipid profile improvements in lupus patients. Each of those studies has treated patients somewhat differently and has shown slightly different results. “But the body of the studies clearly show that when a benefit is looked for, it is found mostly in lowering LDL cholesterol,” Dr. McCune said.

In one study involving lupus patients not on corticosteroids, antimalarial therapy was associated with a 4% drop in total cholesterol at 3 months and a 1% drop at 6 months, compared with baseline levels. In patients on a corticosteroid, antimalarial therapy was associated with an 11% drop in total cholesterol at 3 months and a 9% drop at 6 months (J. Rheumatol. 1999;26:325-30).

Among diabetes patients, antimalarials have been shown to lower glucose levels in non-insulin-dependent patients. They also reduce insulin requirements in insulin-dependent patients. The dosages used have tended to be much higher than those typically used in rheumatology. However, even at the lower dosages used for treating lupus, it's believed that there is some positive effect on glucose tolerance, Dr. McCune said.

Dehydroepiandrosterone, which can be steroid sparing when it is added to lupus treatment, may produce increases in bone density that could offset steroid-induced osteopenia. But this has not been shown in patients with lupus, and the evidence is not definitive.

Statins clearly have immunomodulatory effects and have been shown to help prevent transplant rejection and to improve rheumatoid arthritis symptoms. However, at present there are no trials of statins used in patients with lupus, Dr. McCune said.

BOSTON — High-dose intravenous chemotherapy and autologous stem cell transplantation significantly improve the survival and organ response of some patients with primary amyloidosis, a longitudinal analysis has shown.

Until recently, the prognosis for patients with primary amyloidosis has been poor, with median survival rates of just 1-2 years, said Martha Skinner, M.D., at a meeting on advances in rheumatology sponsored by Harvard Medical School.

Primary amyloidosis, also called AL amyloidosis, involves an overproduction of amyloid light (AL) chain proteins caused by an underlying plasma cell abnormality. The excess proteins build up in tissues and organs, disrupting the structure and function of the heart, liver, kidneys, spleen, intestines, skin, and nervous system. Amyloid cardiomyopathy is a particularly fatal complication of the disease.

Conventional treatment with low-dose oral melphalan has been associated with a very low response rate, said Dr. Skinner, director of the amyloid program at Boston University Medical Center. Recently, however, aggressive treatment with high-dose intravenous melphalan followed by stem cell replacement or rescue has proven to be a more effective therapy, she said. In selected patients, this regimen has resulted in hematologic remission, improved survival rates, and reversal of amyloid-related disease, according to a review of outcome data.

Dr. Skinner and her colleagues analyzed data for 701 consecutive patients with AL amyloidosis who participated in six separate trials over a period of 8 years. They looked for evidence of persistent disease after treatment, and they assessed duration of survival and organ function.

Of the combined study populations, 394 patients were eligible for high-dose melphalan (100-200 mg/m2) and stem cell transplantation based on organ involvement and clinical status. Of these, 312 patients initiated treatment. The remaining 82 eligible patients did not proceed with treatment by choice or because of disease progression.

Among the treated patients, 40% had a complete hematologic response, defined as no evidence of an underlying plasma cell dyscrasia 1 year after treatment. Of those who remained in complete remission 1 year after treatment, 8% had relapses within 2 years, but none had relapses after 2 years, said Dr. Skinner.

Patients with a complete hematologic response had greater statistically significant improvements in end-organ disease, compared with treated patients who had evidence of persistent plasma cell dyscrasia, she said.

The hematologic and end-organ responses to treatment were accompanied by measurable and sustained quality of life improvements based on Short-Form Health Survey (SF-36) scores, said Dr. Skinner. At baseline, the scores were significantly lower on all eight SF-36 scales, compared with age-matched population norms. At 1 year, all of the scores had improved, with the mental component summary scores reaching the population norm. The physical component summary scores, which were lower than the population norm but still improved, were higher in the subgroup of patients who achieved a complete hematologic response, she said.

Mortality within 100 days of treatment was 13%, said Dr. Skinner, noting that patients in the treatment group who had cardiomyopathy had the highest mortality, compared with the other patients in the treatment group. The median survival of the treatment group was 4.6 years, Dr. Skinner said. Of 137 treated patients with heart involvement, approximately half were alive after 1.5 years, compared with 6.5 years for those treated patients without heart involvement. Half of the patients who were not eligible for the aggressive treatment died within 4 months.

The results should be taken in context, Dr. Skinner advised. “Patients were collected from multiple studies.”

BOSTON — High-dose intravenous chemotherapy and autologous stem cell transplantation significantly improve the survival and organ response of some patients with primary amyloidosis, a longitudinal analysis has shown.

Until recently, the prognosis for patients with primary amyloidosis has been poor, with median survival rates of just 1-2 years, said Martha Skinner, M.D., at a meeting on advances in rheumatology sponsored by Harvard Medical School.

Primary amyloidosis, also called AL amyloidosis, involves an overproduction of amyloid light (AL) chain proteins caused by an underlying plasma cell abnormality. The excess proteins build up in tissues and organs, disrupting the structure and function of the heart, liver, kidneys, spleen, intestines, skin, and nervous system. Amyloid cardiomyopathy is a particularly fatal complication of the disease.

Conventional treatment with low-dose oral melphalan has been associated with a very low response rate, said Dr. Skinner, director of the amyloid program at Boston University Medical Center. Recently, however, aggressive treatment with high-dose intravenous melphalan followed by stem cell replacement or rescue has proven to be a more effective therapy, she said. In selected patients, this regimen has resulted in hematologic remission, improved survival rates, and reversal of amyloid-related disease, according to a review of outcome data.

Dr. Skinner and her colleagues analyzed data for 701 consecutive patients with AL amyloidosis who participated in six separate trials over a period of 8 years. They looked for evidence of persistent disease after treatment, and they assessed duration of survival and organ function.

Of the combined study populations, 394 patients were eligible for high-dose melphalan (100-200 mg/m2) and stem cell transplantation based on organ involvement and clinical status. Of these, 312 patients initiated treatment. The remaining 82 eligible patients did not proceed with treatment by choice or because of disease progression.

Among the treated patients, 40% had a complete hematologic response, defined as no evidence of an underlying plasma cell dyscrasia 1 year after treatment. Of those who remained in complete remission 1 year after treatment, 8% had relapses within 2 years, but none had relapses after 2 years, said Dr. Skinner.

Patients with a complete hematologic response had greater statistically significant improvements in end-organ disease, compared with treated patients who had evidence of persistent plasma cell dyscrasia, she said.

The hematologic and end-organ responses to treatment were accompanied by measurable and sustained quality of life improvements based on Short-Form Health Survey (SF-36) scores, said Dr. Skinner. At baseline, the scores were significantly lower on all eight SF-36 scales, compared with age-matched population norms. At 1 year, all of the scores had improved, with the mental component summary scores reaching the population norm. The physical component summary scores, which were lower than the population norm but still improved, were higher in the subgroup of patients who achieved a complete hematologic response, she said.

Mortality within 100 days of treatment was 13%, said Dr. Skinner, noting that patients in the treatment group who had cardiomyopathy had the highest mortality, compared with the other patients in the treatment group. The median survival of the treatment group was 4.6 years, Dr. Skinner said. Of 137 treated patients with heart involvement, approximately half were alive after 1.5 years, compared with 6.5 years for those treated patients without heart involvement. Half of the patients who were not eligible for the aggressive treatment died within 4 months.

The results should be taken in context, Dr. Skinner advised. “Patients were collected from multiple studies.”

BOSTON — High-dose intravenous chemotherapy and autologous stem cell transplantation significantly improve the survival and organ response of some patients with primary amyloidosis, a longitudinal analysis has shown.

Until recently, the prognosis for patients with primary amyloidosis has been poor, with median survival rates of just 1-2 years, said Martha Skinner, M.D., at a meeting on advances in rheumatology sponsored by Harvard Medical School.

Primary amyloidosis, also called AL amyloidosis, involves an overproduction of amyloid light (AL) chain proteins caused by an underlying plasma cell abnormality. The excess proteins build up in tissues and organs, disrupting the structure and function of the heart, liver, kidneys, spleen, intestines, skin, and nervous system. Amyloid cardiomyopathy is a particularly fatal complication of the disease.

Conventional treatment with low-dose oral melphalan has been associated with a very low response rate, said Dr. Skinner, director of the amyloid program at Boston University Medical Center. Recently, however, aggressive treatment with high-dose intravenous melphalan followed by stem cell replacement or rescue has proven to be a more effective therapy, she said. In selected patients, this regimen has resulted in hematologic remission, improved survival rates, and reversal of amyloid-related disease, according to a review of outcome data.

Dr. Skinner and her colleagues analyzed data for 701 consecutive patients with AL amyloidosis who participated in six separate trials over a period of 8 years. They looked for evidence of persistent disease after treatment, and they assessed duration of survival and organ function.

Of the combined study populations, 394 patients were eligible for high-dose melphalan (100-200 mg/m2) and stem cell transplantation based on organ involvement and clinical status. Of these, 312 patients initiated treatment. The remaining 82 eligible patients did not proceed with treatment by choice or because of disease progression.

Among the treated patients, 40% had a complete hematologic response, defined as no evidence of an underlying plasma cell dyscrasia 1 year after treatment. Of those who remained in complete remission 1 year after treatment, 8% had relapses within 2 years, but none had relapses after 2 years, said Dr. Skinner.

Patients with a complete hematologic response had greater statistically significant improvements in end-organ disease, compared with treated patients who had evidence of persistent plasma cell dyscrasia, she said.

The hematologic and end-organ responses to treatment were accompanied by measurable and sustained quality of life improvements based on Short-Form Health Survey (SF-36) scores, said Dr. Skinner. At baseline, the scores were significantly lower on all eight SF-36 scales, compared with age-matched population norms. At 1 year, all of the scores had improved, with the mental component summary scores reaching the population norm. The physical component summary scores, which were lower than the population norm but still improved, were higher in the subgroup of patients who achieved a complete hematologic response, she said.

Mortality within 100 days of treatment was 13%, said Dr. Skinner, noting that patients in the treatment group who had cardiomyopathy had the highest mortality, compared with the other patients in the treatment group. The median survival of the treatment group was 4.6 years, Dr. Skinner said. Of 137 treated patients with heart involvement, approximately half were alive after 1.5 years, compared with 6.5 years for those treated patients without heart involvement. Half of the patients who were not eligible for the aggressive treatment died within 4 months.

The results should be taken in context, Dr. Skinner advised. “Patients were collected from multiple studies.”