Empathy Can Help Hospitalists Improve Patient Experience, Outcomes

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Empathy Can Help Hospitalists Improve Patient Experience, Outcomes

Empathy: ability to understand and share the feelings of another.

In today’s increasingly hyper-measured healthcare world, we are looking more and more at measures of patient outcomes. The Institute for Healthcare Improvement (IHI) touts the Triple Aim principle as the lens through which we should be approaching our work. The Triple Aim is the three-part goal and simultaneous focus of improving the health of the community and our patients, improving affordability of care, and finally and perhaps most elusively, improving the patient experience. Who wouldn’t want to hit on these admirable goals? How do we do it?

In approaching the health aspect of the Triple Aim, we, as hospitalists, have tried-and-true frameworks of process improvement. Clinical research and peer-reviewed publication advance the knowledge of what medicines and procedures can improve care. Although powerful and generally truthful, this system results in a slow diffusion of practice improvement, not to mention idiosyncratic and nonstandardized care. This has led to a new toolkit of improvement techniques: continuous quality improvement, Lean, and Six Sigma. We learn and adopt these and watch our scores go up at a steady pace.

If all we focus on is the scores, and we lack faith that the scores represent the true experience of patients, then how can we ever truly create a more satisfying experience for our patients?

Improving affordability has its challenges, some huge, like our basic cultural ethos that “more is better.” Yet affordability is still something we can grasp. It is rooted in systems we are all familiar with, from basic personal finance to resource allocation to generally accepted accounting principles. We all can grasp that the current system of pay for widgets is teetering at the edge, just waiting for a shove from CMS to send it to its doom. Once this happens, affordability likely will become something we can start to make serious headway against.

Improving the experience of patients and families is perhaps the toughest of the three and where I would like to focus.

Patients First

First, a question: Are experience scores reflective of the true experience of a patient?

Two weeks after discharge, when patients receive their HCAHPS questionnaire in the mail, do they remember the details of their stay? And who was their doctor anyway? The cardiologist who placed a stent? The on-call doctor? The hospitalist who visited them every morning? If all we focus on is the scores, and we lack faith that the scores represent the true experience of patients, then how can we ever truly create a more satisfying experience for our patients?

I believe that the answer lies with empathy. What’s unique about this part of the Triple Aim is that many of the answers are within us. Gaining empathy with our patients requires us to ask questions of them and also to ask questions of ourselves. It requires us to invoke ancient methods of learning and thinking, like walking in another’s shoes for a day or using the Golden Rule. Experience doesn’t lend itself to being taught by PowerPoint. It must be lived and channeled back and out through our emotional selves as empathy.

Using the wisdom of patients themselves is one way to understand their needs and develop the empathy to motivate us to change how we do things in health care. Many organizations around the country have used some form of patient focus group to help learn from patients. Park Nicollet, a large health system in Minnesota, has incorporated family councils in nearly every clinic and care area. They usually are patients or caregivers from the area, bound together by a common disease or location. They dedicate their time, often meeting monthly, to share their stories, give opinions on care processes, and even to shape the design of a care area. Currently, there are more than 100 patient councils in the system, and the number continues to grow.

 

 

Film, when done skillfully, is a powerful tool in helping us gain empathy. The Cleveland Clinic has produced an amazing short film called “Empathy: The Human Connection to Patient Care.” It follows patients, families, and staff through the care system. As the camera focuses on each person, floating text appears near them, explaining their situation, inner thoughts, or fears, all overlaid by an emotional piano score. Tears will flow. Understanding follows.

Jim Merlino, MD, Cleveland Clinic’s chief experience officer, explains, “We need to understand that being on the other side of health care is frightening, and our job, our responsibility as people responsible for other people, is to help ease that fear.” Cleveland Clinic has done a remarkable job in reminding us why we went in to health care.

Morgan Spurlock of “Super Size Me” fame produced a reality series called “30 Days.” In each episode, a participant spent 30 days in the shoes of another. In the “Life in a Wheelchair” episode, Super Bowl-winning football player Ray Crockett lives in a wheelchair for 30 days and explores what it is like going through recovery and the healthcare system. He meets several rehabbing paraplegics and quadriplegics and accompanies them through their daily lives at home and the hospital. Viewers gain empathy directly in seeing these patients struggle to get better and work with the healthcare system. We also gain empathy watching Crockett gain empathy. The combination is powerful.

In Patients’ Shoes

In addition to listening and observation, we can begin to literally walk in the shoes of our patients.

I recently attended IHI’s International Forum in London. The National Health Service (NHS) in England is using a new tool to help providers understand what it is like for geriatric patients who must navigate the healthcare system with diminished senses and capabilities. Providers put on an age-simulation suit (www.age-simulation-suit.com) that mimics the impairments of aging. Special goggles fog the vision and narrow the visual field. Head mobility is reduced so that it becomes difficult to see beyond the field cuts. Earmuffs reduce high-frequency hearing and the ability to understand speech clearly. The overall suit impedes motion and reduces strength. Thick gloves make it difficult to coordinate fine motions. Wearing this suit and trying to go through a hospital or clinic setting instantly makes the wearer gain empathy for our patients’ needs.

Most important, be a patient. SHM immediate past president Shaun Frost, MD, SFHM, whose personal mission during his tenure was to help the society understand patient experience, explained it best to me. “In one episode in the hospital with a family member, I learned more about patient experience than all the reading and self-educating I have been doing for the last year.”

I think any of us who have been a patient in the hospital, or accompanied a loved one, comes out frustrated that the healthcare system is so convoluted and lacking in clarity for patients. Then there is often a sense of renewal, hopefully,followed by evangelism to spread their newfound empathy to others in the system.

In our busy work lives as hospitalists, it isn’t easy turning our daily focus away from efficiency and productivity. Yet we must always remain mindful of that core idea every one of us wrote down as the heart of our personal statements on our applications to medical school. Do you remember writing something like this? “I want to help people and relieve suffering in their time of need.”

Empathy is the start of our work.


Dr. Kealey is medical director of hospital specialties at HealthPartners Medical Group in St. Paul, Minn. He is an SHM board member and SHM president-elect.

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Empathy: ability to understand and share the feelings of another.

In today’s increasingly hyper-measured healthcare world, we are looking more and more at measures of patient outcomes. The Institute for Healthcare Improvement (IHI) touts the Triple Aim principle as the lens through which we should be approaching our work. The Triple Aim is the three-part goal and simultaneous focus of improving the health of the community and our patients, improving affordability of care, and finally and perhaps most elusively, improving the patient experience. Who wouldn’t want to hit on these admirable goals? How do we do it?

In approaching the health aspect of the Triple Aim, we, as hospitalists, have tried-and-true frameworks of process improvement. Clinical research and peer-reviewed publication advance the knowledge of what medicines and procedures can improve care. Although powerful and generally truthful, this system results in a slow diffusion of practice improvement, not to mention idiosyncratic and nonstandardized care. This has led to a new toolkit of improvement techniques: continuous quality improvement, Lean, and Six Sigma. We learn and adopt these and watch our scores go up at a steady pace.

If all we focus on is the scores, and we lack faith that the scores represent the true experience of patients, then how can we ever truly create a more satisfying experience for our patients?

Improving affordability has its challenges, some huge, like our basic cultural ethos that “more is better.” Yet affordability is still something we can grasp. It is rooted in systems we are all familiar with, from basic personal finance to resource allocation to generally accepted accounting principles. We all can grasp that the current system of pay for widgets is teetering at the edge, just waiting for a shove from CMS to send it to its doom. Once this happens, affordability likely will become something we can start to make serious headway against.

Improving the experience of patients and families is perhaps the toughest of the three and where I would like to focus.

Patients First

First, a question: Are experience scores reflective of the true experience of a patient?

Two weeks after discharge, when patients receive their HCAHPS questionnaire in the mail, do they remember the details of their stay? And who was their doctor anyway? The cardiologist who placed a stent? The on-call doctor? The hospitalist who visited them every morning? If all we focus on is the scores, and we lack faith that the scores represent the true experience of patients, then how can we ever truly create a more satisfying experience for our patients?

I believe that the answer lies with empathy. What’s unique about this part of the Triple Aim is that many of the answers are within us. Gaining empathy with our patients requires us to ask questions of them and also to ask questions of ourselves. It requires us to invoke ancient methods of learning and thinking, like walking in another’s shoes for a day or using the Golden Rule. Experience doesn’t lend itself to being taught by PowerPoint. It must be lived and channeled back and out through our emotional selves as empathy.

Using the wisdom of patients themselves is one way to understand their needs and develop the empathy to motivate us to change how we do things in health care. Many organizations around the country have used some form of patient focus group to help learn from patients. Park Nicollet, a large health system in Minnesota, has incorporated family councils in nearly every clinic and care area. They usually are patients or caregivers from the area, bound together by a common disease or location. They dedicate their time, often meeting monthly, to share their stories, give opinions on care processes, and even to shape the design of a care area. Currently, there are more than 100 patient councils in the system, and the number continues to grow.

 

 

Film, when done skillfully, is a powerful tool in helping us gain empathy. The Cleveland Clinic has produced an amazing short film called “Empathy: The Human Connection to Patient Care.” It follows patients, families, and staff through the care system. As the camera focuses on each person, floating text appears near them, explaining their situation, inner thoughts, or fears, all overlaid by an emotional piano score. Tears will flow. Understanding follows.

Jim Merlino, MD, Cleveland Clinic’s chief experience officer, explains, “We need to understand that being on the other side of health care is frightening, and our job, our responsibility as people responsible for other people, is to help ease that fear.” Cleveland Clinic has done a remarkable job in reminding us why we went in to health care.

Morgan Spurlock of “Super Size Me” fame produced a reality series called “30 Days.” In each episode, a participant spent 30 days in the shoes of another. In the “Life in a Wheelchair” episode, Super Bowl-winning football player Ray Crockett lives in a wheelchair for 30 days and explores what it is like going through recovery and the healthcare system. He meets several rehabbing paraplegics and quadriplegics and accompanies them through their daily lives at home and the hospital. Viewers gain empathy directly in seeing these patients struggle to get better and work with the healthcare system. We also gain empathy watching Crockett gain empathy. The combination is powerful.

In Patients’ Shoes

In addition to listening and observation, we can begin to literally walk in the shoes of our patients.

I recently attended IHI’s International Forum in London. The National Health Service (NHS) in England is using a new tool to help providers understand what it is like for geriatric patients who must navigate the healthcare system with diminished senses and capabilities. Providers put on an age-simulation suit (www.age-simulation-suit.com) that mimics the impairments of aging. Special goggles fog the vision and narrow the visual field. Head mobility is reduced so that it becomes difficult to see beyond the field cuts. Earmuffs reduce high-frequency hearing and the ability to understand speech clearly. The overall suit impedes motion and reduces strength. Thick gloves make it difficult to coordinate fine motions. Wearing this suit and trying to go through a hospital or clinic setting instantly makes the wearer gain empathy for our patients’ needs.

Most important, be a patient. SHM immediate past president Shaun Frost, MD, SFHM, whose personal mission during his tenure was to help the society understand patient experience, explained it best to me. “In one episode in the hospital with a family member, I learned more about patient experience than all the reading and self-educating I have been doing for the last year.”

I think any of us who have been a patient in the hospital, or accompanied a loved one, comes out frustrated that the healthcare system is so convoluted and lacking in clarity for patients. Then there is often a sense of renewal, hopefully,followed by evangelism to spread their newfound empathy to others in the system.

In our busy work lives as hospitalists, it isn’t easy turning our daily focus away from efficiency and productivity. Yet we must always remain mindful of that core idea every one of us wrote down as the heart of our personal statements on our applications to medical school. Do you remember writing something like this? “I want to help people and relieve suffering in their time of need.”

Empathy is the start of our work.


Dr. Kealey is medical director of hospital specialties at HealthPartners Medical Group in St. Paul, Minn. He is an SHM board member and SHM president-elect.

Empathy: ability to understand and share the feelings of another.

In today’s increasingly hyper-measured healthcare world, we are looking more and more at measures of patient outcomes. The Institute for Healthcare Improvement (IHI) touts the Triple Aim principle as the lens through which we should be approaching our work. The Triple Aim is the three-part goal and simultaneous focus of improving the health of the community and our patients, improving affordability of care, and finally and perhaps most elusively, improving the patient experience. Who wouldn’t want to hit on these admirable goals? How do we do it?

In approaching the health aspect of the Triple Aim, we, as hospitalists, have tried-and-true frameworks of process improvement. Clinical research and peer-reviewed publication advance the knowledge of what medicines and procedures can improve care. Although powerful and generally truthful, this system results in a slow diffusion of practice improvement, not to mention idiosyncratic and nonstandardized care. This has led to a new toolkit of improvement techniques: continuous quality improvement, Lean, and Six Sigma. We learn and adopt these and watch our scores go up at a steady pace.

If all we focus on is the scores, and we lack faith that the scores represent the true experience of patients, then how can we ever truly create a more satisfying experience for our patients?

Improving affordability has its challenges, some huge, like our basic cultural ethos that “more is better.” Yet affordability is still something we can grasp. It is rooted in systems we are all familiar with, from basic personal finance to resource allocation to generally accepted accounting principles. We all can grasp that the current system of pay for widgets is teetering at the edge, just waiting for a shove from CMS to send it to its doom. Once this happens, affordability likely will become something we can start to make serious headway against.

Improving the experience of patients and families is perhaps the toughest of the three and where I would like to focus.

Patients First

First, a question: Are experience scores reflective of the true experience of a patient?

Two weeks after discharge, when patients receive their HCAHPS questionnaire in the mail, do they remember the details of their stay? And who was their doctor anyway? The cardiologist who placed a stent? The on-call doctor? The hospitalist who visited them every morning? If all we focus on is the scores, and we lack faith that the scores represent the true experience of patients, then how can we ever truly create a more satisfying experience for our patients?

I believe that the answer lies with empathy. What’s unique about this part of the Triple Aim is that many of the answers are within us. Gaining empathy with our patients requires us to ask questions of them and also to ask questions of ourselves. It requires us to invoke ancient methods of learning and thinking, like walking in another’s shoes for a day or using the Golden Rule. Experience doesn’t lend itself to being taught by PowerPoint. It must be lived and channeled back and out through our emotional selves as empathy.

Using the wisdom of patients themselves is one way to understand their needs and develop the empathy to motivate us to change how we do things in health care. Many organizations around the country have used some form of patient focus group to help learn from patients. Park Nicollet, a large health system in Minnesota, has incorporated family councils in nearly every clinic and care area. They usually are patients or caregivers from the area, bound together by a common disease or location. They dedicate their time, often meeting monthly, to share their stories, give opinions on care processes, and even to shape the design of a care area. Currently, there are more than 100 patient councils in the system, and the number continues to grow.

 

 

Film, when done skillfully, is a powerful tool in helping us gain empathy. The Cleveland Clinic has produced an amazing short film called “Empathy: The Human Connection to Patient Care.” It follows patients, families, and staff through the care system. As the camera focuses on each person, floating text appears near them, explaining their situation, inner thoughts, or fears, all overlaid by an emotional piano score. Tears will flow. Understanding follows.

Jim Merlino, MD, Cleveland Clinic’s chief experience officer, explains, “We need to understand that being on the other side of health care is frightening, and our job, our responsibility as people responsible for other people, is to help ease that fear.” Cleveland Clinic has done a remarkable job in reminding us why we went in to health care.

Morgan Spurlock of “Super Size Me” fame produced a reality series called “30 Days.” In each episode, a participant spent 30 days in the shoes of another. In the “Life in a Wheelchair” episode, Super Bowl-winning football player Ray Crockett lives in a wheelchair for 30 days and explores what it is like going through recovery and the healthcare system. He meets several rehabbing paraplegics and quadriplegics and accompanies them through their daily lives at home and the hospital. Viewers gain empathy directly in seeing these patients struggle to get better and work with the healthcare system. We also gain empathy watching Crockett gain empathy. The combination is powerful.

In Patients’ Shoes

In addition to listening and observation, we can begin to literally walk in the shoes of our patients.

I recently attended IHI’s International Forum in London. The National Health Service (NHS) in England is using a new tool to help providers understand what it is like for geriatric patients who must navigate the healthcare system with diminished senses and capabilities. Providers put on an age-simulation suit (www.age-simulation-suit.com) that mimics the impairments of aging. Special goggles fog the vision and narrow the visual field. Head mobility is reduced so that it becomes difficult to see beyond the field cuts. Earmuffs reduce high-frequency hearing and the ability to understand speech clearly. The overall suit impedes motion and reduces strength. Thick gloves make it difficult to coordinate fine motions. Wearing this suit and trying to go through a hospital or clinic setting instantly makes the wearer gain empathy for our patients’ needs.

Most important, be a patient. SHM immediate past president Shaun Frost, MD, SFHM, whose personal mission during his tenure was to help the society understand patient experience, explained it best to me. “In one episode in the hospital with a family member, I learned more about patient experience than all the reading and self-educating I have been doing for the last year.”

I think any of us who have been a patient in the hospital, or accompanied a loved one, comes out frustrated that the healthcare system is so convoluted and lacking in clarity for patients. Then there is often a sense of renewal, hopefully,followed by evangelism to spread their newfound empathy to others in the system.

In our busy work lives as hospitalists, it isn’t easy turning our daily focus away from efficiency and productivity. Yet we must always remain mindful of that core idea every one of us wrote down as the heart of our personal statements on our applications to medical school. Do you remember writing something like this? “I want to help people and relieve suffering in their time of need.”

Empathy is the start of our work.


Dr. Kealey is medical director of hospital specialties at HealthPartners Medical Group in St. Paul, Minn. He is an SHM board member and SHM president-elect.

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Medicare Outlines Anticipated Funding Changes Under Affordable Care Act

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Medicare Outlines Anticipated Funding Changes Under Affordable Care Act

The Centers for Medicare & Medicaid Services (CMS) recently released a few Fact Sheets on how they anticipate funding changes on a few of their programs that were implemented (or sustained) under the Affordable Care Act. As a background, CMS pays most acute-care hospitals by prospectively determining payment based on a patient’s diagnosis and the severity of illness within that diagnosis (e.g. “MS-DRG”). These payment amounts are updated annually after evaluating several factors, including the costs associated with the delivery of care.

One of the most major changes described in the Fact Sheet that will affect hospitalists is how CMS will review inpatient stays based on the number of nights in the hospital. CMS has proposed that any patient who stays in the hospital for two or more “midnights” should be appropriate for payment under Medicare Part A. For those who stay in the hospital for only one (or zero) midnights, payment under Medicare Part A will only be appropriate if:

  1. There is sufficient documentation at the time of admission that the anticipated length of stay is two or more nights; and.
  2. Further documentation that circumstances changed, and the hospital stay ended prematurely because of those changes.

Overall for hospitalists, this should substantially simplify the admitting process, whereby most inpatients being admitted with the anticipation of two or more nights should qualify for an inpatient stay. This also reduces the administrative burden of correcting the “inpatient” versus “observation” designation, which keeps many hospital staffs entirely too busy. This change also should relieve a significant burden from the patients and their families, who if kept in observation for a period of time, may have to pay substantially out of pocket to make up for the difference between the cost of the stay and the reimbursement from CMS for observation status. So this is one of the moves that CMS is making to simplify (and not complicate) an already too-complicated payment system. This should go into effect October 2013 and will be a sigh of much relief from many of us.

Overall for hospitalists, this should substantially simplify the admitting process, whereby most inpatients being admitted with the anticipation of two or more nights should qualify for an inpatient stay.

A few other anticipated changes that will affect hospitalists include:

Payments for Unfunded Care

Another major change that will go into affect October 2013 is the amount of monies received by hospitals that care for unfunded patients. These payments historically have been made to “Disproportionate Share Hospitals” (DSH), which are hospitals that care for a higher percentage of unfunded patients. Under the Affordable Care Act, only 25% of these payments will be distributed to DSH hospitals; the remaining 75% will be reduced based on the number of uninsured in the U.S., then redistributed to DSH hospitals based on their portion of uninsured care delivered.

Most DSH hospitals should expect a decrease in DSH payments, the amount of which will depend on their share of unfunded patients.

Any reduction in the “bottom line” to the hospital can affect hospitalists, especially those who are directly employed by the hospital.

Hospital-Acquired Conditions

CMS has long had the Hospital-Acquired Condition (HAC) program in effect, which has the ability to reduce the amount of payment for inpatients who acquire a HAC during their hospital stay. Starting in October 2014, CMS will impose additional financial penalties for hospitals with high HAC rates.

Specifically, those hospitals in the highest 25th percentile of HAC rates will be penalized 1% of their overall CMS payments. Another proposed change is that the following be included in the HAC reduction plan (two “domains” of measures):

 

 

  • Domain No. 1: Six of the AHRQ Patient Safety Indicators (PSIs), including pressure ulcers, foreign bodies left in after surgery, iatrogenic pneumothorax, postoperative physiologic or metabolic derangements, postoperative VTE, and accidental puncture/laceration.
  • Domain No. 2: Central-line-associated bloodstream infections (CLABSI) and catheter-associated urinary tract infections (CAUTIs).

The domains will be weighted equally, and an average score will determine the total score. There will be some methodology for risk adjustment, and hospitals will be given a review and comment period to validate their own scores.

Most hospitalists have at least indirect control over many of these HACs,and all need to pay very close attention to their hospital’s rates of these now and in the future.

Readmissions

As we all know, the Hospital Readmission Reduction program went into effect October 2012; it placed 1% of CMS payments at risk. This will increase to 2% of payments as of October 2013. CMS will continue to use AMI, CHF, and pneumonia as the three conditions under which the readmissions are measured but will put in some methodology to account for planned readmissions.

In addition, in October 2014, they plan to add readmission rates for COPD and for hip/knee arthroplasty.

Hospitalists will continue to need to progress their transitions of care programs, at least for these five patients conditions but more likely (and more effectively) for all hospital discharges.

Quality Measures

Currently more than 99% of acute-care hospitals participate in the pay-for-reporting quality program through CMS, the results of which have been displayed on the Hospital Compare website (www.hospitalcompare.hhs.gov) for years. The program started in 2004 with 10 quality metrics and now includes 57 metrics. These include process and outcome measures for AMI, CHF, and pneumonia, as well as process measures for surgical care, HACs, and patient-satisfaction surveys, among others.

This program will continue to expand over time, including hospital-acquired MRSA and Clostridium difficile rates. The few hospitals not participating will have their CMS annual payments reduced by 2%.

EHR Incentives

CMS is evaluating ways to reduce the burden of reporting by aligning EHR incentives with the Inpatient Quality Reporting program.

Summary

After an open commentary period, the Final Rule will be published Aug. 1, and will become effective for discharges on or after Oct. 1. Although CMS will continue to expand the total number of measures that need to be reported, and the penalties for non-reporting or low performance will continue to escalate, CMS is at least attempting to reduce the overall burden of reporting by combining measures and programs over time and using EHRs to facilitate the bulk of reporting over time.

The global message to hospitalists is: Continue to focus on reducing the burden of HACs, enhance throughput, and carefully and thoughtfully transition patients to the next provider after their hospital discharge. All in all, although at times this can feel overwhelming, these changes represent the right direction to move for high-quality and safe patient care.


Dr. Scheurer is a hospitalist and chief quality officer at the Medical University of South Carolina in Charleston. She is physician editor of The Hospitalist. Email her at [email protected].

Reference

  1. Centers for Medicare & Medicaid. Fact Sheets: CMS proposals to improve quality of care during hospital inpatient stays. Centers for Medicare & Medicaid website. Available at: www.cms.gov/apps/media/press/factsheet.asp?Counter=4586&intNumPerPage=10&checkDate=&checkKey=&srchType=1&numDays=3500&srchOpt=0&srchData=&keywordType=All&chkNewsType=6&intPage=&showAll=&pYear=&year=&desc=&cboOrder=date. Accessed May 1, 2013.
Issue
The Hospitalist - 2013(07)
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The Centers for Medicare & Medicaid Services (CMS) recently released a few Fact Sheets on how they anticipate funding changes on a few of their programs that were implemented (or sustained) under the Affordable Care Act. As a background, CMS pays most acute-care hospitals by prospectively determining payment based on a patient’s diagnosis and the severity of illness within that diagnosis (e.g. “MS-DRG”). These payment amounts are updated annually after evaluating several factors, including the costs associated with the delivery of care.

One of the most major changes described in the Fact Sheet that will affect hospitalists is how CMS will review inpatient stays based on the number of nights in the hospital. CMS has proposed that any patient who stays in the hospital for two or more “midnights” should be appropriate for payment under Medicare Part A. For those who stay in the hospital for only one (or zero) midnights, payment under Medicare Part A will only be appropriate if:

  1. There is sufficient documentation at the time of admission that the anticipated length of stay is two or more nights; and.
  2. Further documentation that circumstances changed, and the hospital stay ended prematurely because of those changes.

Overall for hospitalists, this should substantially simplify the admitting process, whereby most inpatients being admitted with the anticipation of two or more nights should qualify for an inpatient stay. This also reduces the administrative burden of correcting the “inpatient” versus “observation” designation, which keeps many hospital staffs entirely too busy. This change also should relieve a significant burden from the patients and their families, who if kept in observation for a period of time, may have to pay substantially out of pocket to make up for the difference between the cost of the stay and the reimbursement from CMS for observation status. So this is one of the moves that CMS is making to simplify (and not complicate) an already too-complicated payment system. This should go into effect October 2013 and will be a sigh of much relief from many of us.

Overall for hospitalists, this should substantially simplify the admitting process, whereby most inpatients being admitted with the anticipation of two or more nights should qualify for an inpatient stay.

A few other anticipated changes that will affect hospitalists include:

Payments for Unfunded Care

Another major change that will go into affect October 2013 is the amount of monies received by hospitals that care for unfunded patients. These payments historically have been made to “Disproportionate Share Hospitals” (DSH), which are hospitals that care for a higher percentage of unfunded patients. Under the Affordable Care Act, only 25% of these payments will be distributed to DSH hospitals; the remaining 75% will be reduced based on the number of uninsured in the U.S., then redistributed to DSH hospitals based on their portion of uninsured care delivered.

Most DSH hospitals should expect a decrease in DSH payments, the amount of which will depend on their share of unfunded patients.

Any reduction in the “bottom line” to the hospital can affect hospitalists, especially those who are directly employed by the hospital.

Hospital-Acquired Conditions

CMS has long had the Hospital-Acquired Condition (HAC) program in effect, which has the ability to reduce the amount of payment for inpatients who acquire a HAC during their hospital stay. Starting in October 2014, CMS will impose additional financial penalties for hospitals with high HAC rates.

Specifically, those hospitals in the highest 25th percentile of HAC rates will be penalized 1% of their overall CMS payments. Another proposed change is that the following be included in the HAC reduction plan (two “domains” of measures):

 

 

  • Domain No. 1: Six of the AHRQ Patient Safety Indicators (PSIs), including pressure ulcers, foreign bodies left in after surgery, iatrogenic pneumothorax, postoperative physiologic or metabolic derangements, postoperative VTE, and accidental puncture/laceration.
  • Domain No. 2: Central-line-associated bloodstream infections (CLABSI) and catheter-associated urinary tract infections (CAUTIs).

The domains will be weighted equally, and an average score will determine the total score. There will be some methodology for risk adjustment, and hospitals will be given a review and comment period to validate their own scores.

Most hospitalists have at least indirect control over many of these HACs,and all need to pay very close attention to their hospital’s rates of these now and in the future.

Readmissions

As we all know, the Hospital Readmission Reduction program went into effect October 2012; it placed 1% of CMS payments at risk. This will increase to 2% of payments as of October 2013. CMS will continue to use AMI, CHF, and pneumonia as the three conditions under which the readmissions are measured but will put in some methodology to account for planned readmissions.

In addition, in October 2014, they plan to add readmission rates for COPD and for hip/knee arthroplasty.

Hospitalists will continue to need to progress their transitions of care programs, at least for these five patients conditions but more likely (and more effectively) for all hospital discharges.

Quality Measures

Currently more than 99% of acute-care hospitals participate in the pay-for-reporting quality program through CMS, the results of which have been displayed on the Hospital Compare website (www.hospitalcompare.hhs.gov) for years. The program started in 2004 with 10 quality metrics and now includes 57 metrics. These include process and outcome measures for AMI, CHF, and pneumonia, as well as process measures for surgical care, HACs, and patient-satisfaction surveys, among others.

This program will continue to expand over time, including hospital-acquired MRSA and Clostridium difficile rates. The few hospitals not participating will have their CMS annual payments reduced by 2%.

EHR Incentives

CMS is evaluating ways to reduce the burden of reporting by aligning EHR incentives with the Inpatient Quality Reporting program.

Summary

After an open commentary period, the Final Rule will be published Aug. 1, and will become effective for discharges on or after Oct. 1. Although CMS will continue to expand the total number of measures that need to be reported, and the penalties for non-reporting or low performance will continue to escalate, CMS is at least attempting to reduce the overall burden of reporting by combining measures and programs over time and using EHRs to facilitate the bulk of reporting over time.

The global message to hospitalists is: Continue to focus on reducing the burden of HACs, enhance throughput, and carefully and thoughtfully transition patients to the next provider after their hospital discharge. All in all, although at times this can feel overwhelming, these changes represent the right direction to move for high-quality and safe patient care.


Dr. Scheurer is a hospitalist and chief quality officer at the Medical University of South Carolina in Charleston. She is physician editor of The Hospitalist. Email her at [email protected].

Reference

  1. Centers for Medicare & Medicaid. Fact Sheets: CMS proposals to improve quality of care during hospital inpatient stays. Centers for Medicare & Medicaid website. Available at: www.cms.gov/apps/media/press/factsheet.asp?Counter=4586&intNumPerPage=10&checkDate=&checkKey=&srchType=1&numDays=3500&srchOpt=0&srchData=&keywordType=All&chkNewsType=6&intPage=&showAll=&pYear=&year=&desc=&cboOrder=date. Accessed May 1, 2013.

The Centers for Medicare & Medicaid Services (CMS) recently released a few Fact Sheets on how they anticipate funding changes on a few of their programs that were implemented (or sustained) under the Affordable Care Act. As a background, CMS pays most acute-care hospitals by prospectively determining payment based on a patient’s diagnosis and the severity of illness within that diagnosis (e.g. “MS-DRG”). These payment amounts are updated annually after evaluating several factors, including the costs associated with the delivery of care.

One of the most major changes described in the Fact Sheet that will affect hospitalists is how CMS will review inpatient stays based on the number of nights in the hospital. CMS has proposed that any patient who stays in the hospital for two or more “midnights” should be appropriate for payment under Medicare Part A. For those who stay in the hospital for only one (or zero) midnights, payment under Medicare Part A will only be appropriate if:

  1. There is sufficient documentation at the time of admission that the anticipated length of stay is two or more nights; and.
  2. Further documentation that circumstances changed, and the hospital stay ended prematurely because of those changes.

Overall for hospitalists, this should substantially simplify the admitting process, whereby most inpatients being admitted with the anticipation of two or more nights should qualify for an inpatient stay. This also reduces the administrative burden of correcting the “inpatient” versus “observation” designation, which keeps many hospital staffs entirely too busy. This change also should relieve a significant burden from the patients and their families, who if kept in observation for a period of time, may have to pay substantially out of pocket to make up for the difference between the cost of the stay and the reimbursement from CMS for observation status. So this is one of the moves that CMS is making to simplify (and not complicate) an already too-complicated payment system. This should go into effect October 2013 and will be a sigh of much relief from many of us.

Overall for hospitalists, this should substantially simplify the admitting process, whereby most inpatients being admitted with the anticipation of two or more nights should qualify for an inpatient stay.

A few other anticipated changes that will affect hospitalists include:

Payments for Unfunded Care

Another major change that will go into affect October 2013 is the amount of monies received by hospitals that care for unfunded patients. These payments historically have been made to “Disproportionate Share Hospitals” (DSH), which are hospitals that care for a higher percentage of unfunded patients. Under the Affordable Care Act, only 25% of these payments will be distributed to DSH hospitals; the remaining 75% will be reduced based on the number of uninsured in the U.S., then redistributed to DSH hospitals based on their portion of uninsured care delivered.

Most DSH hospitals should expect a decrease in DSH payments, the amount of which will depend on their share of unfunded patients.

Any reduction in the “bottom line” to the hospital can affect hospitalists, especially those who are directly employed by the hospital.

Hospital-Acquired Conditions

CMS has long had the Hospital-Acquired Condition (HAC) program in effect, which has the ability to reduce the amount of payment for inpatients who acquire a HAC during their hospital stay. Starting in October 2014, CMS will impose additional financial penalties for hospitals with high HAC rates.

Specifically, those hospitals in the highest 25th percentile of HAC rates will be penalized 1% of their overall CMS payments. Another proposed change is that the following be included in the HAC reduction plan (two “domains” of measures):

 

 

  • Domain No. 1: Six of the AHRQ Patient Safety Indicators (PSIs), including pressure ulcers, foreign bodies left in after surgery, iatrogenic pneumothorax, postoperative physiologic or metabolic derangements, postoperative VTE, and accidental puncture/laceration.
  • Domain No. 2: Central-line-associated bloodstream infections (CLABSI) and catheter-associated urinary tract infections (CAUTIs).

The domains will be weighted equally, and an average score will determine the total score. There will be some methodology for risk adjustment, and hospitals will be given a review and comment period to validate their own scores.

Most hospitalists have at least indirect control over many of these HACs,and all need to pay very close attention to their hospital’s rates of these now and in the future.

Readmissions

As we all know, the Hospital Readmission Reduction program went into effect October 2012; it placed 1% of CMS payments at risk. This will increase to 2% of payments as of October 2013. CMS will continue to use AMI, CHF, and pneumonia as the three conditions under which the readmissions are measured but will put in some methodology to account for planned readmissions.

In addition, in October 2014, they plan to add readmission rates for COPD and for hip/knee arthroplasty.

Hospitalists will continue to need to progress their transitions of care programs, at least for these five patients conditions but more likely (and more effectively) for all hospital discharges.

Quality Measures

Currently more than 99% of acute-care hospitals participate in the pay-for-reporting quality program through CMS, the results of which have been displayed on the Hospital Compare website (www.hospitalcompare.hhs.gov) for years. The program started in 2004 with 10 quality metrics and now includes 57 metrics. These include process and outcome measures for AMI, CHF, and pneumonia, as well as process measures for surgical care, HACs, and patient-satisfaction surveys, among others.

This program will continue to expand over time, including hospital-acquired MRSA and Clostridium difficile rates. The few hospitals not participating will have their CMS annual payments reduced by 2%.

EHR Incentives

CMS is evaluating ways to reduce the burden of reporting by aligning EHR incentives with the Inpatient Quality Reporting program.

Summary

After an open commentary period, the Final Rule will be published Aug. 1, and will become effective for discharges on or after Oct. 1. Although CMS will continue to expand the total number of measures that need to be reported, and the penalties for non-reporting or low performance will continue to escalate, CMS is at least attempting to reduce the overall burden of reporting by combining measures and programs over time and using EHRs to facilitate the bulk of reporting over time.

The global message to hospitalists is: Continue to focus on reducing the burden of HACs, enhance throughput, and carefully and thoughtfully transition patients to the next provider after their hospital discharge. All in all, although at times this can feel overwhelming, these changes represent the right direction to move for high-quality and safe patient care.


Dr. Scheurer is a hospitalist and chief quality officer at the Medical University of South Carolina in Charleston. She is physician editor of The Hospitalist. Email her at [email protected].

Reference

  1. Centers for Medicare & Medicaid. Fact Sheets: CMS proposals to improve quality of care during hospital inpatient stays. Centers for Medicare & Medicaid website. Available at: www.cms.gov/apps/media/press/factsheet.asp?Counter=4586&intNumPerPage=10&checkDate=&checkKey=&srchType=1&numDays=3500&srchOpt=0&srchData=&keywordType=All&chkNewsType=6&intPage=&showAll=&pYear=&year=&desc=&cboOrder=date. Accessed May 1, 2013.
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Steps Hospitalists Should Take to Reduce Turnaround Time of Death Certificates

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Funeral-home representatives sometimes make multiple trips to a hospital or doctor’s office to get a death certificate signed, often waiting in the lobby for hours. I first realized this in the 1980s when starting post-residency practice as a hospitalist. I began asking these guys (they are nearly always men, in my experience) how much time they typically invest getting each certificate signed. They told of walking halfway across a golf course to catch the doctor on the 13th hole or making the 90-minute drive (each way) to a doctor’s office, sometimes finding the doctor had just left, only to repeat the process several times before getting the signature.

When the Clinton administration made electronic signatures via the Internet valid, I thought about starting a business charging funeral homes something like $200 for getting the doctor to sign it electronically within 48 hours. I would use about half of the $200 to provide an incentive for the doctor to sign quickly (sign within 48 hours, and you’ll get a $100 gift card!), then use the rest to fund the company. Since funeral homes probably spend much more than $200 per certificate paying their staff to drive around getting signatures on paper, I thought they would jump at this idea.

I never pursued it, but that doesn’t stop me from loudly proclaiming to friends and family that it was a “can’t-miss” blockbuster Internet business idea. Of course, I never tested that theory, but it makes for fun chest-thumping at parties.

Lack of a death certificate can hold up burial or cremation, and things like life-insurance payouts and estate settlement are delayed. For a grieving family, these things only add to their pain.

A number of states, including Florida, Texas, and others, now have in place online completion of death certificates. Indiana has required use of its online death certificate since 2011; there is no option to use paper. I suspect nearly every state will do the same before long. But that alone won’t ensure timely completion. Doctors and others who complete the certificates need to ensure they respond quickly, something they often fail to do.

It Really Matters

Lack of a death certificate can hold up burial or cremation, and things like life-insurance payouts and estate settlement are delayed. For a grieving family, these things only add to their pain.

I’m aware of a tragic case from a few years ago in which a certificate was passed around to a number of doctors, each of whom thought with some justification that someone else should sign it. It sat in two different mailboxes for many days while the intended recipients were vacationing. All of this delayed the burial, and the poor family had to send updates to loved ones saying, “We don’t know when Dad’s funeral will be.” About three weeks later, the certificate was completed and the funeral held. What a terribly sad story!

Some states have laws governing how quickly certificates must be signed. A thought-provoking 2004 Medical Staff Update from Stanford University says that California requires a signature within 15 hours of death, though I wonder how often this is enforced.

Improving Turnaround Time

There are several things hospitalists could consider to improve timely completion of death certificates:

  • Ensure doctors liberally complete them for one another. Don’t let one doctor’s absence delay, even for a day, getting it completed and signed. This means the “covering” doctor has access to the discharge (death) summary in the medical record.
  • When several doctors in different specialties are caring for a patient at the time of death, nearly any of them could reasonably sign the certificate. It might be appropriate to adopt a policy that whichever doctor (e.g. hospitalist, intensivist, or oncologist) who had contact with the patient and is presented with the certificate should go ahead and sign it rather than passing it along to one of the other specialties, regardless of which served as attending.
  • Consider creating a central access point at your hospital for receipt of death certificates. Ideally, a funeral-home representative can deliver it to one person at the hospital who will do the leg work of getting a doctor to sign it quickly. Delays are likely if the funeral-home representative has to “shop it around” to different departments and physician offices. A hospital staffer should be able to navigate this quickly.
  • Pressure EMR vendors to include some sort of death-certificate functionality in the future. I don’t know if some have it already, but it seems like it shouldn’t be too difficult for an EMR to spit out a prefilled certificate in much the same way e-prescribing works. It could even be delivered electronically to the funeral home.
  • For hospitalists with 24-hour, on-site presence, it could be reasonable to have an on-duty hospitalist complete the certificate at the time of death rather than waiting for the funeral home to initiate the process. This was standard when I was a resident, and it may be a practical approach in many settings.
  • Consider copying one hospital I worked with previously: They created a hospitalist salary bonus for timely completion. I assure you this policy was very effective.
 

 

Follow up on Direct Admissions

In the April 2013 issue, I wrote about the challenges associated with direct admissions (“Hospitalist Workload,” p. 69). I heard from a number of people, including Dr. Rob Young, a talented hospitalist who pointed me to a paper by his colleagues at Northwestern University (Am J Emerg Med. 2012;30(3):432-439). It makes sense that the safety of direct admission is influenced by the patient’s diagnosis, and sepsis patients are safer stopping in the ED first. And it can be tricky to sort all of this out in advance.

Dr. Mujtaba Ali-Khan, a hospitalist practicing in the Houston area, made me aware of the Direct Admission System for Hospitals (DASH), a commercial product he and a colleague have developed. I don’t have any experience with it and so can’t comment on its value, but you can learn more for yourself on YouTube (http://www.youtube.com/watch?v=HUG_vQgKvE0). What a clever idea for them to create a hospital “boarding pass” that the direct-admission patient presents on arrival to the hospital.

—John Nelson, MD, MHM


Dr. Nelson has been a practicing hospitalist since 1988. He is co-founder and past president of SHM, and principal in Nelson Flores Hospital Medicine Consultants. He is co-director for SHM’s “Best Practices in Managing a Hospital Medicine Program” course. Write to him at [email protected].

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Funeral-home representatives sometimes make multiple trips to a hospital or doctor’s office to get a death certificate signed, often waiting in the lobby for hours. I first realized this in the 1980s when starting post-residency practice as a hospitalist. I began asking these guys (they are nearly always men, in my experience) how much time they typically invest getting each certificate signed. They told of walking halfway across a golf course to catch the doctor on the 13th hole or making the 90-minute drive (each way) to a doctor’s office, sometimes finding the doctor had just left, only to repeat the process several times before getting the signature.

When the Clinton administration made electronic signatures via the Internet valid, I thought about starting a business charging funeral homes something like $200 for getting the doctor to sign it electronically within 48 hours. I would use about half of the $200 to provide an incentive for the doctor to sign quickly (sign within 48 hours, and you’ll get a $100 gift card!), then use the rest to fund the company. Since funeral homes probably spend much more than $200 per certificate paying their staff to drive around getting signatures on paper, I thought they would jump at this idea.

I never pursued it, but that doesn’t stop me from loudly proclaiming to friends and family that it was a “can’t-miss” blockbuster Internet business idea. Of course, I never tested that theory, but it makes for fun chest-thumping at parties.

Lack of a death certificate can hold up burial or cremation, and things like life-insurance payouts and estate settlement are delayed. For a grieving family, these things only add to their pain.

A number of states, including Florida, Texas, and others, now have in place online completion of death certificates. Indiana has required use of its online death certificate since 2011; there is no option to use paper. I suspect nearly every state will do the same before long. But that alone won’t ensure timely completion. Doctors and others who complete the certificates need to ensure they respond quickly, something they often fail to do.

It Really Matters

Lack of a death certificate can hold up burial or cremation, and things like life-insurance payouts and estate settlement are delayed. For a grieving family, these things only add to their pain.

I’m aware of a tragic case from a few years ago in which a certificate was passed around to a number of doctors, each of whom thought with some justification that someone else should sign it. It sat in two different mailboxes for many days while the intended recipients were vacationing. All of this delayed the burial, and the poor family had to send updates to loved ones saying, “We don’t know when Dad’s funeral will be.” About three weeks later, the certificate was completed and the funeral held. What a terribly sad story!

Some states have laws governing how quickly certificates must be signed. A thought-provoking 2004 Medical Staff Update from Stanford University says that California requires a signature within 15 hours of death, though I wonder how often this is enforced.

Improving Turnaround Time

There are several things hospitalists could consider to improve timely completion of death certificates:

  • Ensure doctors liberally complete them for one another. Don’t let one doctor’s absence delay, even for a day, getting it completed and signed. This means the “covering” doctor has access to the discharge (death) summary in the medical record.
  • When several doctors in different specialties are caring for a patient at the time of death, nearly any of them could reasonably sign the certificate. It might be appropriate to adopt a policy that whichever doctor (e.g. hospitalist, intensivist, or oncologist) who had contact with the patient and is presented with the certificate should go ahead and sign it rather than passing it along to one of the other specialties, regardless of which served as attending.
  • Consider creating a central access point at your hospital for receipt of death certificates. Ideally, a funeral-home representative can deliver it to one person at the hospital who will do the leg work of getting a doctor to sign it quickly. Delays are likely if the funeral-home representative has to “shop it around” to different departments and physician offices. A hospital staffer should be able to navigate this quickly.
  • Pressure EMR vendors to include some sort of death-certificate functionality in the future. I don’t know if some have it already, but it seems like it shouldn’t be too difficult for an EMR to spit out a prefilled certificate in much the same way e-prescribing works. It could even be delivered electronically to the funeral home.
  • For hospitalists with 24-hour, on-site presence, it could be reasonable to have an on-duty hospitalist complete the certificate at the time of death rather than waiting for the funeral home to initiate the process. This was standard when I was a resident, and it may be a practical approach in many settings.
  • Consider copying one hospital I worked with previously: They created a hospitalist salary bonus for timely completion. I assure you this policy was very effective.
 

 

Follow up on Direct Admissions

In the April 2013 issue, I wrote about the challenges associated with direct admissions (“Hospitalist Workload,” p. 69). I heard from a number of people, including Dr. Rob Young, a talented hospitalist who pointed me to a paper by his colleagues at Northwestern University (Am J Emerg Med. 2012;30(3):432-439). It makes sense that the safety of direct admission is influenced by the patient’s diagnosis, and sepsis patients are safer stopping in the ED first. And it can be tricky to sort all of this out in advance.

Dr. Mujtaba Ali-Khan, a hospitalist practicing in the Houston area, made me aware of the Direct Admission System for Hospitals (DASH), a commercial product he and a colleague have developed. I don’t have any experience with it and so can’t comment on its value, but you can learn more for yourself on YouTube (http://www.youtube.com/watch?v=HUG_vQgKvE0). What a clever idea for them to create a hospital “boarding pass” that the direct-admission patient presents on arrival to the hospital.

—John Nelson, MD, MHM


Dr. Nelson has been a practicing hospitalist since 1988. He is co-founder and past president of SHM, and principal in Nelson Flores Hospital Medicine Consultants. He is co-director for SHM’s “Best Practices in Managing a Hospital Medicine Program” course. Write to him at [email protected].

Funeral-home representatives sometimes make multiple trips to a hospital or doctor’s office to get a death certificate signed, often waiting in the lobby for hours. I first realized this in the 1980s when starting post-residency practice as a hospitalist. I began asking these guys (they are nearly always men, in my experience) how much time they typically invest getting each certificate signed. They told of walking halfway across a golf course to catch the doctor on the 13th hole or making the 90-minute drive (each way) to a doctor’s office, sometimes finding the doctor had just left, only to repeat the process several times before getting the signature.

When the Clinton administration made electronic signatures via the Internet valid, I thought about starting a business charging funeral homes something like $200 for getting the doctor to sign it electronically within 48 hours. I would use about half of the $200 to provide an incentive for the doctor to sign quickly (sign within 48 hours, and you’ll get a $100 gift card!), then use the rest to fund the company. Since funeral homes probably spend much more than $200 per certificate paying their staff to drive around getting signatures on paper, I thought they would jump at this idea.

I never pursued it, but that doesn’t stop me from loudly proclaiming to friends and family that it was a “can’t-miss” blockbuster Internet business idea. Of course, I never tested that theory, but it makes for fun chest-thumping at parties.

Lack of a death certificate can hold up burial or cremation, and things like life-insurance payouts and estate settlement are delayed. For a grieving family, these things only add to their pain.

A number of states, including Florida, Texas, and others, now have in place online completion of death certificates. Indiana has required use of its online death certificate since 2011; there is no option to use paper. I suspect nearly every state will do the same before long. But that alone won’t ensure timely completion. Doctors and others who complete the certificates need to ensure they respond quickly, something they often fail to do.

It Really Matters

Lack of a death certificate can hold up burial or cremation, and things like life-insurance payouts and estate settlement are delayed. For a grieving family, these things only add to their pain.

I’m aware of a tragic case from a few years ago in which a certificate was passed around to a number of doctors, each of whom thought with some justification that someone else should sign it. It sat in two different mailboxes for many days while the intended recipients were vacationing. All of this delayed the burial, and the poor family had to send updates to loved ones saying, “We don’t know when Dad’s funeral will be.” About three weeks later, the certificate was completed and the funeral held. What a terribly sad story!

Some states have laws governing how quickly certificates must be signed. A thought-provoking 2004 Medical Staff Update from Stanford University says that California requires a signature within 15 hours of death, though I wonder how often this is enforced.

Improving Turnaround Time

There are several things hospitalists could consider to improve timely completion of death certificates:

  • Ensure doctors liberally complete them for one another. Don’t let one doctor’s absence delay, even for a day, getting it completed and signed. This means the “covering” doctor has access to the discharge (death) summary in the medical record.
  • When several doctors in different specialties are caring for a patient at the time of death, nearly any of them could reasonably sign the certificate. It might be appropriate to adopt a policy that whichever doctor (e.g. hospitalist, intensivist, or oncologist) who had contact with the patient and is presented with the certificate should go ahead and sign it rather than passing it along to one of the other specialties, regardless of which served as attending.
  • Consider creating a central access point at your hospital for receipt of death certificates. Ideally, a funeral-home representative can deliver it to one person at the hospital who will do the leg work of getting a doctor to sign it quickly. Delays are likely if the funeral-home representative has to “shop it around” to different departments and physician offices. A hospital staffer should be able to navigate this quickly.
  • Pressure EMR vendors to include some sort of death-certificate functionality in the future. I don’t know if some have it already, but it seems like it shouldn’t be too difficult for an EMR to spit out a prefilled certificate in much the same way e-prescribing works. It could even be delivered electronically to the funeral home.
  • For hospitalists with 24-hour, on-site presence, it could be reasonable to have an on-duty hospitalist complete the certificate at the time of death rather than waiting for the funeral home to initiate the process. This was standard when I was a resident, and it may be a practical approach in many settings.
  • Consider copying one hospital I worked with previously: They created a hospitalist salary bonus for timely completion. I assure you this policy was very effective.
 

 

Follow up on Direct Admissions

In the April 2013 issue, I wrote about the challenges associated with direct admissions (“Hospitalist Workload,” p. 69). I heard from a number of people, including Dr. Rob Young, a talented hospitalist who pointed me to a paper by his colleagues at Northwestern University (Am J Emerg Med. 2012;30(3):432-439). It makes sense that the safety of direct admission is influenced by the patient’s diagnosis, and sepsis patients are safer stopping in the ED first. And it can be tricky to sort all of this out in advance.

Dr. Mujtaba Ali-Khan, a hospitalist practicing in the Houston area, made me aware of the Direct Admission System for Hospitals (DASH), a commercial product he and a colleague have developed. I don’t have any experience with it and so can’t comment on its value, but you can learn more for yourself on YouTube (http://www.youtube.com/watch?v=HUG_vQgKvE0). What a clever idea for them to create a hospital “boarding pass” that the direct-admission patient presents on arrival to the hospital.

—John Nelson, MD, MHM


Dr. Nelson has been a practicing hospitalist since 1988. He is co-founder and past president of SHM, and principal in Nelson Flores Hospital Medicine Consultants. He is co-director for SHM’s “Best Practices in Managing a Hospital Medicine Program” course. Write to him at [email protected].

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Hospitalists Should Research Salary Range by Market Before Negotiating a Job Offer

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Dr. Hospitalist

I am a third-year internal-medicine resident and currently looking for a nocturnist opportunity. I have no experience in negotiating a job or salary. When I interview for a job, should I negotiate for salary? How do I know that the salary is correct and what others in the same group are getting? Thanks for the help.

–Santhosh Mannem, New York City

Dr. Hospitalist responds:

Salary discussions are always intriguing, mainly because you won’t really know what everyone else is getting paid. There are several places to get some information. To begin, find out the general salary range for the market in which you want to work. Just because an annual salary might be $240,000 in Emporia, Kan., doesn’t mean a thing if you are looking for a job in Salt Lake City or Seattle. You can use the online resources through SHM (www.hospitalmedicine.org/survey) to paint a pretty good picture of salary by region, but remember that these are ranges only.

When I think of job offers, I like to take total compensation and break it down by category. For example, benefits are not negotiable—your employer cannot vary the health insurance coverage they provide by physician. Still, you need to consider benefits as an important part of the package. A good health insurance plan won’t mean as much to a single physician as it would to one with a family, so consider your individual needs. I strongly encourage you to make a line item for every potential benefit: health, dental, disability, life, continuing medical education (CME), professional dues, retirement plans (potentially with an employer match), malpractice insurance costs, and so on. A job with a “salary” of $300,000 but no benefits would pale in comparison to a job paying $250,000 with full benefits.

Don’t discount the value of benefits; get the numbers and assign a dollar amount. If the group is not being transparent on benefits, walk away.

With strict regard to salary, you probably will get little to no information as to what the rest of the group members are paid. Feel free to ask, but expect some vague answers. Most often, there is a fairly tight convergence of salaries within a given market, and it’s always better to interview for more than one job in the same location. You mentioned that you’d like to work as a nocturnist, which is good. These positions are recruited heavily and tend to command a higher initial salary.

Overall, your ability to negotiate a higher salary is going to be rather limited. However, there is another calculation worth mentioning: You need to find out how much you are being paid per unit of work so you can compare jobs. Here are some of the items to help you figure out a formula that works for you: annual salary, contracted shifts per year/month, pay per shift, admits/census per shift, number of weekends, and potential bonus thresholds. Use these numbers (metrics) to more accurately compare different jobs. There is no magic formula; it just depends on what is important to you, but you will get a much better picture if you combine these metrics with your benefit analysis.

As a nocturnist, I would not expect to hit any productivity metrics. If you are that busy, it’s probably a miserable job. In a business sense, nights almost always lose money.

One thing that can always be negotiated: a signing bonus and/or loan forgiveness. Often, a practice won’t want to continually offer higher starting salaries since eventually this causes wage creep across the practice. However, they can be much more flexible when it comes to “one-time” payments. This keeps the overall salary structure for the practice intact and is usually much more agreeable for your employer. As always, it’s a supply-and-demand issue, but if you are a nocturnist looking at a high-demand area, I would negotiate hard for a signing bonus and maybe even a contract-renewal bonus after your first year.

 

 

It never hurts to get creative, either. I remember negotiating my first job; I offered to sign a two-year contract (instead of one) if they would let me take off six months the first year. They said yes, I did some traveling that first year on my new salary, and I stayed with the practice for 11 years. Don’t get so caught up in salary numbers that you lose sight of what’s really important to you and whether the job would be the right fit.

Good luck and welcome to hospital medicine. You’ll love it.


Do you have a problem or concern that you’d like Dr. Hospitalist to address? Email your questions to [email protected].

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Dr. Hospitalist

I am a third-year internal-medicine resident and currently looking for a nocturnist opportunity. I have no experience in negotiating a job or salary. When I interview for a job, should I negotiate for salary? How do I know that the salary is correct and what others in the same group are getting? Thanks for the help.

–Santhosh Mannem, New York City

Dr. Hospitalist responds:

Salary discussions are always intriguing, mainly because you won’t really know what everyone else is getting paid. There are several places to get some information. To begin, find out the general salary range for the market in which you want to work. Just because an annual salary might be $240,000 in Emporia, Kan., doesn’t mean a thing if you are looking for a job in Salt Lake City or Seattle. You can use the online resources through SHM (www.hospitalmedicine.org/survey) to paint a pretty good picture of salary by region, but remember that these are ranges only.

When I think of job offers, I like to take total compensation and break it down by category. For example, benefits are not negotiable—your employer cannot vary the health insurance coverage they provide by physician. Still, you need to consider benefits as an important part of the package. A good health insurance plan won’t mean as much to a single physician as it would to one with a family, so consider your individual needs. I strongly encourage you to make a line item for every potential benefit: health, dental, disability, life, continuing medical education (CME), professional dues, retirement plans (potentially with an employer match), malpractice insurance costs, and so on. A job with a “salary” of $300,000 but no benefits would pale in comparison to a job paying $250,000 with full benefits.

Don’t discount the value of benefits; get the numbers and assign a dollar amount. If the group is not being transparent on benefits, walk away.

With strict regard to salary, you probably will get little to no information as to what the rest of the group members are paid. Feel free to ask, but expect some vague answers. Most often, there is a fairly tight convergence of salaries within a given market, and it’s always better to interview for more than one job in the same location. You mentioned that you’d like to work as a nocturnist, which is good. These positions are recruited heavily and tend to command a higher initial salary.

Overall, your ability to negotiate a higher salary is going to be rather limited. However, there is another calculation worth mentioning: You need to find out how much you are being paid per unit of work so you can compare jobs. Here are some of the items to help you figure out a formula that works for you: annual salary, contracted shifts per year/month, pay per shift, admits/census per shift, number of weekends, and potential bonus thresholds. Use these numbers (metrics) to more accurately compare different jobs. There is no magic formula; it just depends on what is important to you, but you will get a much better picture if you combine these metrics with your benefit analysis.

As a nocturnist, I would not expect to hit any productivity metrics. If you are that busy, it’s probably a miserable job. In a business sense, nights almost always lose money.

One thing that can always be negotiated: a signing bonus and/or loan forgiveness. Often, a practice won’t want to continually offer higher starting salaries since eventually this causes wage creep across the practice. However, they can be much more flexible when it comes to “one-time” payments. This keeps the overall salary structure for the practice intact and is usually much more agreeable for your employer. As always, it’s a supply-and-demand issue, but if you are a nocturnist looking at a high-demand area, I would negotiate hard for a signing bonus and maybe even a contract-renewal bonus after your first year.

 

 

It never hurts to get creative, either. I remember negotiating my first job; I offered to sign a two-year contract (instead of one) if they would let me take off six months the first year. They said yes, I did some traveling that first year on my new salary, and I stayed with the practice for 11 years. Don’t get so caught up in salary numbers that you lose sight of what’s really important to you and whether the job would be the right fit.

Good luck and welcome to hospital medicine. You’ll love it.


Do you have a problem or concern that you’d like Dr. Hospitalist to address? Email your questions to [email protected].

Dr. Hospitalist

I am a third-year internal-medicine resident and currently looking for a nocturnist opportunity. I have no experience in negotiating a job or salary. When I interview for a job, should I negotiate for salary? How do I know that the salary is correct and what others in the same group are getting? Thanks for the help.

–Santhosh Mannem, New York City

Dr. Hospitalist responds:

Salary discussions are always intriguing, mainly because you won’t really know what everyone else is getting paid. There are several places to get some information. To begin, find out the general salary range for the market in which you want to work. Just because an annual salary might be $240,000 in Emporia, Kan., doesn’t mean a thing if you are looking for a job in Salt Lake City or Seattle. You can use the online resources through SHM (www.hospitalmedicine.org/survey) to paint a pretty good picture of salary by region, but remember that these are ranges only.

When I think of job offers, I like to take total compensation and break it down by category. For example, benefits are not negotiable—your employer cannot vary the health insurance coverage they provide by physician. Still, you need to consider benefits as an important part of the package. A good health insurance plan won’t mean as much to a single physician as it would to one with a family, so consider your individual needs. I strongly encourage you to make a line item for every potential benefit: health, dental, disability, life, continuing medical education (CME), professional dues, retirement plans (potentially with an employer match), malpractice insurance costs, and so on. A job with a “salary” of $300,000 but no benefits would pale in comparison to a job paying $250,000 with full benefits.

Don’t discount the value of benefits; get the numbers and assign a dollar amount. If the group is not being transparent on benefits, walk away.

With strict regard to salary, you probably will get little to no information as to what the rest of the group members are paid. Feel free to ask, but expect some vague answers. Most often, there is a fairly tight convergence of salaries within a given market, and it’s always better to interview for more than one job in the same location. You mentioned that you’d like to work as a nocturnist, which is good. These positions are recruited heavily and tend to command a higher initial salary.

Overall, your ability to negotiate a higher salary is going to be rather limited. However, there is another calculation worth mentioning: You need to find out how much you are being paid per unit of work so you can compare jobs. Here are some of the items to help you figure out a formula that works for you: annual salary, contracted shifts per year/month, pay per shift, admits/census per shift, number of weekends, and potential bonus thresholds. Use these numbers (metrics) to more accurately compare different jobs. There is no magic formula; it just depends on what is important to you, but you will get a much better picture if you combine these metrics with your benefit analysis.

As a nocturnist, I would not expect to hit any productivity metrics. If you are that busy, it’s probably a miserable job. In a business sense, nights almost always lose money.

One thing that can always be negotiated: a signing bonus and/or loan forgiveness. Often, a practice won’t want to continually offer higher starting salaries since eventually this causes wage creep across the practice. However, they can be much more flexible when it comes to “one-time” payments. This keeps the overall salary structure for the practice intact and is usually much more agreeable for your employer. As always, it’s a supply-and-demand issue, but if you are a nocturnist looking at a high-demand area, I would negotiate hard for a signing bonus and maybe even a contract-renewal bonus after your first year.

 

 

It never hurts to get creative, either. I remember negotiating my first job; I offered to sign a two-year contract (instead of one) if they would let me take off six months the first year. They said yes, I did some traveling that first year on my new salary, and I stayed with the practice for 11 years. Don’t get so caught up in salary numbers that you lose sight of what’s really important to you and whether the job would be the right fit.

Good luck and welcome to hospital medicine. You’ll love it.


Do you have a problem or concern that you’d like Dr. Hospitalist to address? Email your questions to [email protected].

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An Encounter With Unflattering Light

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ANSWER
The correct answer is dermatoheliosis (choice “d”), also correctly termed photoaging. This condition manifests as a number of specific skin changes, including the items named (choices “a,” “b,” and “c”)—all of which were present on this patient.

DISCUSSION
The consequences of chronic overexposure to UV radiation constitute the most common reason patients present to dermatology practices in the United States. The bulk of this damage takes decades to appear, by which time patients have forgotten about their earlier sun exposure (in fact, they often deny any exposure) and even the painful sunburns that taught them to avoid the sun in the first place.

In general, the effects of sunburns sustained in childhood or young adulthood do not usually manifest until the patient is in his/her 50s or 60s, although patients who are less sun-tolerant (our definition of “fair”) may show signs of damage considerably earlier.

However, with the popularity of artificial tanning among teenagers (and even preteens in some cases), evidence of sun damage is being seen at younger ages than ever. Basal cell carcinomas, once unheard of in teenagers, are being found with increasing frequency in this age-group. In patients ages 12 to 15, there has been a 100-fold increase in the incidence of melanoma—theorized to be due, in part, to the effects of artificial tanning.

This particular patient is typical of cases in which sun damage was obtained more passively. At one time in the US, having a tan was decidedly unfashionable; it marked one as a member of “the lower classes.” But that all began to change after WWI: Hemlines and hairlines rose, Prohibition created a new generation of drinkers and scofflaws, clothing began to be more revealing, and suddenly it was fashionable for women to shave their legs and get a tan.

About that same time, many men began to ignore the long-held tradition of wearing hats and long sleeves when outside, inevitably tanned, and thus gained approval from the opposite sex. Most went off to war in the 1940s, many to the Pacific theater, where they had even more exposure to the sun.

Following WWII, a great number of these men returned to their jobs as farmers, ranchers, or construction workers. Golfing became the “in” sport during leisure time. It’s this generation we’re seeing now for sun-related pathology. Even if they had been inclined to use it, effective sunscreen was not generally available until the early 1970s.

The patient depicted here has a typical collection of the pre-cancerous sun damage known as dermatoheliosis: solar elastosis, actinic keratoses, telangiectasias, and solar atrophy (which affects the arms more than the face). The latter, along with the effects of wind, heat, cold, smoking, and drinking alcohol, constitute the main causes of extrinsic aging.

TREATMENT
Short of heroic efforts, not much will be done for this patient’s dermatoheliosis. However, he was strongly advised to return to dermatology twice a year to watch for the arrival of the basal cell and squamous cell carcinomas that are almost certainly headed his way.

 

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ANSWER
The correct answer is dermatoheliosis (choice “d”), also correctly termed photoaging. This condition manifests as a number of specific skin changes, including the items named (choices “a,” “b,” and “c”)—all of which were present on this patient.

DISCUSSION
The consequences of chronic overexposure to UV radiation constitute the most common reason patients present to dermatology practices in the United States. The bulk of this damage takes decades to appear, by which time patients have forgotten about their earlier sun exposure (in fact, they often deny any exposure) and even the painful sunburns that taught them to avoid the sun in the first place.

In general, the effects of sunburns sustained in childhood or young adulthood do not usually manifest until the patient is in his/her 50s or 60s, although patients who are less sun-tolerant (our definition of “fair”) may show signs of damage considerably earlier.

However, with the popularity of artificial tanning among teenagers (and even preteens in some cases), evidence of sun damage is being seen at younger ages than ever. Basal cell carcinomas, once unheard of in teenagers, are being found with increasing frequency in this age-group. In patients ages 12 to 15, there has been a 100-fold increase in the incidence of melanoma—theorized to be due, in part, to the effects of artificial tanning.

This particular patient is typical of cases in which sun damage was obtained more passively. At one time in the US, having a tan was decidedly unfashionable; it marked one as a member of “the lower classes.” But that all began to change after WWI: Hemlines and hairlines rose, Prohibition created a new generation of drinkers and scofflaws, clothing began to be more revealing, and suddenly it was fashionable for women to shave their legs and get a tan.

About that same time, many men began to ignore the long-held tradition of wearing hats and long sleeves when outside, inevitably tanned, and thus gained approval from the opposite sex. Most went off to war in the 1940s, many to the Pacific theater, where they had even more exposure to the sun.

Following WWII, a great number of these men returned to their jobs as farmers, ranchers, or construction workers. Golfing became the “in” sport during leisure time. It’s this generation we’re seeing now for sun-related pathology. Even if they had been inclined to use it, effective sunscreen was not generally available until the early 1970s.

The patient depicted here has a typical collection of the pre-cancerous sun damage known as dermatoheliosis: solar elastosis, actinic keratoses, telangiectasias, and solar atrophy (which affects the arms more than the face). The latter, along with the effects of wind, heat, cold, smoking, and drinking alcohol, constitute the main causes of extrinsic aging.

TREATMENT
Short of heroic efforts, not much will be done for this patient’s dermatoheliosis. However, he was strongly advised to return to dermatology twice a year to watch for the arrival of the basal cell and squamous cell carcinomas that are almost certainly headed his way.

 

ANSWER
The correct answer is dermatoheliosis (choice “d”), also correctly termed photoaging. This condition manifests as a number of specific skin changes, including the items named (choices “a,” “b,” and “c”)—all of which were present on this patient.

DISCUSSION
The consequences of chronic overexposure to UV radiation constitute the most common reason patients present to dermatology practices in the United States. The bulk of this damage takes decades to appear, by which time patients have forgotten about their earlier sun exposure (in fact, they often deny any exposure) and even the painful sunburns that taught them to avoid the sun in the first place.

In general, the effects of sunburns sustained in childhood or young adulthood do not usually manifest until the patient is in his/her 50s or 60s, although patients who are less sun-tolerant (our definition of “fair”) may show signs of damage considerably earlier.

However, with the popularity of artificial tanning among teenagers (and even preteens in some cases), evidence of sun damage is being seen at younger ages than ever. Basal cell carcinomas, once unheard of in teenagers, are being found with increasing frequency in this age-group. In patients ages 12 to 15, there has been a 100-fold increase in the incidence of melanoma—theorized to be due, in part, to the effects of artificial tanning.

This particular patient is typical of cases in which sun damage was obtained more passively. At one time in the US, having a tan was decidedly unfashionable; it marked one as a member of “the lower classes.” But that all began to change after WWI: Hemlines and hairlines rose, Prohibition created a new generation of drinkers and scofflaws, clothing began to be more revealing, and suddenly it was fashionable for women to shave their legs and get a tan.

About that same time, many men began to ignore the long-held tradition of wearing hats and long sleeves when outside, inevitably tanned, and thus gained approval from the opposite sex. Most went off to war in the 1940s, many to the Pacific theater, where they had even more exposure to the sun.

Following WWII, a great number of these men returned to their jobs as farmers, ranchers, or construction workers. Golfing became the “in” sport during leisure time. It’s this generation we’re seeing now for sun-related pathology. Even if they had been inclined to use it, effective sunscreen was not generally available until the early 1970s.

The patient depicted here has a typical collection of the pre-cancerous sun damage known as dermatoheliosis: solar elastosis, actinic keratoses, telangiectasias, and solar atrophy (which affects the arms more than the face). The latter, along with the effects of wind, heat, cold, smoking, and drinking alcohol, constitute the main causes of extrinsic aging.

TREATMENT
Short of heroic efforts, not much will be done for this patient’s dermatoheliosis. However, he was strongly advised to return to dermatology twice a year to watch for the arrival of the basal cell and squamous cell carcinomas that are almost certainly headed his way.

 

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During a recent trip, this 77-year-old man stayed in a hotel in which the bathroom lighting was considerably brighter than that at home—allowing him to see a number of skin changes he hadn’t noticed before. As a result, he presents to dermatology for an evaluation. The patient’s forehead, as well as his cheeks and nose, look curiously mottled (pink and white), with a rough, scar-like, pebbly surface that resembles chicken skin. There are also numerous 1- to 3-mm rough, scaly, papular lesions and multiple faint telangiectasias. In sun-exposed areas, such as his hands and arms, the skin is rough, dry, and exceptionally thin, with light and dark color changes; this is in sharp contrast to the relatively pristine texture and uniformly light color of the volar forearms and other areas that are not exposed to the sun. History taking reveals that, as a young man, the patient spent a great deal of time outdoors, both at work and in his free time. He never wore a hat or used any other form of sun protection. Since age 50, he has had several skin cancers removed from his face and back. Despite this, he is not seeing a dermatology provider regularly.

 

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What I wish I'd learned in med school

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You might remember from medical school that psychiatrists use a five Axis system when evaluating patients. (Or at least they used to. The recent fifth edition of the Diagnostic and Statistical Manual of Mental Disorders eliminated the Axis system.)

Axis I refers to psychiatric pathology, such as major depressive disorder, bipolar disorder, or generalized anxiety disorder. Axis II refers to personality disorders, such as borderline personality disorder, narcissistic personality disorder, and obsessive-compulsive personality disorder. Axis III covers the medical conditions that the patient has. Axis IV, quite appropriately, lists social and environmental factors contributing to the pathology. Axis V is the global assessment of function.

This five Axis system at the very least reminds us that the individual is more than just the sum of his or her illnesses. Rather than existing in a vacuum, the individual interacts with the world. The system acknowledges that the individual influences the environment (through Axis V) and is influenced by it (Axis IV).

Though we are not psychiatrists, I do think that rheumatologists are generally attuned to the five Axis system anyway. We may not explicitly identify the axes, but we are most definitely interested in our patients’ level of function and how much support is available to them. We are familiar with depression and anxiety, and we don’t shy away from frank discussions with our patients about their emotional well-being.

But where I find my education lacking is in how to manage patients with Axis II (personality) disorders. And yet, I dare say, this is no less important than the other axes. At the very least, it affects my interaction with the patient.

For example, a patient with newly diagnosed rheumatoid arthritis who also has obsessive-compulsive personality disorder was extremely anxious and perseverated on his risk of lymphoma to the point of sleepless nights and frequent phone calls to me. There are patients with narcissistic personality disorder who feel entitled to special treatment and are unhappy even with standard care. Patients with histrionic personality disorder are emotionally labile and have a tendency toward hyperbole.

Most problematic for me are patients with borderline personality disorder. I meet one or two of them every year. By definition they split the world into absolutes, good and bad. They have a pathologic fear of being abandoned, so they heap you with praises that feel contrived and insincere, yet they will roll their eyeballs and speak disparagingly of your colleagues – mostly a bad sign. They are impulsive, argumentative, and frequently self-destructive. These traits make it difficult to manage their care appropriately, with challenges that run the gamut from potential patient noncompliance to exhausting physician goodwill. But they are patients, and we have a responsibility to provide them with the best possible care.

I envy the physician who can talk to these patients, address their concerns, gain their trust, and still be able to set boundaries and maintain objectivity. No one taught me how to do these things. No one even warned me that I would need to do these things. Truthfully, though, these are skills that cannot be taught effectively in a classroom setting. Rather, in this, as in many other situations, experience is the best teacher.

Dr. Chan practices rheumatology in Pawtucket, R.I.

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You might remember from medical school that psychiatrists use a five Axis system when evaluating patients. (Or at least they used to. The recent fifth edition of the Diagnostic and Statistical Manual of Mental Disorders eliminated the Axis system.)

Axis I refers to psychiatric pathology, such as major depressive disorder, bipolar disorder, or generalized anxiety disorder. Axis II refers to personality disorders, such as borderline personality disorder, narcissistic personality disorder, and obsessive-compulsive personality disorder. Axis III covers the medical conditions that the patient has. Axis IV, quite appropriately, lists social and environmental factors contributing to the pathology. Axis V is the global assessment of function.

This five Axis system at the very least reminds us that the individual is more than just the sum of his or her illnesses. Rather than existing in a vacuum, the individual interacts with the world. The system acknowledges that the individual influences the environment (through Axis V) and is influenced by it (Axis IV).

Though we are not psychiatrists, I do think that rheumatologists are generally attuned to the five Axis system anyway. We may not explicitly identify the axes, but we are most definitely interested in our patients’ level of function and how much support is available to them. We are familiar with depression and anxiety, and we don’t shy away from frank discussions with our patients about their emotional well-being.

But where I find my education lacking is in how to manage patients with Axis II (personality) disorders. And yet, I dare say, this is no less important than the other axes. At the very least, it affects my interaction with the patient.

For example, a patient with newly diagnosed rheumatoid arthritis who also has obsessive-compulsive personality disorder was extremely anxious and perseverated on his risk of lymphoma to the point of sleepless nights and frequent phone calls to me. There are patients with narcissistic personality disorder who feel entitled to special treatment and are unhappy even with standard care. Patients with histrionic personality disorder are emotionally labile and have a tendency toward hyperbole.

Most problematic for me are patients with borderline personality disorder. I meet one or two of them every year. By definition they split the world into absolutes, good and bad. They have a pathologic fear of being abandoned, so they heap you with praises that feel contrived and insincere, yet they will roll their eyeballs and speak disparagingly of your colleagues – mostly a bad sign. They are impulsive, argumentative, and frequently self-destructive. These traits make it difficult to manage their care appropriately, with challenges that run the gamut from potential patient noncompliance to exhausting physician goodwill. But they are patients, and we have a responsibility to provide them with the best possible care.

I envy the physician who can talk to these patients, address their concerns, gain their trust, and still be able to set boundaries and maintain objectivity. No one taught me how to do these things. No one even warned me that I would need to do these things. Truthfully, though, these are skills that cannot be taught effectively in a classroom setting. Rather, in this, as in many other situations, experience is the best teacher.

Dr. Chan practices rheumatology in Pawtucket, R.I.

You might remember from medical school that psychiatrists use a five Axis system when evaluating patients. (Or at least they used to. The recent fifth edition of the Diagnostic and Statistical Manual of Mental Disorders eliminated the Axis system.)

Axis I refers to psychiatric pathology, such as major depressive disorder, bipolar disorder, or generalized anxiety disorder. Axis II refers to personality disorders, such as borderline personality disorder, narcissistic personality disorder, and obsessive-compulsive personality disorder. Axis III covers the medical conditions that the patient has. Axis IV, quite appropriately, lists social and environmental factors contributing to the pathology. Axis V is the global assessment of function.

This five Axis system at the very least reminds us that the individual is more than just the sum of his or her illnesses. Rather than existing in a vacuum, the individual interacts with the world. The system acknowledges that the individual influences the environment (through Axis V) and is influenced by it (Axis IV).

Though we are not psychiatrists, I do think that rheumatologists are generally attuned to the five Axis system anyway. We may not explicitly identify the axes, but we are most definitely interested in our patients’ level of function and how much support is available to them. We are familiar with depression and anxiety, and we don’t shy away from frank discussions with our patients about their emotional well-being.

But where I find my education lacking is in how to manage patients with Axis II (personality) disorders. And yet, I dare say, this is no less important than the other axes. At the very least, it affects my interaction with the patient.

For example, a patient with newly diagnosed rheumatoid arthritis who also has obsessive-compulsive personality disorder was extremely anxious and perseverated on his risk of lymphoma to the point of sleepless nights and frequent phone calls to me. There are patients with narcissistic personality disorder who feel entitled to special treatment and are unhappy even with standard care. Patients with histrionic personality disorder are emotionally labile and have a tendency toward hyperbole.

Most problematic for me are patients with borderline personality disorder. I meet one or two of them every year. By definition they split the world into absolutes, good and bad. They have a pathologic fear of being abandoned, so they heap you with praises that feel contrived and insincere, yet they will roll their eyeballs and speak disparagingly of your colleagues – mostly a bad sign. They are impulsive, argumentative, and frequently self-destructive. These traits make it difficult to manage their care appropriately, with challenges that run the gamut from potential patient noncompliance to exhausting physician goodwill. But they are patients, and we have a responsibility to provide them with the best possible care.

I envy the physician who can talk to these patients, address their concerns, gain their trust, and still be able to set boundaries and maintain objectivity. No one taught me how to do these things. No one even warned me that I would need to do these things. Truthfully, though, these are skills that cannot be taught effectively in a classroom setting. Rather, in this, as in many other situations, experience is the best teacher.

Dr. Chan practices rheumatology in Pawtucket, R.I.

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Anxiety during pregnancy

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What is the best treatment for plant-induced contact dermatitis?

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IT’S UNCLEAR which treatment is best, because there have been no head-to-head comparisons of treatments for Rhus (plant-induced) contact dermatitis. That said, topical high-potency steroids slightly improve pruritus and the appearance of the rash (strength of recommendation [SOR]: B, small cohort studies).

Neither topical pimecrolimus (an immunomodulatory drug) nor jewelweed extract are helpful (SOR: B, 1 small randomized controlled trial [RCT]).
Oral steroids improve symptoms in severe cases (SOR: C, expert opinion).

 

It’s unclear which treatment is best, because there have been no head-to-head comparisons of treatments for Rhus (plant-induced) contact dermatitis. That said, topical high-potency steroids slightly improve pruritus and the appearance of the rash (strength of recommendation [SOR]: B, small cohort studies).

Neither topical pimecrolimus (an immunomodulatory drug) nor jewelweed extract are helpful (SOR: B, 1 small randomized controlled trial [RCT]).

Oral steroids improve symptoms in severe cases (SOR: C, expert opinion).

Evidence summary

Two prospective, self-controlled cohort studies (N=30) showed that high-potency topical steroids improved symptoms associated with artificially induced Rhus dermatitis in a group with a history of that type of dermatitis.

The first study found that 0.05% clobetasol propionate ointment applied twice a day significantly reduced overall vesiculation, erythema, induration, and pruritus compared with the control (P<.05, .01, .01, and .05, respectively).1 Investigators evaluated erythema, induration, and pruritus on a scale of 0 to 3 (absent, mild, moderate, or severe) and graded vesiculation on a similar 0- to 3-point scale (a frank bulla was graded 3). They started treatment at 12, 24, and 48 hours after exposure and followed patients for 14 days. The greatest difference in mean scores—a reduction in vesiculation scores of approximately 1 point—occurred between 2 and 7 days of therapy.

The second study compared improvement in symptoms of Rhus dermatitis with daily application of topical steroids of different potencies and a control ointment.2 Investigators evaluated healing using a 0- to 4-point scale (0=clearing and 4=marked edema, erythema, and vesiculation). They found that lower-potency topical steroids such as 1% hydrocortisone and 0.1% triamcinolone were equivalent to the control ointment, but high-potency (class IV) steroid ointments produced significant improvement in symptoms (by a mean of 1.07 points vs the control ointment; supporting statistics not given).

A systematic review of contact dermatitis treatment and prevention identified 4 “good-quality” RCTs that evaluated effective remedies for nickel-induced allergic contact dermatitis in a predominantly female Caucasian population.3 All found that moderately high-potency topical steroid therapy improved symptoms, but heterogeneity among the studies made it impossible to determine the best agent.

Topical immunomodulatory drugs and jewelweed are no help

In a double-blinded RCT of 12 adults with a history of Rhus dermatitis and a significant reaction to tincture of poison ivy, topical pimecrolimus didn’t improve the duration or severity of symptoms (P=nonsignificant).4

A similar RCT from a dermatology clinic of 10 adults with confirmed sensitivity to poison oak or ivy found that topical jewelweed extract didn’t improve symptoms of artificially induced Rhus dermatitis. Investigators didn’t report P values.5

Oral steroids haven’t been studied

No studies have evaluated the effectiveness of oral steroids for Rhus dermatitis. Expert opinion recommends prednisone (60 mg daily, tapered over 14 days) for severe and widespread cases of poison ivy dermatitis.6,7

Recommendations

The American Academy of Allergy, Asthma, and Immunology and the American College of Allergy, Asthma, and Immunology jointly recommend topical corticosteroids as firstline treatment for localized allergic contact dermatitis. They advise giving systemic corticosteroids for lesions covering more than 20% of body surface area (for example, prednisone 0.5-1 mg/kg per day for 5-7 days, then 50% of the dose for another 5-7 days).6

The American Academy of Dermatology hasn’t issued guidelines on plant-induced dermatitis.

A dermatology textbook states that topical steroids are effective during the early stages of an outbreak, when vesicles and blisters aren’t yet present, and that systemic steroids are extremely effective for severe outbreaks. The authors recommend treating weepy lesions with tepid baths, wet to dry soaks, or calamine lotion to dry the lesions.7

References

1. Vernon HJ, Olsen EA. A controlled trial of clobetasol propionate ointment 0.05% in the treatment of experimentally induced Rhus dermatitis. J Am Acad Dermatol. 1990;23:829-832.

2. Kaidbey KH, Kligman AM. Assay of topical corticosteroids: efficacy of suppression of experimental Rhus dermatitis in humans. Arch Dermatol. 1976;112:808-813.

3. Saary J, Qureshi R, Palda V, et al. A systematic review of contact dermatitis treatment and prevention. J Am Acad Dermatol. 2005;53:845.

4. Amrol D, Keitel D, Hagaman D, et al. Topical pimecrolimus in the treatment of human allergic contact dermatitis. Ann Allergy Asthma Immunol. 2003;91:563-566.

5. Long D, Ballentine NH, Marks JG Jr. Treatment of poison ivy/ oak allergic contact dermatitis with an extract of jewelweed. Am J Contact Dermatol. 1997;8:150-153.

6. American Academy of Allergy, Asthma and Immunology; American College of Allergy, Asthma and Immunology. Contact dermatitis: a practice parameter. Ann Allergy Asthma Immunol. 2006;97(suppl 2):S1-S38.

7. Habif TP. Contact dermatitis and patch testing. In: Habif TP. Clinical Dermatology: A Color Guide to Diagnosis and Therapy. 5th ed. St. Louis, Mo: Mosby; 2010:130-153.

Author and Disclosure Information

Joshua Eaton, MD;
Paul Crawford, MD;
Rita Smith, MLS, MBA

Nellis Family Medicine Residency, Nellis Air Force Base, Nev (Drs. Eaton and Crawford); Wilford Hall Ambulatory Surgical Center, Lackland Air Force Base, Tex (Ms. Smith)

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The Journal of Family Practice - 62(06)
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contact dermatitis; vesiculation; plant-induced; jewelweed; immunomodulatory; Rhus; clobetasol; ointment; erythema; Joshua Eaton; MD; Paul Crawford; MD; Rita Smith; MLS; MBA; Brian Crownover; MD
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Joshua Eaton, MD;
Paul Crawford, MD;
Rita Smith, MLS, MBA

Nellis Family Medicine Residency, Nellis Air Force Base, Nev (Drs. Eaton and Crawford); Wilford Hall Ambulatory Surgical Center, Lackland Air Force Base, Tex (Ms. Smith)

Author and Disclosure Information

Joshua Eaton, MD;
Paul Crawford, MD;
Rita Smith, MLS, MBA

Nellis Family Medicine Residency, Nellis Air Force Base, Nev (Drs. Eaton and Crawford); Wilford Hall Ambulatory Surgical Center, Lackland Air Force Base, Tex (Ms. Smith)

EVIDENCE-BASED ANSWER

IT’S UNCLEAR which treatment is best, because there have been no head-to-head comparisons of treatments for Rhus (plant-induced) contact dermatitis. That said, topical high-potency steroids slightly improve pruritus and the appearance of the rash (strength of recommendation [SOR]: B, small cohort studies).

Neither topical pimecrolimus (an immunomodulatory drug) nor jewelweed extract are helpful (SOR: B, 1 small randomized controlled trial [RCT]).
Oral steroids improve symptoms in severe cases (SOR: C, expert opinion).

 

It’s unclear which treatment is best, because there have been no head-to-head comparisons of treatments for Rhus (plant-induced) contact dermatitis. That said, topical high-potency steroids slightly improve pruritus and the appearance of the rash (strength of recommendation [SOR]: B, small cohort studies).

Neither topical pimecrolimus (an immunomodulatory drug) nor jewelweed extract are helpful (SOR: B, 1 small randomized controlled trial [RCT]).

Oral steroids improve symptoms in severe cases (SOR: C, expert opinion).

Evidence summary

Two prospective, self-controlled cohort studies (N=30) showed that high-potency topical steroids improved symptoms associated with artificially induced Rhus dermatitis in a group with a history of that type of dermatitis.

The first study found that 0.05% clobetasol propionate ointment applied twice a day significantly reduced overall vesiculation, erythema, induration, and pruritus compared with the control (P<.05, .01, .01, and .05, respectively).1 Investigators evaluated erythema, induration, and pruritus on a scale of 0 to 3 (absent, mild, moderate, or severe) and graded vesiculation on a similar 0- to 3-point scale (a frank bulla was graded 3). They started treatment at 12, 24, and 48 hours after exposure and followed patients for 14 days. The greatest difference in mean scores—a reduction in vesiculation scores of approximately 1 point—occurred between 2 and 7 days of therapy.

The second study compared improvement in symptoms of Rhus dermatitis with daily application of topical steroids of different potencies and a control ointment.2 Investigators evaluated healing using a 0- to 4-point scale (0=clearing and 4=marked edema, erythema, and vesiculation). They found that lower-potency topical steroids such as 1% hydrocortisone and 0.1% triamcinolone were equivalent to the control ointment, but high-potency (class IV) steroid ointments produced significant improvement in symptoms (by a mean of 1.07 points vs the control ointment; supporting statistics not given).

A systematic review of contact dermatitis treatment and prevention identified 4 “good-quality” RCTs that evaluated effective remedies for nickel-induced allergic contact dermatitis in a predominantly female Caucasian population.3 All found that moderately high-potency topical steroid therapy improved symptoms, but heterogeneity among the studies made it impossible to determine the best agent.

Topical immunomodulatory drugs and jewelweed are no help

In a double-blinded RCT of 12 adults with a history of Rhus dermatitis and a significant reaction to tincture of poison ivy, topical pimecrolimus didn’t improve the duration or severity of symptoms (P=nonsignificant).4

A similar RCT from a dermatology clinic of 10 adults with confirmed sensitivity to poison oak or ivy found that topical jewelweed extract didn’t improve symptoms of artificially induced Rhus dermatitis. Investigators didn’t report P values.5

Oral steroids haven’t been studied

No studies have evaluated the effectiveness of oral steroids for Rhus dermatitis. Expert opinion recommends prednisone (60 mg daily, tapered over 14 days) for severe and widespread cases of poison ivy dermatitis.6,7

Recommendations

The American Academy of Allergy, Asthma, and Immunology and the American College of Allergy, Asthma, and Immunology jointly recommend topical corticosteroids as firstline treatment for localized allergic contact dermatitis. They advise giving systemic corticosteroids for lesions covering more than 20% of body surface area (for example, prednisone 0.5-1 mg/kg per day for 5-7 days, then 50% of the dose for another 5-7 days).6

The American Academy of Dermatology hasn’t issued guidelines on plant-induced dermatitis.

A dermatology textbook states that topical steroids are effective during the early stages of an outbreak, when vesicles and blisters aren’t yet present, and that systemic steroids are extremely effective for severe outbreaks. The authors recommend treating weepy lesions with tepid baths, wet to dry soaks, or calamine lotion to dry the lesions.7

EVIDENCE-BASED ANSWER

IT’S UNCLEAR which treatment is best, because there have been no head-to-head comparisons of treatments for Rhus (plant-induced) contact dermatitis. That said, topical high-potency steroids slightly improve pruritus and the appearance of the rash (strength of recommendation [SOR]: B, small cohort studies).

Neither topical pimecrolimus (an immunomodulatory drug) nor jewelweed extract are helpful (SOR: B, 1 small randomized controlled trial [RCT]).
Oral steroids improve symptoms in severe cases (SOR: C, expert opinion).

 

It’s unclear which treatment is best, because there have been no head-to-head comparisons of treatments for Rhus (plant-induced) contact dermatitis. That said, topical high-potency steroids slightly improve pruritus and the appearance of the rash (strength of recommendation [SOR]: B, small cohort studies).

Neither topical pimecrolimus (an immunomodulatory drug) nor jewelweed extract are helpful (SOR: B, 1 small randomized controlled trial [RCT]).

Oral steroids improve symptoms in severe cases (SOR: C, expert opinion).

Evidence summary

Two prospective, self-controlled cohort studies (N=30) showed that high-potency topical steroids improved symptoms associated with artificially induced Rhus dermatitis in a group with a history of that type of dermatitis.

The first study found that 0.05% clobetasol propionate ointment applied twice a day significantly reduced overall vesiculation, erythema, induration, and pruritus compared with the control (P<.05, .01, .01, and .05, respectively).1 Investigators evaluated erythema, induration, and pruritus on a scale of 0 to 3 (absent, mild, moderate, or severe) and graded vesiculation on a similar 0- to 3-point scale (a frank bulla was graded 3). They started treatment at 12, 24, and 48 hours after exposure and followed patients for 14 days. The greatest difference in mean scores—a reduction in vesiculation scores of approximately 1 point—occurred between 2 and 7 days of therapy.

The second study compared improvement in symptoms of Rhus dermatitis with daily application of topical steroids of different potencies and a control ointment.2 Investigators evaluated healing using a 0- to 4-point scale (0=clearing and 4=marked edema, erythema, and vesiculation). They found that lower-potency topical steroids such as 1% hydrocortisone and 0.1% triamcinolone were equivalent to the control ointment, but high-potency (class IV) steroid ointments produced significant improvement in symptoms (by a mean of 1.07 points vs the control ointment; supporting statistics not given).

A systematic review of contact dermatitis treatment and prevention identified 4 “good-quality” RCTs that evaluated effective remedies for nickel-induced allergic contact dermatitis in a predominantly female Caucasian population.3 All found that moderately high-potency topical steroid therapy improved symptoms, but heterogeneity among the studies made it impossible to determine the best agent.

Topical immunomodulatory drugs and jewelweed are no help

In a double-blinded RCT of 12 adults with a history of Rhus dermatitis and a significant reaction to tincture of poison ivy, topical pimecrolimus didn’t improve the duration or severity of symptoms (P=nonsignificant).4

A similar RCT from a dermatology clinic of 10 adults with confirmed sensitivity to poison oak or ivy found that topical jewelweed extract didn’t improve symptoms of artificially induced Rhus dermatitis. Investigators didn’t report P values.5

Oral steroids haven’t been studied

No studies have evaluated the effectiveness of oral steroids for Rhus dermatitis. Expert opinion recommends prednisone (60 mg daily, tapered over 14 days) for severe and widespread cases of poison ivy dermatitis.6,7

Recommendations

The American Academy of Allergy, Asthma, and Immunology and the American College of Allergy, Asthma, and Immunology jointly recommend topical corticosteroids as firstline treatment for localized allergic contact dermatitis. They advise giving systemic corticosteroids for lesions covering more than 20% of body surface area (for example, prednisone 0.5-1 mg/kg per day for 5-7 days, then 50% of the dose for another 5-7 days).6

The American Academy of Dermatology hasn’t issued guidelines on plant-induced dermatitis.

A dermatology textbook states that topical steroids are effective during the early stages of an outbreak, when vesicles and blisters aren’t yet present, and that systemic steroids are extremely effective for severe outbreaks. The authors recommend treating weepy lesions with tepid baths, wet to dry soaks, or calamine lotion to dry the lesions.7

References

1. Vernon HJ, Olsen EA. A controlled trial of clobetasol propionate ointment 0.05% in the treatment of experimentally induced Rhus dermatitis. J Am Acad Dermatol. 1990;23:829-832.

2. Kaidbey KH, Kligman AM. Assay of topical corticosteroids: efficacy of suppression of experimental Rhus dermatitis in humans. Arch Dermatol. 1976;112:808-813.

3. Saary J, Qureshi R, Palda V, et al. A systematic review of contact dermatitis treatment and prevention. J Am Acad Dermatol. 2005;53:845.

4. Amrol D, Keitel D, Hagaman D, et al. Topical pimecrolimus in the treatment of human allergic contact dermatitis. Ann Allergy Asthma Immunol. 2003;91:563-566.

5. Long D, Ballentine NH, Marks JG Jr. Treatment of poison ivy/ oak allergic contact dermatitis with an extract of jewelweed. Am J Contact Dermatol. 1997;8:150-153.

6. American Academy of Allergy, Asthma and Immunology; American College of Allergy, Asthma and Immunology. Contact dermatitis: a practice parameter. Ann Allergy Asthma Immunol. 2006;97(suppl 2):S1-S38.

7. Habif TP. Contact dermatitis and patch testing. In: Habif TP. Clinical Dermatology: A Color Guide to Diagnosis and Therapy. 5th ed. St. Louis, Mo: Mosby; 2010:130-153.

References

1. Vernon HJ, Olsen EA. A controlled trial of clobetasol propionate ointment 0.05% in the treatment of experimentally induced Rhus dermatitis. J Am Acad Dermatol. 1990;23:829-832.

2. Kaidbey KH, Kligman AM. Assay of topical corticosteroids: efficacy of suppression of experimental Rhus dermatitis in humans. Arch Dermatol. 1976;112:808-813.

3. Saary J, Qureshi R, Palda V, et al. A systematic review of contact dermatitis treatment and prevention. J Am Acad Dermatol. 2005;53:845.

4. Amrol D, Keitel D, Hagaman D, et al. Topical pimecrolimus in the treatment of human allergic contact dermatitis. Ann Allergy Asthma Immunol. 2003;91:563-566.

5. Long D, Ballentine NH, Marks JG Jr. Treatment of poison ivy/ oak allergic contact dermatitis with an extract of jewelweed. Am J Contact Dermatol. 1997;8:150-153.

6. American Academy of Allergy, Asthma and Immunology; American College of Allergy, Asthma and Immunology. Contact dermatitis: a practice parameter. Ann Allergy Asthma Immunol. 2006;97(suppl 2):S1-S38.

7. Habif TP. Contact dermatitis and patch testing. In: Habif TP. Clinical Dermatology: A Color Guide to Diagnosis and Therapy. 5th ed. St. Louis, Mo: Mosby; 2010:130-153.

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Evidence-based answers from the Family Physicians Inquiries Network

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Recurrent abdominal pain and vomiting

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Recurrent abdominal pain and vomiting

A 32-year-old man presents to the emergency department with excruciating abdominal pain associated with multiple episodes of vomiting for the past 2 days. He reports no fevers, headaches, diarrhea, constipation, hematochezia, melena, musculoskeletal symptoms, or weight loss. His abdominal pain is generalized and crampy. It does not radiate and has no precipitating factors. The pain is relieved only with intravenous narcotics.

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He does not smoke, drink alcohol, or use illicit drugs. He has no known drug or food allergies. He says that his current condition causes him emotional stress that affects his performance at work.

About a year ago, after a complicated surgical procedure, he needed chronic high-dose narcotics. A few months later, he developed multiple bouts of abdominal pain and vomiting that required hospital visits. He now takes oral oxycodone 10–15 mg every 4–6 hours.

On admission, his vital signs are stable, but he is in excruciating pain. He is alert and oriented to person, place, and time. His sclera are anicteric, and the pupils are equal, round, and reactive to light. Lung and heart examinations are normal. The abdomen is soft and nondistended but tender in all four quadrants without guarding; the liver and spleen are not palpable, and no abdominal masses are detected. He has no skin rash, joint swelling or tenderness, or peripheral edema. The neurologic examination is normal. Computed tomography (CT) of the abdomen with contrast shows no signs of bowel obstruction, pancreatic calcifications or edema, cholecystitis, or hepatobiliary disease. Results of initial laboratory testing are shown in Table 1.

1. Based on the information available, which is the least likely cause of his symptoms?

  • Acute pancreatitis
  • Cyclic vomiting syndrome
  • Acute intermittent porphyria
  • Gastroparesis

Acute pancreatitis

Acute pancreatitis is the least likely cause of his symptoms. It is commonly caused by gallstones, alcohol, hypertriglyceridemia, and certain drugs.1 The associated abdominal pain is usually epigastric, radiates to the back, and is accompanied by nausea or vomiting, or both. The onset of pain is sudden and rapidly increases in severity within 30 minutes. CT shows enlargement of the pancreas with diffuse edema, heterogeneity of pancreatic parenchyma, peripancreatic stranding, and peripancreatic fluid collections.1 The diagnosis is based on two of the following three criteria: abdominal pain characteristic of acute pancreatitis; a serum amylase or lipase concentration three or more times the upper limit of normal; and characteristic findings of acute pancreatitis on CT.1

Cyclic vomiting syndrome

Cyclic vomiting syndrome is thought to be caused by episodic dysautonomia, mitochondrial DNA mutations, and hypothalamic emetic response oversensitivity,2–4 but the exact pathogenesis is unknown. The syndrome has been strongly linked to migraine and to the chronic excessive use of cannabinoids.5–9 The Rome III diagnostic criteria10 are the following: the vomiting episodes are stereotypical, ie, they are acute and last for less than 1 week; the patient has had three or more episodes in the previous year; and the patient has no nausea or vomiting between episodes. The patient must meet all three criteria. A history of migraine or a family history of migraine further supports the diagnosis.

Acute intermittent porphyria

Acute intermittent porphyria is characterized by neurovisceral symptoms such as convulsions, paresis, autonomic dysfunction, constipation, and diarrhea that result from the overproduction of porphyrin precursors and deficiency of porphobilinogen deaminase.11

Most patients have poorly localized, severe, steady abdominal pain that develops over hours to days and that may persist for days to weeks.11 Since the pain is neuropathic, abdominal tenderness is usually minimal during an acute attack. Other clues include signs of ileus, such as constipation, nausea, abdominal distention, or decreased bowel sounds; bladder dysfunction, eg, urinary retention, incontinence, or dysuria; reddish-brown urine; and sensory neuropathy of the chest, back, and extremities.11 Blistering skin lesions are usually not seen. The presence of porphobilinogen in the urine confirms the diagnosis.11

Gastroparesis

Gastroparesis is a result of discoordination between the sympathetic and parasympathetic nervous systems, neurons, and smooth muscles within the stomach, causing a decrease in gastric motility. Common causes are diabetes,12 scleroderma,13 and neurologic disorders.14 It can also be iatrogenic,15 resulting from visceral nerve injury and drug treatment with narcotics, calcium channel blockers, muscarinic cholinergic antagonists, or certain antidepressants. Symptoms are related to gastric stasis, ie, abdominal pain from gastric distention, bloating, vomiting, and early satiety.15 Abdominal pain may worsen after eating, and vomitus usually consists of recently ingested food. These patients may have abdominal distension or tenderness and succussion splash. After excluding possible mechanical obstruction, a gastric-emptying study may be necessary to make the diagnosis.15

CASE CONTINUED

A serum and urine drug screen in our patient is positive only for opioids. Urine measures of delta-aminolevulinic acid and porphobilinogen are normal. CT angiography of the abdomen shows no signs of mesenteric vascular occlusion. Esophagogastroduodenoscopy shows antral gastritis, but the esophagus and duodenum appear normal, and colonoscopy is normal as well. Histologic study of biopsy specimens obtained during endoscopy is unrevealing. A gastric-emptying study shows delayed emptying. The patient’s abdominal pain and vomiting persist with the initial dose of intravenous narcotic but resolve with escalating doses. When asked, the patient denies an excessive need for hot baths.

 

 

2. Which is the most likely diagnosis at this point?

  • Narcotic bowel syndrome
  • Opioid withdrawal
  • Crohn disease
  • Chronic pancreatitis
  • Chronic mesenteric ischemia
  • Cannabinoid hyperemesis

Narcotic bowel syndrome

Narcotic bowel syndrome is the most likely diagnosis. Grunkemeier et al16 described it as chronic or frequently recurring abdominal pain that is treated with narcotics, either chronically or acutely with high doses, and that includes all the following features16:

  • The pain worsens or resolves incompletely with continued or increasing doses of narcotics
  • The pain markedly worsens when the narcotic dose is decreased, and decreases when the drug is reinstituted (the “soarand-crash” effect)
  • The frequency, duration, and intensity of the pain episodes gradually increase
  • The nature of the pain and its intensity are not explained by a current or previous gastrointestinal diagnosis.16

This syndrome is common in patients who receive high doses of narcotics for postoperative pain or for other, nonmalignant causes of pain. Patients eventually become dependent on the drugs but are not aware that chronic use activates and facilitates areas in the brain that enhance the perception of pain.16 A study of a rat model of narcotic bowel syndrome17 showed that morphine-induced hyperalgesia depends on central sensitization involving the activation of spinal microglia. This eventually results in concomitant peripheral sensitization involving the colonic mucosal neuroimmune system, and also in central or peripheral activation of opioid kappa-receptors by dynorphin release.17

Patients tend to present with chronic or intermittent colicky abdominal pain that requires escalating doses of narcotics. Eventually, they develop tachyphylaxis and shortened pain-free periods and will require even higher doses of narcotics. This ultimately enhances the perception of pain and worsens opioid bowel symptoms, causing a vicious circle of pain and more narcotic use.16

Laboratory tests are usually normal, and imaging may show only ileus. Gastric emptying may be delayed in patients who have either narcotic bowel syndrome or gastroparesis, but since abdominal pain from narcotic bowel syndrome is a result of central and visceral hypersensitivity, these patients perceive more severe abdominal pain than patients with gastroparesis alone.

Opioid withdrawal

Symptoms of opioid withdrawal may appear as soon as 6 to 24 hours after cessation of the opioid in patients known to be dependent on opioids. These patients present with crampy abdominal pain with nausea.18 Other symptoms include agitation, rhinorrhea, lacrimation, excessive yawning, arthralgias, papillary dilation, and piloerection.18

Our patient did not have the typical signs of opioid withdrawal.

Crohn disease

Crohn disease is a multisystem disorder with specific clinical and pathologic features. It is characterized by focal, asymmetric, transmural, and occasionally granulomatous inflammation primarily affecting the gastrointestinal tract.19 Characteristic symptoms include abdominal pain, chronic diarrhea with or without rectal bleeding, and weight loss. Extraintestinal signs may include anemia and inflammatory changes in the eyes, skin, and joints. The diagnosis is based on endoscopic, radiographic, and pathologic findings.19

Our patient did not have diarrhea or signs of Crohn disease on CT, endoscopy, or histology.

Chronic pancreatitis

Chronic pancreatitis involves progressive inflammatory changes resulting in permanent structural damage to the pancreas and subsequent exocrine and endocrine dysfunction.20 Patients have epigastric abdominal pain that often radiates to the back20; it is associated with eating and is partly relieved with leaning forward. Symptoms of pancreatic insufficiency such as fat malabsorption (resulting in steatorrhea and fat-soluble vitamin deficiency) and diabetes are common. Calcifications within the pancreas on CT suggest chronic pancreatitis.20 Serum lipase and amylase levels may be normal or slightly elevated.20

Our patient’s abdominal pain was not typical of pancreatitis. He had no signs or symptoms of pancreatic insufficiency and no calcifications within the pancreas.

Chronic mesenteric ischemia

Chronic mesenteric ischemia (“intestinal angina”) is caused by a reduction in intestinal blood flow as a result of occlusion, vasospasm, or hypoperfusion of the mesenteric vasculature.21 It is commonly seen in patients who smoke or who have atherosclerotic vascular disease. These patients have chronic dull or crampy abdominal pain that usually occurs within 1 hour after eating.21 To avoid pain, patients avoid eating, resulting in weight loss.21 CT angiography with multi-detector CT is as effective as angiography (the gold standard) in depicting splanchnic arterial anatomy.22

Our patient is young and has no known risk factors for atherosclerosis such as smoking. His abdominal pain is more intermittent than chronic and is not associated with eating.

Cannabinoid hyperemesis

Cannabinoid hyperemesis should be considered in patients with long-term cannabis use presenting with cyclic vomiting, abdominal pain, compulsive use of hot showers, and improvement of symptoms with cannabis cessation.23 Although cannabinoids have been recognized for their antiemetic effects, long-term use may eventually cause autonomic instability and disturbances in the hypothalamic-pituitary-adrenal axis, resulting in cyclic vomiting and thermoregulatory impairment.23

Although our patient presented with multiple episodes of vomiting and abdominal pain, he denied using marijuana, he tested negative for tetrahydrocannabinol, and he did not associate any relief of his symptoms with hot baths.

CASE CONTINUED

Our patient receives intravenous hydration, antiemetics, and a narcotic in tapering intravenous doses, and his symptoms gradually improve. He is discharged from the hospital. However, a few weeks later he is readmitted with the same symptoms of abdominal pain and nausea.

 

 

3. What is the cornerstone of treatment for narcotic bowel syndrome?

  • Establishing a therapeutic relationship
  • Detoxification
  • Supportive management with intravenous fluids, antiemetics, and stool-softeners
  • Medical management with a short-acting narcotic, clonidine, lorazepam, and desipramine

MANAGEMENT OF NARCOTIC BOWEL SYNDROME

An effective therapeutic relationship with the patient is the cornerstone of treatment and should be established before starting detoxification.17 The physician must first learn to accept that the patient’s condition is real and must show genuine empathy as well as provide information about the pathophysiologic basis of the condition, the rationale for withholding narcotics, and the detrimental role narcotics play in the vicious circle of pain.

Detoxification involves gradually withdrawing the narcotic and substituting a nonnarcotic such as an antidepressant for pain control, as well as prescribing a drug such as a benzodiazepine or clonidine to prevent withdrawal symptoms and a laxative to prevent constipation.17,24 The physician must reassure the patient that he or she will not be abandoned in pain and that all medications will be continuously adjusted as needed to keep him or her comfortable throughout the detoxification process.17,24 The physician must continuously gauge the patient’s willingness to continue with treatment and must also be readily available to address the patient’s concerns in a timely manner.17,24 Involving family members and friends may provide additional support to the patient. Referral to a functional gastrointestinal motility program, a pain specialist, and a psychologist may also be considered.17,24 Follow-up care is essential, even after the withdrawal program has ended.17,24

BACK TO THE PATIENT

After successfully establishing a therapeutic relationship and discussing the treatment plan with our patient, we started him on the same dosage of narcotic that he had been receiving, calculated in intravenous morphine equivalents to achieve maximal comfort, and then decreased the dosage by 10% to 33% daily until he was completely off narcotics. An antidepressant and a benzodiazepine were given simultaneously with narcotic tapering. Oral clonidine (0.1–0.4 mg/day) was given after the narcotic dosage was reduced to about half, and polyethylene glycol was given as needed for constipation. The total duration of detoxification was 7 days.

The patient was referred to a psychologist for cognitive-behavioral and relaxation therapy, as well as for encouragement and support. At 6 months, he had had no recurrence of symptoms.

TAKE-HOME MESSAGE

In the United States, the number of patients taking a narcotic for nonmalignant pain is increasing, 25 and physicians should be more aware of complications such as narcotic bowel syndrome.

Narcotic bowel syndrome should be suspected in any patient with prolonged narcotic use presenting with multiple recurrent episodes of abdominal pain after other causes are ruled out.

Establishing a good therapeutic relationship with the patient is the cornerstone of successful treatment. Patients who understand their condition and are willing to be treated tend to have better outcomes.

Supportive treatment, symptom relief, and emotional support during detoxification increase compliance.

References
  1. Banks PA, Freeman ML; Practice Parameters Committee of the American College of Gastroenterology. Practice guidelines in acute pancreatitis. Am J Gastroenterol 2006; 101:23792400.
  2. Boles RG, Adams K, Ito M, Li BU. Maternal inheritance in cyclic vomiting syndrome with neuromuscular disease. Am J Med Genet A 2003; 120A:474482.
  3. Wang Q, Ito M, Adams K, et al. Mitochondrial DNA control region sequence variation in migraine headache and cyclic vomiting syndrome. Am J Med Genet A 2004; 131:5058.
  4. Taché Y. Cyclic vomiting syndrome: the corticotropinreleasing-factor hypothesis. Dig Dis Sci 1999; 44(suppl 8):79S86S.
  5. Withers GD, Silburn SR, Forbes DA. Precipitants and aetiology of cyclic vomiting syndrome. Acta Paediatr 1998; 87:272277.
  6. Whitney HB. Cyclic vomiting. A brief review of this affection as illustrated by a typical case. Arch Pediatr 1898; 15:839845.
  7. Stickler GB. Relationship between cyclic vomiting syndrome and migraine. Clin Pediatr (Phila) 2005; 44:505508.
  8. Li BU, Murray RD, Heitlinger LA, Robbins JL, Hayes JR. Is cyclic vomiting syndrome related to migraine? J Pediatr 1999; 134:567572.
  9. Allen JH, de Moore GM, Heddle R, Twartz JC. Cannabinoid hyperemesis: cyclical hyperemesis in association with chronic cannabis abuse. Gut 2004; 53:15661570.
  10. Rome Foundation. Rome III disorders and diagnostic criteria. http://www.romecriteria.org/criteria/. Accessed February 27, 2013.
  11. Anderson KE, Bloomer JR, Bonkovsky HL, et al. Recommendations for the diagnosis and treatment of the acute porphyrias. Ann Intern Med 2005; 142:439450.
  12. Camilleri M. Clinical practice. Diabetic gastroparesis. N Engl J Med 2007; 356:820829.
  13. Maddern GJ, Horowitz M, Jamieson GG, Chatterton BE, Collins PJ, Roberts-Thomson P. Abnormalities of esophageal and gastric emptying in progressive systemic sclerosis. Gastroenterology 1984; 87:922926.
  14. Jost WH. Gastrointestinal dysfunction in Parkinson’s disease. J Neurol Sci 2010; 289:6973.
  15. Parkman HP, Hasler WL, Fisher RS; American Gastroenterological Association. American Gastroenterological Association technical review on the diagnosis and treatment of gastroparesis. Gastroenterology 2004; 127:15921622.
  16. Grunkemeier DM, Cassara JE, Dalton CB, Drossman DA. The narcotic bowel syndrome: clinical features, pathophysiology, and management. Clin Gastroenterol Hepatol 2007; 5:11261139.
  17. Agostini S, Eutamene H, Cartier C, et al. Evidence of central and peripheral sensitization in a rat model of narcotic bowel-like syndrome. Gastroenterology 2010; 139:553563,563.e1e5.
  18. Nicholls L, Bragaw L, Ruetsch C. Opioid dependence treatment and guidelines. J Manag Care Pharm 2010; 16(1 suppl B):S14S21.
  19. Lichtenstein GR, Hanauer SB, Sandborn WJ; Practice Parameters Committee of American College of Gastroenterology. Management of Crohn’s disease in adults. Am J Gastroenterol 2009; 104:465483.
  20. Steer ML, Waxman I, Freedman S. Chronic pancreatitis. N Engl J Med 1995; 332:14821490.
  21. American Gastroenterological Association Medical Position Statement: guidelines on intestinal ischemia. Gastroenterology 2000; 118:951953.
  22. Savastano S, Teso S, Corrà S, Fantozzi O, Miotto D. Multislice CT angiography of the celiac and superior mesenteric arteries: comparison with arteriographic findings. Radiol Med 2002; 103:456463.
  23. Simonetto DA, Oxentenko AS, Herman ML, Szostek JH. Cannabinoid hyperemesis: a case series of 98 patients. Mayo Clin Proc 2012; 87:114119.
  24. Drossman DA, Morris CB, Edwards H, et al. Diagnosis, characterization, and 3-month outcome after detoxification of 39 patients with narcotic bowel syndrome. Am J Gastroenterol 2012; 107:14261440.
  25. Trescot AM, Boswell MV, Atluri SL, et al. Opioid guidelines in the management of chronic non-cancer pain. Pain Physician 2006; 9:139.
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Maged Rizk, MD
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Address: Markus Agito, MD, Department of Internal Medicine, Akron General Medical Center, 400 Wabash Avenue, Akron, OH 44307; e-mail: [email protected]

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Maged Rizk, MD
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Address: Markus Agito, MD, Department of Internal Medicine, Akron General Medical Center, 400 Wabash Avenue, Akron, OH 44307; e-mail: [email protected]

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Department of Internal Medicine, Akron General Medical Center, Akron, OH

Maged Rizk, MD
Quality Improvement Officer, Digestive Disease Institute, Cleveland Clinic; Assistant Professor, Cleveland Clinic Lerner College of Medicine of Case Western Reserve University, Cleveland, OH

Address: Markus Agito, MD, Department of Internal Medicine, Akron General Medical Center, 400 Wabash Avenue, Akron, OH 44307; e-mail: [email protected]

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A 32-year-old man presents to the emergency department with excruciating abdominal pain associated with multiple episodes of vomiting for the past 2 days. He reports no fevers, headaches, diarrhea, constipation, hematochezia, melena, musculoskeletal symptoms, or weight loss. His abdominal pain is generalized and crampy. It does not radiate and has no precipitating factors. The pain is relieved only with intravenous narcotics.

See related editorial

He does not smoke, drink alcohol, or use illicit drugs. He has no known drug or food allergies. He says that his current condition causes him emotional stress that affects his performance at work.

About a year ago, after a complicated surgical procedure, he needed chronic high-dose narcotics. A few months later, he developed multiple bouts of abdominal pain and vomiting that required hospital visits. He now takes oral oxycodone 10–15 mg every 4–6 hours.

On admission, his vital signs are stable, but he is in excruciating pain. He is alert and oriented to person, place, and time. His sclera are anicteric, and the pupils are equal, round, and reactive to light. Lung and heart examinations are normal. The abdomen is soft and nondistended but tender in all four quadrants without guarding; the liver and spleen are not palpable, and no abdominal masses are detected. He has no skin rash, joint swelling or tenderness, or peripheral edema. The neurologic examination is normal. Computed tomography (CT) of the abdomen with contrast shows no signs of bowel obstruction, pancreatic calcifications or edema, cholecystitis, or hepatobiliary disease. Results of initial laboratory testing are shown in Table 1.

1. Based on the information available, which is the least likely cause of his symptoms?

  • Acute pancreatitis
  • Cyclic vomiting syndrome
  • Acute intermittent porphyria
  • Gastroparesis

Acute pancreatitis

Acute pancreatitis is the least likely cause of his symptoms. It is commonly caused by gallstones, alcohol, hypertriglyceridemia, and certain drugs.1 The associated abdominal pain is usually epigastric, radiates to the back, and is accompanied by nausea or vomiting, or both. The onset of pain is sudden and rapidly increases in severity within 30 minutes. CT shows enlargement of the pancreas with diffuse edema, heterogeneity of pancreatic parenchyma, peripancreatic stranding, and peripancreatic fluid collections.1 The diagnosis is based on two of the following three criteria: abdominal pain characteristic of acute pancreatitis; a serum amylase or lipase concentration three or more times the upper limit of normal; and characteristic findings of acute pancreatitis on CT.1

Cyclic vomiting syndrome

Cyclic vomiting syndrome is thought to be caused by episodic dysautonomia, mitochondrial DNA mutations, and hypothalamic emetic response oversensitivity,2–4 but the exact pathogenesis is unknown. The syndrome has been strongly linked to migraine and to the chronic excessive use of cannabinoids.5–9 The Rome III diagnostic criteria10 are the following: the vomiting episodes are stereotypical, ie, they are acute and last for less than 1 week; the patient has had three or more episodes in the previous year; and the patient has no nausea or vomiting between episodes. The patient must meet all three criteria. A history of migraine or a family history of migraine further supports the diagnosis.

Acute intermittent porphyria

Acute intermittent porphyria is characterized by neurovisceral symptoms such as convulsions, paresis, autonomic dysfunction, constipation, and diarrhea that result from the overproduction of porphyrin precursors and deficiency of porphobilinogen deaminase.11

Most patients have poorly localized, severe, steady abdominal pain that develops over hours to days and that may persist for days to weeks.11 Since the pain is neuropathic, abdominal tenderness is usually minimal during an acute attack. Other clues include signs of ileus, such as constipation, nausea, abdominal distention, or decreased bowel sounds; bladder dysfunction, eg, urinary retention, incontinence, or dysuria; reddish-brown urine; and sensory neuropathy of the chest, back, and extremities.11 Blistering skin lesions are usually not seen. The presence of porphobilinogen in the urine confirms the diagnosis.11

Gastroparesis

Gastroparesis is a result of discoordination between the sympathetic and parasympathetic nervous systems, neurons, and smooth muscles within the stomach, causing a decrease in gastric motility. Common causes are diabetes,12 scleroderma,13 and neurologic disorders.14 It can also be iatrogenic,15 resulting from visceral nerve injury and drug treatment with narcotics, calcium channel blockers, muscarinic cholinergic antagonists, or certain antidepressants. Symptoms are related to gastric stasis, ie, abdominal pain from gastric distention, bloating, vomiting, and early satiety.15 Abdominal pain may worsen after eating, and vomitus usually consists of recently ingested food. These patients may have abdominal distension or tenderness and succussion splash. After excluding possible mechanical obstruction, a gastric-emptying study may be necessary to make the diagnosis.15

CASE CONTINUED

A serum and urine drug screen in our patient is positive only for opioids. Urine measures of delta-aminolevulinic acid and porphobilinogen are normal. CT angiography of the abdomen shows no signs of mesenteric vascular occlusion. Esophagogastroduodenoscopy shows antral gastritis, but the esophagus and duodenum appear normal, and colonoscopy is normal as well. Histologic study of biopsy specimens obtained during endoscopy is unrevealing. A gastric-emptying study shows delayed emptying. The patient’s abdominal pain and vomiting persist with the initial dose of intravenous narcotic but resolve with escalating doses. When asked, the patient denies an excessive need for hot baths.

 

 

2. Which is the most likely diagnosis at this point?

  • Narcotic bowel syndrome
  • Opioid withdrawal
  • Crohn disease
  • Chronic pancreatitis
  • Chronic mesenteric ischemia
  • Cannabinoid hyperemesis

Narcotic bowel syndrome

Narcotic bowel syndrome is the most likely diagnosis. Grunkemeier et al16 described it as chronic or frequently recurring abdominal pain that is treated with narcotics, either chronically or acutely with high doses, and that includes all the following features16:

  • The pain worsens or resolves incompletely with continued or increasing doses of narcotics
  • The pain markedly worsens when the narcotic dose is decreased, and decreases when the drug is reinstituted (the “soarand-crash” effect)
  • The frequency, duration, and intensity of the pain episodes gradually increase
  • The nature of the pain and its intensity are not explained by a current or previous gastrointestinal diagnosis.16

This syndrome is common in patients who receive high doses of narcotics for postoperative pain or for other, nonmalignant causes of pain. Patients eventually become dependent on the drugs but are not aware that chronic use activates and facilitates areas in the brain that enhance the perception of pain.16 A study of a rat model of narcotic bowel syndrome17 showed that morphine-induced hyperalgesia depends on central sensitization involving the activation of spinal microglia. This eventually results in concomitant peripheral sensitization involving the colonic mucosal neuroimmune system, and also in central or peripheral activation of opioid kappa-receptors by dynorphin release.17

Patients tend to present with chronic or intermittent colicky abdominal pain that requires escalating doses of narcotics. Eventually, they develop tachyphylaxis and shortened pain-free periods and will require even higher doses of narcotics. This ultimately enhances the perception of pain and worsens opioid bowel symptoms, causing a vicious circle of pain and more narcotic use.16

Laboratory tests are usually normal, and imaging may show only ileus. Gastric emptying may be delayed in patients who have either narcotic bowel syndrome or gastroparesis, but since abdominal pain from narcotic bowel syndrome is a result of central and visceral hypersensitivity, these patients perceive more severe abdominal pain than patients with gastroparesis alone.

Opioid withdrawal

Symptoms of opioid withdrawal may appear as soon as 6 to 24 hours after cessation of the opioid in patients known to be dependent on opioids. These patients present with crampy abdominal pain with nausea.18 Other symptoms include agitation, rhinorrhea, lacrimation, excessive yawning, arthralgias, papillary dilation, and piloerection.18

Our patient did not have the typical signs of opioid withdrawal.

Crohn disease

Crohn disease is a multisystem disorder with specific clinical and pathologic features. It is characterized by focal, asymmetric, transmural, and occasionally granulomatous inflammation primarily affecting the gastrointestinal tract.19 Characteristic symptoms include abdominal pain, chronic diarrhea with or without rectal bleeding, and weight loss. Extraintestinal signs may include anemia and inflammatory changes in the eyes, skin, and joints. The diagnosis is based on endoscopic, radiographic, and pathologic findings.19

Our patient did not have diarrhea or signs of Crohn disease on CT, endoscopy, or histology.

Chronic pancreatitis

Chronic pancreatitis involves progressive inflammatory changes resulting in permanent structural damage to the pancreas and subsequent exocrine and endocrine dysfunction.20 Patients have epigastric abdominal pain that often radiates to the back20; it is associated with eating and is partly relieved with leaning forward. Symptoms of pancreatic insufficiency such as fat malabsorption (resulting in steatorrhea and fat-soluble vitamin deficiency) and diabetes are common. Calcifications within the pancreas on CT suggest chronic pancreatitis.20 Serum lipase and amylase levels may be normal or slightly elevated.20

Our patient’s abdominal pain was not typical of pancreatitis. He had no signs or symptoms of pancreatic insufficiency and no calcifications within the pancreas.

Chronic mesenteric ischemia

Chronic mesenteric ischemia (“intestinal angina”) is caused by a reduction in intestinal blood flow as a result of occlusion, vasospasm, or hypoperfusion of the mesenteric vasculature.21 It is commonly seen in patients who smoke or who have atherosclerotic vascular disease. These patients have chronic dull or crampy abdominal pain that usually occurs within 1 hour after eating.21 To avoid pain, patients avoid eating, resulting in weight loss.21 CT angiography with multi-detector CT is as effective as angiography (the gold standard) in depicting splanchnic arterial anatomy.22

Our patient is young and has no known risk factors for atherosclerosis such as smoking. His abdominal pain is more intermittent than chronic and is not associated with eating.

Cannabinoid hyperemesis

Cannabinoid hyperemesis should be considered in patients with long-term cannabis use presenting with cyclic vomiting, abdominal pain, compulsive use of hot showers, and improvement of symptoms with cannabis cessation.23 Although cannabinoids have been recognized for their antiemetic effects, long-term use may eventually cause autonomic instability and disturbances in the hypothalamic-pituitary-adrenal axis, resulting in cyclic vomiting and thermoregulatory impairment.23

Although our patient presented with multiple episodes of vomiting and abdominal pain, he denied using marijuana, he tested negative for tetrahydrocannabinol, and he did not associate any relief of his symptoms with hot baths.

CASE CONTINUED

Our patient receives intravenous hydration, antiemetics, and a narcotic in tapering intravenous doses, and his symptoms gradually improve. He is discharged from the hospital. However, a few weeks later he is readmitted with the same symptoms of abdominal pain and nausea.

 

 

3. What is the cornerstone of treatment for narcotic bowel syndrome?

  • Establishing a therapeutic relationship
  • Detoxification
  • Supportive management with intravenous fluids, antiemetics, and stool-softeners
  • Medical management with a short-acting narcotic, clonidine, lorazepam, and desipramine

MANAGEMENT OF NARCOTIC BOWEL SYNDROME

An effective therapeutic relationship with the patient is the cornerstone of treatment and should be established before starting detoxification.17 The physician must first learn to accept that the patient’s condition is real and must show genuine empathy as well as provide information about the pathophysiologic basis of the condition, the rationale for withholding narcotics, and the detrimental role narcotics play in the vicious circle of pain.

Detoxification involves gradually withdrawing the narcotic and substituting a nonnarcotic such as an antidepressant for pain control, as well as prescribing a drug such as a benzodiazepine or clonidine to prevent withdrawal symptoms and a laxative to prevent constipation.17,24 The physician must reassure the patient that he or she will not be abandoned in pain and that all medications will be continuously adjusted as needed to keep him or her comfortable throughout the detoxification process.17,24 The physician must continuously gauge the patient’s willingness to continue with treatment and must also be readily available to address the patient’s concerns in a timely manner.17,24 Involving family members and friends may provide additional support to the patient. Referral to a functional gastrointestinal motility program, a pain specialist, and a psychologist may also be considered.17,24 Follow-up care is essential, even after the withdrawal program has ended.17,24

BACK TO THE PATIENT

After successfully establishing a therapeutic relationship and discussing the treatment plan with our patient, we started him on the same dosage of narcotic that he had been receiving, calculated in intravenous morphine equivalents to achieve maximal comfort, and then decreased the dosage by 10% to 33% daily until he was completely off narcotics. An antidepressant and a benzodiazepine were given simultaneously with narcotic tapering. Oral clonidine (0.1–0.4 mg/day) was given after the narcotic dosage was reduced to about half, and polyethylene glycol was given as needed for constipation. The total duration of detoxification was 7 days.

The patient was referred to a psychologist for cognitive-behavioral and relaxation therapy, as well as for encouragement and support. At 6 months, he had had no recurrence of symptoms.

TAKE-HOME MESSAGE

In the United States, the number of patients taking a narcotic for nonmalignant pain is increasing, 25 and physicians should be more aware of complications such as narcotic bowel syndrome.

Narcotic bowel syndrome should be suspected in any patient with prolonged narcotic use presenting with multiple recurrent episodes of abdominal pain after other causes are ruled out.

Establishing a good therapeutic relationship with the patient is the cornerstone of successful treatment. Patients who understand their condition and are willing to be treated tend to have better outcomes.

Supportive treatment, symptom relief, and emotional support during detoxification increase compliance.

A 32-year-old man presents to the emergency department with excruciating abdominal pain associated with multiple episodes of vomiting for the past 2 days. He reports no fevers, headaches, diarrhea, constipation, hematochezia, melena, musculoskeletal symptoms, or weight loss. His abdominal pain is generalized and crampy. It does not radiate and has no precipitating factors. The pain is relieved only with intravenous narcotics.

See related editorial

He does not smoke, drink alcohol, or use illicit drugs. He has no known drug or food allergies. He says that his current condition causes him emotional stress that affects his performance at work.

About a year ago, after a complicated surgical procedure, he needed chronic high-dose narcotics. A few months later, he developed multiple bouts of abdominal pain and vomiting that required hospital visits. He now takes oral oxycodone 10–15 mg every 4–6 hours.

On admission, his vital signs are stable, but he is in excruciating pain. He is alert and oriented to person, place, and time. His sclera are anicteric, and the pupils are equal, round, and reactive to light. Lung and heart examinations are normal. The abdomen is soft and nondistended but tender in all four quadrants without guarding; the liver and spleen are not palpable, and no abdominal masses are detected. He has no skin rash, joint swelling or tenderness, or peripheral edema. The neurologic examination is normal. Computed tomography (CT) of the abdomen with contrast shows no signs of bowel obstruction, pancreatic calcifications or edema, cholecystitis, or hepatobiliary disease. Results of initial laboratory testing are shown in Table 1.

1. Based on the information available, which is the least likely cause of his symptoms?

  • Acute pancreatitis
  • Cyclic vomiting syndrome
  • Acute intermittent porphyria
  • Gastroparesis

Acute pancreatitis

Acute pancreatitis is the least likely cause of his symptoms. It is commonly caused by gallstones, alcohol, hypertriglyceridemia, and certain drugs.1 The associated abdominal pain is usually epigastric, radiates to the back, and is accompanied by nausea or vomiting, or both. The onset of pain is sudden and rapidly increases in severity within 30 minutes. CT shows enlargement of the pancreas with diffuse edema, heterogeneity of pancreatic parenchyma, peripancreatic stranding, and peripancreatic fluid collections.1 The diagnosis is based on two of the following three criteria: abdominal pain characteristic of acute pancreatitis; a serum amylase or lipase concentration three or more times the upper limit of normal; and characteristic findings of acute pancreatitis on CT.1

Cyclic vomiting syndrome

Cyclic vomiting syndrome is thought to be caused by episodic dysautonomia, mitochondrial DNA mutations, and hypothalamic emetic response oversensitivity,2–4 but the exact pathogenesis is unknown. The syndrome has been strongly linked to migraine and to the chronic excessive use of cannabinoids.5–9 The Rome III diagnostic criteria10 are the following: the vomiting episodes are stereotypical, ie, they are acute and last for less than 1 week; the patient has had three or more episodes in the previous year; and the patient has no nausea or vomiting between episodes. The patient must meet all three criteria. A history of migraine or a family history of migraine further supports the diagnosis.

Acute intermittent porphyria

Acute intermittent porphyria is characterized by neurovisceral symptoms such as convulsions, paresis, autonomic dysfunction, constipation, and diarrhea that result from the overproduction of porphyrin precursors and deficiency of porphobilinogen deaminase.11

Most patients have poorly localized, severe, steady abdominal pain that develops over hours to days and that may persist for days to weeks.11 Since the pain is neuropathic, abdominal tenderness is usually minimal during an acute attack. Other clues include signs of ileus, such as constipation, nausea, abdominal distention, or decreased bowel sounds; bladder dysfunction, eg, urinary retention, incontinence, or dysuria; reddish-brown urine; and sensory neuropathy of the chest, back, and extremities.11 Blistering skin lesions are usually not seen. The presence of porphobilinogen in the urine confirms the diagnosis.11

Gastroparesis

Gastroparesis is a result of discoordination between the sympathetic and parasympathetic nervous systems, neurons, and smooth muscles within the stomach, causing a decrease in gastric motility. Common causes are diabetes,12 scleroderma,13 and neurologic disorders.14 It can also be iatrogenic,15 resulting from visceral nerve injury and drug treatment with narcotics, calcium channel blockers, muscarinic cholinergic antagonists, or certain antidepressants. Symptoms are related to gastric stasis, ie, abdominal pain from gastric distention, bloating, vomiting, and early satiety.15 Abdominal pain may worsen after eating, and vomitus usually consists of recently ingested food. These patients may have abdominal distension or tenderness and succussion splash. After excluding possible mechanical obstruction, a gastric-emptying study may be necessary to make the diagnosis.15

CASE CONTINUED

A serum and urine drug screen in our patient is positive only for opioids. Urine measures of delta-aminolevulinic acid and porphobilinogen are normal. CT angiography of the abdomen shows no signs of mesenteric vascular occlusion. Esophagogastroduodenoscopy shows antral gastritis, but the esophagus and duodenum appear normal, and colonoscopy is normal as well. Histologic study of biopsy specimens obtained during endoscopy is unrevealing. A gastric-emptying study shows delayed emptying. The patient’s abdominal pain and vomiting persist with the initial dose of intravenous narcotic but resolve with escalating doses. When asked, the patient denies an excessive need for hot baths.

 

 

2. Which is the most likely diagnosis at this point?

  • Narcotic bowel syndrome
  • Opioid withdrawal
  • Crohn disease
  • Chronic pancreatitis
  • Chronic mesenteric ischemia
  • Cannabinoid hyperemesis

Narcotic bowel syndrome

Narcotic bowel syndrome is the most likely diagnosis. Grunkemeier et al16 described it as chronic or frequently recurring abdominal pain that is treated with narcotics, either chronically or acutely with high doses, and that includes all the following features16:

  • The pain worsens or resolves incompletely with continued or increasing doses of narcotics
  • The pain markedly worsens when the narcotic dose is decreased, and decreases when the drug is reinstituted (the “soarand-crash” effect)
  • The frequency, duration, and intensity of the pain episodes gradually increase
  • The nature of the pain and its intensity are not explained by a current or previous gastrointestinal diagnosis.16

This syndrome is common in patients who receive high doses of narcotics for postoperative pain or for other, nonmalignant causes of pain. Patients eventually become dependent on the drugs but are not aware that chronic use activates and facilitates areas in the brain that enhance the perception of pain.16 A study of a rat model of narcotic bowel syndrome17 showed that morphine-induced hyperalgesia depends on central sensitization involving the activation of spinal microglia. This eventually results in concomitant peripheral sensitization involving the colonic mucosal neuroimmune system, and also in central or peripheral activation of opioid kappa-receptors by dynorphin release.17

Patients tend to present with chronic or intermittent colicky abdominal pain that requires escalating doses of narcotics. Eventually, they develop tachyphylaxis and shortened pain-free periods and will require even higher doses of narcotics. This ultimately enhances the perception of pain and worsens opioid bowel symptoms, causing a vicious circle of pain and more narcotic use.16

Laboratory tests are usually normal, and imaging may show only ileus. Gastric emptying may be delayed in patients who have either narcotic bowel syndrome or gastroparesis, but since abdominal pain from narcotic bowel syndrome is a result of central and visceral hypersensitivity, these patients perceive more severe abdominal pain than patients with gastroparesis alone.

Opioid withdrawal

Symptoms of opioid withdrawal may appear as soon as 6 to 24 hours after cessation of the opioid in patients known to be dependent on opioids. These patients present with crampy abdominal pain with nausea.18 Other symptoms include agitation, rhinorrhea, lacrimation, excessive yawning, arthralgias, papillary dilation, and piloerection.18

Our patient did not have the typical signs of opioid withdrawal.

Crohn disease

Crohn disease is a multisystem disorder with specific clinical and pathologic features. It is characterized by focal, asymmetric, transmural, and occasionally granulomatous inflammation primarily affecting the gastrointestinal tract.19 Characteristic symptoms include abdominal pain, chronic diarrhea with or without rectal bleeding, and weight loss. Extraintestinal signs may include anemia and inflammatory changes in the eyes, skin, and joints. The diagnosis is based on endoscopic, radiographic, and pathologic findings.19

Our patient did not have diarrhea or signs of Crohn disease on CT, endoscopy, or histology.

Chronic pancreatitis

Chronic pancreatitis involves progressive inflammatory changes resulting in permanent structural damage to the pancreas and subsequent exocrine and endocrine dysfunction.20 Patients have epigastric abdominal pain that often radiates to the back20; it is associated with eating and is partly relieved with leaning forward. Symptoms of pancreatic insufficiency such as fat malabsorption (resulting in steatorrhea and fat-soluble vitamin deficiency) and diabetes are common. Calcifications within the pancreas on CT suggest chronic pancreatitis.20 Serum lipase and amylase levels may be normal or slightly elevated.20

Our patient’s abdominal pain was not typical of pancreatitis. He had no signs or symptoms of pancreatic insufficiency and no calcifications within the pancreas.

Chronic mesenteric ischemia

Chronic mesenteric ischemia (“intestinal angina”) is caused by a reduction in intestinal blood flow as a result of occlusion, vasospasm, or hypoperfusion of the mesenteric vasculature.21 It is commonly seen in patients who smoke or who have atherosclerotic vascular disease. These patients have chronic dull or crampy abdominal pain that usually occurs within 1 hour after eating.21 To avoid pain, patients avoid eating, resulting in weight loss.21 CT angiography with multi-detector CT is as effective as angiography (the gold standard) in depicting splanchnic arterial anatomy.22

Our patient is young and has no known risk factors for atherosclerosis such as smoking. His abdominal pain is more intermittent than chronic and is not associated with eating.

Cannabinoid hyperemesis

Cannabinoid hyperemesis should be considered in patients with long-term cannabis use presenting with cyclic vomiting, abdominal pain, compulsive use of hot showers, and improvement of symptoms with cannabis cessation.23 Although cannabinoids have been recognized for their antiemetic effects, long-term use may eventually cause autonomic instability and disturbances in the hypothalamic-pituitary-adrenal axis, resulting in cyclic vomiting and thermoregulatory impairment.23

Although our patient presented with multiple episodes of vomiting and abdominal pain, he denied using marijuana, he tested negative for tetrahydrocannabinol, and he did not associate any relief of his symptoms with hot baths.

CASE CONTINUED

Our patient receives intravenous hydration, antiemetics, and a narcotic in tapering intravenous doses, and his symptoms gradually improve. He is discharged from the hospital. However, a few weeks later he is readmitted with the same symptoms of abdominal pain and nausea.

 

 

3. What is the cornerstone of treatment for narcotic bowel syndrome?

  • Establishing a therapeutic relationship
  • Detoxification
  • Supportive management with intravenous fluids, antiemetics, and stool-softeners
  • Medical management with a short-acting narcotic, clonidine, lorazepam, and desipramine

MANAGEMENT OF NARCOTIC BOWEL SYNDROME

An effective therapeutic relationship with the patient is the cornerstone of treatment and should be established before starting detoxification.17 The physician must first learn to accept that the patient’s condition is real and must show genuine empathy as well as provide information about the pathophysiologic basis of the condition, the rationale for withholding narcotics, and the detrimental role narcotics play in the vicious circle of pain.

Detoxification involves gradually withdrawing the narcotic and substituting a nonnarcotic such as an antidepressant for pain control, as well as prescribing a drug such as a benzodiazepine or clonidine to prevent withdrawal symptoms and a laxative to prevent constipation.17,24 The physician must reassure the patient that he or she will not be abandoned in pain and that all medications will be continuously adjusted as needed to keep him or her comfortable throughout the detoxification process.17,24 The physician must continuously gauge the patient’s willingness to continue with treatment and must also be readily available to address the patient’s concerns in a timely manner.17,24 Involving family members and friends may provide additional support to the patient. Referral to a functional gastrointestinal motility program, a pain specialist, and a psychologist may also be considered.17,24 Follow-up care is essential, even after the withdrawal program has ended.17,24

BACK TO THE PATIENT

After successfully establishing a therapeutic relationship and discussing the treatment plan with our patient, we started him on the same dosage of narcotic that he had been receiving, calculated in intravenous morphine equivalents to achieve maximal comfort, and then decreased the dosage by 10% to 33% daily until he was completely off narcotics. An antidepressant and a benzodiazepine were given simultaneously with narcotic tapering. Oral clonidine (0.1–0.4 mg/day) was given after the narcotic dosage was reduced to about half, and polyethylene glycol was given as needed for constipation. The total duration of detoxification was 7 days.

The patient was referred to a psychologist for cognitive-behavioral and relaxation therapy, as well as for encouragement and support. At 6 months, he had had no recurrence of symptoms.

TAKE-HOME MESSAGE

In the United States, the number of patients taking a narcotic for nonmalignant pain is increasing, 25 and physicians should be more aware of complications such as narcotic bowel syndrome.

Narcotic bowel syndrome should be suspected in any patient with prolonged narcotic use presenting with multiple recurrent episodes of abdominal pain after other causes are ruled out.

Establishing a good therapeutic relationship with the patient is the cornerstone of successful treatment. Patients who understand their condition and are willing to be treated tend to have better outcomes.

Supportive treatment, symptom relief, and emotional support during detoxification increase compliance.

References
  1. Banks PA, Freeman ML; Practice Parameters Committee of the American College of Gastroenterology. Practice guidelines in acute pancreatitis. Am J Gastroenterol 2006; 101:23792400.
  2. Boles RG, Adams K, Ito M, Li BU. Maternal inheritance in cyclic vomiting syndrome with neuromuscular disease. Am J Med Genet A 2003; 120A:474482.
  3. Wang Q, Ito M, Adams K, et al. Mitochondrial DNA control region sequence variation in migraine headache and cyclic vomiting syndrome. Am J Med Genet A 2004; 131:5058.
  4. Taché Y. Cyclic vomiting syndrome: the corticotropinreleasing-factor hypothesis. Dig Dis Sci 1999; 44(suppl 8):79S86S.
  5. Withers GD, Silburn SR, Forbes DA. Precipitants and aetiology of cyclic vomiting syndrome. Acta Paediatr 1998; 87:272277.
  6. Whitney HB. Cyclic vomiting. A brief review of this affection as illustrated by a typical case. Arch Pediatr 1898; 15:839845.
  7. Stickler GB. Relationship between cyclic vomiting syndrome and migraine. Clin Pediatr (Phila) 2005; 44:505508.
  8. Li BU, Murray RD, Heitlinger LA, Robbins JL, Hayes JR. Is cyclic vomiting syndrome related to migraine? J Pediatr 1999; 134:567572.
  9. Allen JH, de Moore GM, Heddle R, Twartz JC. Cannabinoid hyperemesis: cyclical hyperemesis in association with chronic cannabis abuse. Gut 2004; 53:15661570.
  10. Rome Foundation. Rome III disorders and diagnostic criteria. http://www.romecriteria.org/criteria/. Accessed February 27, 2013.
  11. Anderson KE, Bloomer JR, Bonkovsky HL, et al. Recommendations for the diagnosis and treatment of the acute porphyrias. Ann Intern Med 2005; 142:439450.
  12. Camilleri M. Clinical practice. Diabetic gastroparesis. N Engl J Med 2007; 356:820829.
  13. Maddern GJ, Horowitz M, Jamieson GG, Chatterton BE, Collins PJ, Roberts-Thomson P. Abnormalities of esophageal and gastric emptying in progressive systemic sclerosis. Gastroenterology 1984; 87:922926.
  14. Jost WH. Gastrointestinal dysfunction in Parkinson’s disease. J Neurol Sci 2010; 289:6973.
  15. Parkman HP, Hasler WL, Fisher RS; American Gastroenterological Association. American Gastroenterological Association technical review on the diagnosis and treatment of gastroparesis. Gastroenterology 2004; 127:15921622.
  16. Grunkemeier DM, Cassara JE, Dalton CB, Drossman DA. The narcotic bowel syndrome: clinical features, pathophysiology, and management. Clin Gastroenterol Hepatol 2007; 5:11261139.
  17. Agostini S, Eutamene H, Cartier C, et al. Evidence of central and peripheral sensitization in a rat model of narcotic bowel-like syndrome. Gastroenterology 2010; 139:553563,563.e1e5.
  18. Nicholls L, Bragaw L, Ruetsch C. Opioid dependence treatment and guidelines. J Manag Care Pharm 2010; 16(1 suppl B):S14S21.
  19. Lichtenstein GR, Hanauer SB, Sandborn WJ; Practice Parameters Committee of American College of Gastroenterology. Management of Crohn’s disease in adults. Am J Gastroenterol 2009; 104:465483.
  20. Steer ML, Waxman I, Freedman S. Chronic pancreatitis. N Engl J Med 1995; 332:14821490.
  21. American Gastroenterological Association Medical Position Statement: guidelines on intestinal ischemia. Gastroenterology 2000; 118:951953.
  22. Savastano S, Teso S, Corrà S, Fantozzi O, Miotto D. Multislice CT angiography of the celiac and superior mesenteric arteries: comparison with arteriographic findings. Radiol Med 2002; 103:456463.
  23. Simonetto DA, Oxentenko AS, Herman ML, Szostek JH. Cannabinoid hyperemesis: a case series of 98 patients. Mayo Clin Proc 2012; 87:114119.
  24. Drossman DA, Morris CB, Edwards H, et al. Diagnosis, characterization, and 3-month outcome after detoxification of 39 patients with narcotic bowel syndrome. Am J Gastroenterol 2012; 107:14261440.
  25. Trescot AM, Boswell MV, Atluri SL, et al. Opioid guidelines in the management of chronic non-cancer pain. Pain Physician 2006; 9:139.
References
  1. Banks PA, Freeman ML; Practice Parameters Committee of the American College of Gastroenterology. Practice guidelines in acute pancreatitis. Am J Gastroenterol 2006; 101:23792400.
  2. Boles RG, Adams K, Ito M, Li BU. Maternal inheritance in cyclic vomiting syndrome with neuromuscular disease. Am J Med Genet A 2003; 120A:474482.
  3. Wang Q, Ito M, Adams K, et al. Mitochondrial DNA control region sequence variation in migraine headache and cyclic vomiting syndrome. Am J Med Genet A 2004; 131:5058.
  4. Taché Y. Cyclic vomiting syndrome: the corticotropinreleasing-factor hypothesis. Dig Dis Sci 1999; 44(suppl 8):79S86S.
  5. Withers GD, Silburn SR, Forbes DA. Precipitants and aetiology of cyclic vomiting syndrome. Acta Paediatr 1998; 87:272277.
  6. Whitney HB. Cyclic vomiting. A brief review of this affection as illustrated by a typical case. Arch Pediatr 1898; 15:839845.
  7. Stickler GB. Relationship between cyclic vomiting syndrome and migraine. Clin Pediatr (Phila) 2005; 44:505508.
  8. Li BU, Murray RD, Heitlinger LA, Robbins JL, Hayes JR. Is cyclic vomiting syndrome related to migraine? J Pediatr 1999; 134:567572.
  9. Allen JH, de Moore GM, Heddle R, Twartz JC. Cannabinoid hyperemesis: cyclical hyperemesis in association with chronic cannabis abuse. Gut 2004; 53:15661570.
  10. Rome Foundation. Rome III disorders and diagnostic criteria. http://www.romecriteria.org/criteria/. Accessed February 27, 2013.
  11. Anderson KE, Bloomer JR, Bonkovsky HL, et al. Recommendations for the diagnosis and treatment of the acute porphyrias. Ann Intern Med 2005; 142:439450.
  12. Camilleri M. Clinical practice. Diabetic gastroparesis. N Engl J Med 2007; 356:820829.
  13. Maddern GJ, Horowitz M, Jamieson GG, Chatterton BE, Collins PJ, Roberts-Thomson P. Abnormalities of esophageal and gastric emptying in progressive systemic sclerosis. Gastroenterology 1984; 87:922926.
  14. Jost WH. Gastrointestinal dysfunction in Parkinson’s disease. J Neurol Sci 2010; 289:6973.
  15. Parkman HP, Hasler WL, Fisher RS; American Gastroenterological Association. American Gastroenterological Association technical review on the diagnosis and treatment of gastroparesis. Gastroenterology 2004; 127:15921622.
  16. Grunkemeier DM, Cassara JE, Dalton CB, Drossman DA. The narcotic bowel syndrome: clinical features, pathophysiology, and management. Clin Gastroenterol Hepatol 2007; 5:11261139.
  17. Agostini S, Eutamene H, Cartier C, et al. Evidence of central and peripheral sensitization in a rat model of narcotic bowel-like syndrome. Gastroenterology 2010; 139:553563,563.e1e5.
  18. Nicholls L, Bragaw L, Ruetsch C. Opioid dependence treatment and guidelines. J Manag Care Pharm 2010; 16(1 suppl B):S14S21.
  19. Lichtenstein GR, Hanauer SB, Sandborn WJ; Practice Parameters Committee of American College of Gastroenterology. Management of Crohn’s disease in adults. Am J Gastroenterol 2009; 104:465483.
  20. Steer ML, Waxman I, Freedman S. Chronic pancreatitis. N Engl J Med 1995; 332:14821490.
  21. American Gastroenterological Association Medical Position Statement: guidelines on intestinal ischemia. Gastroenterology 2000; 118:951953.
  22. Savastano S, Teso S, Corrà S, Fantozzi O, Miotto D. Multislice CT angiography of the celiac and superior mesenteric arteries: comparison with arteriographic findings. Radiol Med 2002; 103:456463.
  23. Simonetto DA, Oxentenko AS, Herman ML, Szostek JH. Cannabinoid hyperemesis: a case series of 98 patients. Mayo Clin Proc 2012; 87:114119.
  24. Drossman DA, Morris CB, Edwards H, et al. Diagnosis, characterization, and 3-month outcome after detoxification of 39 patients with narcotic bowel syndrome. Am J Gastroenterol 2012; 107:14261440.
  25. Trescot AM, Boswell MV, Atluri SL, et al. Opioid guidelines in the management of chronic non-cancer pain. Pain Physician 2006; 9:139.
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Postoperative pain: Meeting new expectations

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Postoperative pain: Meeting new expectations

One of the most common questions patients ask when they hear that they need surgery is, “How much pain will I have, and how will you manage it?”

Pain is a common human experience that provokes both fear and anxiety, which in some cases can last a lifetime. The medical community has been slow to meet the challenge of managing it. The US National Institutes of Health states that more than 80% of patients suffer postoperative pain, with fewer than 50% receiving adequate relief.1 Patients have spoken out loudly through the Hospital Consumer Assessment of Healthcare Providers and Systems scores, demonstrating that the issue of inadequate postoperative pain management is real.

See related article

Clearly, as the push to tie reimbursement to patient satisfaction grows, clinicians have both a moral and a financial imperative to address postoperative pain.

The management of acute postoperative pain is evolving, and recognition of acute pain has progressed from considering it an afterthought or nuisance to realizing that improperly or inadequately treated postoperative pain can have a number of adverse effects, including debilitating chronic pain syndromes.2 Inadequately treated pain is also contributing to the calamitous rise in addiction to illegal substances and prescription medications.3 The time has come to take responsibility and meet the expectations of our patients.

OPIOIDS HAVE MAJOR DRAWBACKS

Opioid derivatives are potent analgesics and have been the traditional first-line therapy for pain. “Judicious use of opium” for painful maladies has been a mainstay of Western medicine since the 16th century and was described in writings from Mesopotamia and China more than 2,000 years ago.

The ease of administration of these drugs coupled with their efficacy in managing a broad spectrum of pain syndromes has led to their frequent and widespread use, often, unfortunately, without consideration of the potential for negative short-term and long-term consequences. Headache, drowsiness, and pruritus are common adverse effects. Less common is a slowing of bowel motility, leading to constipation, bloating, or nausea. Additionally, in 5% to 10% of patients, narcotics may actually sensitize the nerves and make bowel-related pain worse. This narcotic bowel syndrome, as discussed by Agito and Rizk in this issue of the Journal, may make the patient uncomfortable and may lead to delays in recovery and hospital discharge.4

Opioid-related respiratory depression is especially devastating in the postoperative period, potentially causing respiratory arrest and death. The frequency of drug-induced respiratory depression and clinically significant adverse outcomes prompted the Anesthesia Patient Safety Foundation (APSF) to declare in 2011, “No patient shall be harmed by opioid-induced respiratory depression.”5 The APSF has recommended using new monitoring technology to enhance detection.

While many clinicians have been moving towards aggressive pain-management practice, hospital infrastructure has not kept pace. It is often ill-equipped to adequately monitor breathing patterns and to alert personnel to the need for rapid intervention. In the 21st century, we need to respond to this challenge with a combination of tools and technology, including improved clinical assessment and monitoring equipment that has proven to save lives in the perioperative setting.

A MULTIMODAL APPROACH IS BEST

Pain management professionals have also been moving from a predominantly opioid-based regimen to a more balanced, multimodal approach. The goal is to effectively treat acute postoperative pain while reducing the use of opioids and increasing the use of nonopioid drugs and alternative therapies for both pain management and convalescence.

Studies have shown the benefits of nonopioid drugs such as nonsteroidal anti-inflammatory drugs, paracetamol (intravenous acetaminophen), antidepressants, antiepileptics, and regional or local anesthetics combined with nontraditional treatments such as Reiki, massage therapy, and deep breathing.6

Each patient’s experience of pain is unique and responds to medications and alternative therapies in a distinctly different manner. We should not assume that one intervention is suitable for every patient. It is more beneficial to individualize treatment based on protocols that target different pain pathways. This may lead to better pain management and patient satisfaction while reducing the incidence of drug overdose and unwanted side effects.

WHAT WE NEED TO DO

Although many health care professionals have the authority to prescribe potent anesthetics and analgesics, we believe that there is a lack of adequate education, supervision, and experience, and this exposes patients to risks of prescription drug overdose.7,8 All medical professionals who provide postoperative care need specific education and training to offer the best care to this vulnerable patient population. This includes specific and more extensive training in the appropriate use of controlled medications before receiving their controlled substance registration from the Drug Enforcement Agency. We must also extend education to patients and family members regarding the dangers of drug abuse and the safe use of prescription drugs.8

Finally, we need to engage and communicate more effectively with our patients, especially when they are in acute pain. How long should a patient expect to remain in pain while waiting for an assessment and intervention? The medical community must commit to rapid and consistent coverage throughout the day for all patients experiencing a new or changing pattern of pain not responding to current therapy. Problems do not end at 5 pm or at a shift change. We need to build a process of timely intervention, perhaps by using a model similar to that of the rapid response and resuscitation team, which has been effective in many institutions. When a patient is in pain, minutes spent waiting for relief seem like an eternity. The empathy we show patients by validating, not minimizing, their pain and by following a defined yet tailored therapeutic intervention may not only improve their physical discomfort, but improve their overall patient experience.

Margo McCaffery, RN, a pioneer in pain management nursing, defined pain as “whatever the experiencing person says it is, existing whenever the experiencing person says it does.”9 We have come a long way from the days when attending staff in the post-anesthesia care unit would routinely declare, “Pain never killed anyone.” As caregivers, we need to become engaged, empathetic, and effective as we meet the challenges of managing acute postoperative pain and improving our patients’ experience and outcomes.

References
  1. Relieving Pain in America. Institute of Medicine 2011. National Academies Press (US). 2011 ISBN-13: 978-0-309-21484-1.
  2. Lamacraft G. The link between acute postoperative pain and chronic pain syndromes. South Afr J Anaesth Analg 2012; 18:4550.
  3. Binyamin R, Trescot AM, Datta S, et al. Opioid complications and side effects. Pain Physician 2008; 11:S105S120.
  4. Grunkemeier DMS, Cassara JE, Dalton CB, Drossman DA. The narcotic bowel syndrome: clinical features, pathophysiology, and management. Clin Gastroenterol Hepatol 2007; 5:11261139.
  5. Anesthesia Patient Safety Foundation. Proceedings of “Essential Monitoring Strategies to Detect Clinically Significant Drug-Induced Respiratory Depression in the Postoperative Period” Conference, 2011. http://www.apsf.org/newsletters/pdf/fall_2011.pdf. Accessed May 13, 2013.
  6. So PS, Jiang JY, Qin Y. Touch therapies for pain relief in adults. Cochrane Database of Systematic Reviews 2008, Issue 4. Art. No.: CD006535. DOI: 10.1002/14651858.CD006535.pub2.
  7. Polydorou S, Gunderson EW, Levin FR. Training physicians to treat substance use disorders. Curr Psychiatry Rep 2008; 10:399404.
  8. CDC Grand Rounds. Prescription Drug Overdoses – a U.S Epidemic MMWR January 13, 2012/61(01);10–13.
  9. McCaffery M, Pasero C. Pain: Clinical Manual. 2nd ed. St. Louis: Mosby, 1999.
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Steven R. Insler, DO
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Michael S. O'Connor, DO, MPH
Department of Cardiothoracic Anesthesiology, Anesthesiology Institute, and Department of Critical Care Medicine, Heart and Vascular Institute, Cleveland Clinic

Address: Steven R. Insler, DO, Cardiothoracic Anesthesiology, J4-331, Cleveland Clinic, 9500 Euclid Avenue, Cleveland, OH 44195; e-mail: [email protected]

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Michael S. O'Connor, DO, MPH
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Address: Steven R. Insler, DO, Cardiothoracic Anesthesiology, J4-331, Cleveland Clinic, 9500 Euclid Avenue, Cleveland, OH 44195; e-mail: [email protected]

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Department of Cardiothoracic Anesthesiology and Department of Outcomes Research, Anesthesiology Institute, and Department of Critical Care Medicine, Heart and Vascular Institute, Cleveland Clinic

Michael S. O'Connor, DO, MPH
Department of Cardiothoracic Anesthesiology, Anesthesiology Institute, and Department of Critical Care Medicine, Heart and Vascular Institute, Cleveland Clinic

Address: Steven R. Insler, DO, Cardiothoracic Anesthesiology, J4-331, Cleveland Clinic, 9500 Euclid Avenue, Cleveland, OH 44195; e-mail: [email protected]

Article PDF
Article PDF

One of the most common questions patients ask when they hear that they need surgery is, “How much pain will I have, and how will you manage it?”

Pain is a common human experience that provokes both fear and anxiety, which in some cases can last a lifetime. The medical community has been slow to meet the challenge of managing it. The US National Institutes of Health states that more than 80% of patients suffer postoperative pain, with fewer than 50% receiving adequate relief.1 Patients have spoken out loudly through the Hospital Consumer Assessment of Healthcare Providers and Systems scores, demonstrating that the issue of inadequate postoperative pain management is real.

See related article

Clearly, as the push to tie reimbursement to patient satisfaction grows, clinicians have both a moral and a financial imperative to address postoperative pain.

The management of acute postoperative pain is evolving, and recognition of acute pain has progressed from considering it an afterthought or nuisance to realizing that improperly or inadequately treated postoperative pain can have a number of adverse effects, including debilitating chronic pain syndromes.2 Inadequately treated pain is also contributing to the calamitous rise in addiction to illegal substances and prescription medications.3 The time has come to take responsibility and meet the expectations of our patients.

OPIOIDS HAVE MAJOR DRAWBACKS

Opioid derivatives are potent analgesics and have been the traditional first-line therapy for pain. “Judicious use of opium” for painful maladies has been a mainstay of Western medicine since the 16th century and was described in writings from Mesopotamia and China more than 2,000 years ago.

The ease of administration of these drugs coupled with their efficacy in managing a broad spectrum of pain syndromes has led to their frequent and widespread use, often, unfortunately, without consideration of the potential for negative short-term and long-term consequences. Headache, drowsiness, and pruritus are common adverse effects. Less common is a slowing of bowel motility, leading to constipation, bloating, or nausea. Additionally, in 5% to 10% of patients, narcotics may actually sensitize the nerves and make bowel-related pain worse. This narcotic bowel syndrome, as discussed by Agito and Rizk in this issue of the Journal, may make the patient uncomfortable and may lead to delays in recovery and hospital discharge.4

Opioid-related respiratory depression is especially devastating in the postoperative period, potentially causing respiratory arrest and death. The frequency of drug-induced respiratory depression and clinically significant adverse outcomes prompted the Anesthesia Patient Safety Foundation (APSF) to declare in 2011, “No patient shall be harmed by opioid-induced respiratory depression.”5 The APSF has recommended using new monitoring technology to enhance detection.

While many clinicians have been moving towards aggressive pain-management practice, hospital infrastructure has not kept pace. It is often ill-equipped to adequately monitor breathing patterns and to alert personnel to the need for rapid intervention. In the 21st century, we need to respond to this challenge with a combination of tools and technology, including improved clinical assessment and monitoring equipment that has proven to save lives in the perioperative setting.

A MULTIMODAL APPROACH IS BEST

Pain management professionals have also been moving from a predominantly opioid-based regimen to a more balanced, multimodal approach. The goal is to effectively treat acute postoperative pain while reducing the use of opioids and increasing the use of nonopioid drugs and alternative therapies for both pain management and convalescence.

Studies have shown the benefits of nonopioid drugs such as nonsteroidal anti-inflammatory drugs, paracetamol (intravenous acetaminophen), antidepressants, antiepileptics, and regional or local anesthetics combined with nontraditional treatments such as Reiki, massage therapy, and deep breathing.6

Each patient’s experience of pain is unique and responds to medications and alternative therapies in a distinctly different manner. We should not assume that one intervention is suitable for every patient. It is more beneficial to individualize treatment based on protocols that target different pain pathways. This may lead to better pain management and patient satisfaction while reducing the incidence of drug overdose and unwanted side effects.

WHAT WE NEED TO DO

Although many health care professionals have the authority to prescribe potent anesthetics and analgesics, we believe that there is a lack of adequate education, supervision, and experience, and this exposes patients to risks of prescription drug overdose.7,8 All medical professionals who provide postoperative care need specific education and training to offer the best care to this vulnerable patient population. This includes specific and more extensive training in the appropriate use of controlled medications before receiving their controlled substance registration from the Drug Enforcement Agency. We must also extend education to patients and family members regarding the dangers of drug abuse and the safe use of prescription drugs.8

Finally, we need to engage and communicate more effectively with our patients, especially when they are in acute pain. How long should a patient expect to remain in pain while waiting for an assessment and intervention? The medical community must commit to rapid and consistent coverage throughout the day for all patients experiencing a new or changing pattern of pain not responding to current therapy. Problems do not end at 5 pm or at a shift change. We need to build a process of timely intervention, perhaps by using a model similar to that of the rapid response and resuscitation team, which has been effective in many institutions. When a patient is in pain, minutes spent waiting for relief seem like an eternity. The empathy we show patients by validating, not minimizing, their pain and by following a defined yet tailored therapeutic intervention may not only improve their physical discomfort, but improve their overall patient experience.

Margo McCaffery, RN, a pioneer in pain management nursing, defined pain as “whatever the experiencing person says it is, existing whenever the experiencing person says it does.”9 We have come a long way from the days when attending staff in the post-anesthesia care unit would routinely declare, “Pain never killed anyone.” As caregivers, we need to become engaged, empathetic, and effective as we meet the challenges of managing acute postoperative pain and improving our patients’ experience and outcomes.

One of the most common questions patients ask when they hear that they need surgery is, “How much pain will I have, and how will you manage it?”

Pain is a common human experience that provokes both fear and anxiety, which in some cases can last a lifetime. The medical community has been slow to meet the challenge of managing it. The US National Institutes of Health states that more than 80% of patients suffer postoperative pain, with fewer than 50% receiving adequate relief.1 Patients have spoken out loudly through the Hospital Consumer Assessment of Healthcare Providers and Systems scores, demonstrating that the issue of inadequate postoperative pain management is real.

See related article

Clearly, as the push to tie reimbursement to patient satisfaction grows, clinicians have both a moral and a financial imperative to address postoperative pain.

The management of acute postoperative pain is evolving, and recognition of acute pain has progressed from considering it an afterthought or nuisance to realizing that improperly or inadequately treated postoperative pain can have a number of adverse effects, including debilitating chronic pain syndromes.2 Inadequately treated pain is also contributing to the calamitous rise in addiction to illegal substances and prescription medications.3 The time has come to take responsibility and meet the expectations of our patients.

OPIOIDS HAVE MAJOR DRAWBACKS

Opioid derivatives are potent analgesics and have been the traditional first-line therapy for pain. “Judicious use of opium” for painful maladies has been a mainstay of Western medicine since the 16th century and was described in writings from Mesopotamia and China more than 2,000 years ago.

The ease of administration of these drugs coupled with their efficacy in managing a broad spectrum of pain syndromes has led to their frequent and widespread use, often, unfortunately, without consideration of the potential for negative short-term and long-term consequences. Headache, drowsiness, and pruritus are common adverse effects. Less common is a slowing of bowel motility, leading to constipation, bloating, or nausea. Additionally, in 5% to 10% of patients, narcotics may actually sensitize the nerves and make bowel-related pain worse. This narcotic bowel syndrome, as discussed by Agito and Rizk in this issue of the Journal, may make the patient uncomfortable and may lead to delays in recovery and hospital discharge.4

Opioid-related respiratory depression is especially devastating in the postoperative period, potentially causing respiratory arrest and death. The frequency of drug-induced respiratory depression and clinically significant adverse outcomes prompted the Anesthesia Patient Safety Foundation (APSF) to declare in 2011, “No patient shall be harmed by opioid-induced respiratory depression.”5 The APSF has recommended using new monitoring technology to enhance detection.

While many clinicians have been moving towards aggressive pain-management practice, hospital infrastructure has not kept pace. It is often ill-equipped to adequately monitor breathing patterns and to alert personnel to the need for rapid intervention. In the 21st century, we need to respond to this challenge with a combination of tools and technology, including improved clinical assessment and monitoring equipment that has proven to save lives in the perioperative setting.

A MULTIMODAL APPROACH IS BEST

Pain management professionals have also been moving from a predominantly opioid-based regimen to a more balanced, multimodal approach. The goal is to effectively treat acute postoperative pain while reducing the use of opioids and increasing the use of nonopioid drugs and alternative therapies for both pain management and convalescence.

Studies have shown the benefits of nonopioid drugs such as nonsteroidal anti-inflammatory drugs, paracetamol (intravenous acetaminophen), antidepressants, antiepileptics, and regional or local anesthetics combined with nontraditional treatments such as Reiki, massage therapy, and deep breathing.6

Each patient’s experience of pain is unique and responds to medications and alternative therapies in a distinctly different manner. We should not assume that one intervention is suitable for every patient. It is more beneficial to individualize treatment based on protocols that target different pain pathways. This may lead to better pain management and patient satisfaction while reducing the incidence of drug overdose and unwanted side effects.

WHAT WE NEED TO DO

Although many health care professionals have the authority to prescribe potent anesthetics and analgesics, we believe that there is a lack of adequate education, supervision, and experience, and this exposes patients to risks of prescription drug overdose.7,8 All medical professionals who provide postoperative care need specific education and training to offer the best care to this vulnerable patient population. This includes specific and more extensive training in the appropriate use of controlled medications before receiving their controlled substance registration from the Drug Enforcement Agency. We must also extend education to patients and family members regarding the dangers of drug abuse and the safe use of prescription drugs.8

Finally, we need to engage and communicate more effectively with our patients, especially when they are in acute pain. How long should a patient expect to remain in pain while waiting for an assessment and intervention? The medical community must commit to rapid and consistent coverage throughout the day for all patients experiencing a new or changing pattern of pain not responding to current therapy. Problems do not end at 5 pm or at a shift change. We need to build a process of timely intervention, perhaps by using a model similar to that of the rapid response and resuscitation team, which has been effective in many institutions. When a patient is in pain, minutes spent waiting for relief seem like an eternity. The empathy we show patients by validating, not minimizing, their pain and by following a defined yet tailored therapeutic intervention may not only improve their physical discomfort, but improve their overall patient experience.

Margo McCaffery, RN, a pioneer in pain management nursing, defined pain as “whatever the experiencing person says it is, existing whenever the experiencing person says it does.”9 We have come a long way from the days when attending staff in the post-anesthesia care unit would routinely declare, “Pain never killed anyone.” As caregivers, we need to become engaged, empathetic, and effective as we meet the challenges of managing acute postoperative pain and improving our patients’ experience and outcomes.

References
  1. Relieving Pain in America. Institute of Medicine 2011. National Academies Press (US). 2011 ISBN-13: 978-0-309-21484-1.
  2. Lamacraft G. The link between acute postoperative pain and chronic pain syndromes. South Afr J Anaesth Analg 2012; 18:4550.
  3. Binyamin R, Trescot AM, Datta S, et al. Opioid complications and side effects. Pain Physician 2008; 11:S105S120.
  4. Grunkemeier DMS, Cassara JE, Dalton CB, Drossman DA. The narcotic bowel syndrome: clinical features, pathophysiology, and management. Clin Gastroenterol Hepatol 2007; 5:11261139.
  5. Anesthesia Patient Safety Foundation. Proceedings of “Essential Monitoring Strategies to Detect Clinically Significant Drug-Induced Respiratory Depression in the Postoperative Period” Conference, 2011. http://www.apsf.org/newsletters/pdf/fall_2011.pdf. Accessed May 13, 2013.
  6. So PS, Jiang JY, Qin Y. Touch therapies for pain relief in adults. Cochrane Database of Systematic Reviews 2008, Issue 4. Art. No.: CD006535. DOI: 10.1002/14651858.CD006535.pub2.
  7. Polydorou S, Gunderson EW, Levin FR. Training physicians to treat substance use disorders. Curr Psychiatry Rep 2008; 10:399404.
  8. CDC Grand Rounds. Prescription Drug Overdoses – a U.S Epidemic MMWR January 13, 2012/61(01);10–13.
  9. McCaffery M, Pasero C. Pain: Clinical Manual. 2nd ed. St. Louis: Mosby, 1999.
References
  1. Relieving Pain in America. Institute of Medicine 2011. National Academies Press (US). 2011 ISBN-13: 978-0-309-21484-1.
  2. Lamacraft G. The link between acute postoperative pain and chronic pain syndromes. South Afr J Anaesth Analg 2012; 18:4550.
  3. Binyamin R, Trescot AM, Datta S, et al. Opioid complications and side effects. Pain Physician 2008; 11:S105S120.
  4. Grunkemeier DMS, Cassara JE, Dalton CB, Drossman DA. The narcotic bowel syndrome: clinical features, pathophysiology, and management. Clin Gastroenterol Hepatol 2007; 5:11261139.
  5. Anesthesia Patient Safety Foundation. Proceedings of “Essential Monitoring Strategies to Detect Clinically Significant Drug-Induced Respiratory Depression in the Postoperative Period” Conference, 2011. http://www.apsf.org/newsletters/pdf/fall_2011.pdf. Accessed May 13, 2013.
  6. So PS, Jiang JY, Qin Y. Touch therapies for pain relief in adults. Cochrane Database of Systematic Reviews 2008, Issue 4. Art. No.: CD006535. DOI: 10.1002/14651858.CD006535.pub2.
  7. Polydorou S, Gunderson EW, Levin FR. Training physicians to treat substance use disorders. Curr Psychiatry Rep 2008; 10:399404.
  8. CDC Grand Rounds. Prescription Drug Overdoses – a U.S Epidemic MMWR January 13, 2012/61(01);10–13.
  9. McCaffery M, Pasero C. Pain: Clinical Manual. 2nd ed. St. Louis: Mosby, 1999.
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