CASE 1 › Lola A is a 28-year-old woman with a history of muscular aches and joint pain throughout her body, fatigue, and mental fogginess. She has been seen by a rheumatologist and has been given a diagnosis of fibromyalgia, but just moved to your town and is establishing care. She is feeling desperate because her pain has worsened and the medication previously prescribed (gabapentin 300 mg tid) is no longer working. She asks to try oxycodone.

CASE 2 › Matt P is a 59-year-old truck driver with severe hip osteoarthritis (OA). His orthopedist recommended against hip replacement at this time because of his young age and a heart condition that makes him high risk. His pain makes sitting for long periods very difficult. He presents to you for help because he is worried he will be unable to continue working.

CASE 3 › Keith B is a 56-year-old construction worker who has been suffering from bouts of back pain for many years. The pain has become more debilitating over time; currently, it is constant, and Mr. B can hardly make it through his work day. He has been getting hydrocodone/acetaminophen from urgent care centers and emergency rooms, but he isn’t sure it is helping and is coming to you to assume his pain management.

Chronic pain (defined as pain >3 months in duration), is a complex, heterogeneous condition affecting an estimated 116 million US adults.¹ Much of the management of chronic pain occurs in primary care settings, placing family physicians (FPs) on the front lines of 2 epidemics: that of chronic pain itself and that of the abuse and misuse of opioid pain medications.

In an effort to improve communication about the risks and benefits of opioid therapy and the safety and effectiveness of pain treatments in general, many professional organizations, health care institutions, and recently the Centers for Disease Control and Prevention,² have published guidelines on the use of opioids for non-malignant chronic pain. With these guidelines in mind—and in light of the latest evidence—we propose the paradigm that follows for the treatment of chronic pain. A critical aspect of this paradigm is determining the pathophysiology underlying a patient’s pain in order to develop a well-rounded, multimodal, evidence-based treatment plan. Detailed here is the application of this approach to the treatment of 3 common chronic pain diagnoses: fibromyalgia, osteoarthritis, and low back pain.

Look to the central and peripheral nervous system

Acute pain begins with activation of peripheral nociceptors at the site of injury. This causes depolarization up the spinal cord and through the brain stem to higher cortical centers where the pain is perceived and localized. Descending neural pathways transport both excitatory and inhibitory information from the brain to the periphery via the spinal cord, which either increases or decreases the perception of pain.³

When damage/injury doesn’t correlate with the perception of pain

Until recently, it was assumed that chronic pain worked much the same way as acute pain and was caused by ongoing nociceptive input in the periphery, but research has shown us that the central nervous system can play a large role in the modulation of nociception. This new understanding comes from the lack of evidence pointing to any pain state in which the degree of nociceptive input correlates with the degree of pain experienced.

With central sensitization, pain is often accompanied by other systemic symptoms such as fatigue—often in the setting of little to no actual stimulation of the peripheral nociceptors.For most patients with chronic pain, regardless of their diagnosis, there is some degree of alteration in the processing of nociceptive signals by the central nervous system contributing to the experience of pain.⁴ This alteration is thought to be the result of peripheral nociceptive signaling persisting past the point of tissue healing, leading to a hypersensitivity of nerve fibers; the fibers then continue to respond to low, or even absent, sensory stimuli.

Central sensitization is the term used when this hypersensitivity develops in the superficial, deep, and ventral cord nerves. When this happens, pain is often accompanied by other systemic symptoms such as fatigue and slowed cognitive processing, often in the setting of little to no actual stimulation of the peripheral nociceptors.³ (For more on this, see “A new paradigm for pain?” J Fam Pract. 2016;65:598-605 or go to http://www.mdedge.com/jfponline/article/111257/pain/new-paradigm-pain.)

TABLE 1⁴ lists the possible mechanisms of pain, which can be broken down into 4 categories: peripheral nociceptive (inflammatory or mechanical), peripheral neuropathic (underlying damage to a peripheral nerve), central (referring to when the central nervous system is the primary entity involved in maintaining the pain), or any combination of the 3.

As pain becomes chronic, multiple mechanisms overlap

It is important to remember that for any single pain diagnosis, there is likely to be—at least initially—a principle underlying mechanism generating the pain. But as the pain becomes chronic, an overlap of multiple mechanisms develops, with central sensitization often playing a more dominant role than peripheral stimulation (regardless of the diagnosis).

For example, in a patient with rheumatoid arthritis (RA), peripheral nociceptive input (in the form of inflammation) is likely the initial mechanism at work, but as time goes on, central processing becomes more involved. The patient may then begin to experience pain that is disproportional to what is generally expected with RA and may develop other somatic symptoms. The diagnosis then becomes pain primarily related to RA with central sensitization, and both need to be addressed in a treatment plan. In rheumatic conditions, comorbid fibromyalgia (indicative of central sensitization) is thought to occur in 15% to 30% of patients.⁵

FPs can utilize the underlying mechanisms to cut across diagnostic labels and tailor treatments to those that are most likely to be effective. For a patient with more prominent peripheral involvement, a procedural intervention such as injections or surgery alone may suffice, whereas a broader approach including psychotherapy, medications, exercise, and other lifestyle interventions may be necessary for a patient with pain caused predominantly by central sensitization.

Addressing both peripheral and central components is essential. One prospective, observational cohort study of more than 600 patients scheduled for unilateral total knee or total hip arthroplasty found that those patients with a higher degree of centralization of pain (as measured by widespread pain index and modified fibromyalgia screening scales⁶) were less likely to report improvement in the affected body part and in overall body pain following the surgery.⁷

There is a high degree of overlap among many of the chronic pain syndromes (fibromyalgia, irritable bowel syndrome, interstitial cystitis, chronic headaches) that have been found to have a central sensitization component.⁸ Providers of primary care are aptly positioned to recognize central sensitization as the underlying pathology and target treatment effectively.

Tailor the treatment plan to the underlying mechanisms of pain

As with any chronic condition, a thorough work-up (complete with history, physical exam, and diagnostic testing, as appropriate) is indicated. In the setting of chronic pain, it’s important to identify both the primary mechanism, as well as secondary factors that may be contributing to the patient’s pain, before developing your treatment plan. These secondary factors may include co-occurring affect disorders,⁹ a history of trauma,¹⁰ poor sleep,¹¹ and tobacco use,¹² among others. A history of trauma, for example, co-exists with many pain syndromes. For these patients, central sensitization is responsible for much of their pain. As a result, traditional cognitive behavioral therapy (CBT) may not be the best option because of its focus on accepting pain as a chronic diagnosis; more trauma-focused treatments such as those dealing in emotional awareness and understanding of the central nervous system’s role in chronic pain need to be considered.¹³

3 common conditions. Below we present evidence-based treatment approaches for 3 conditions that are typically associated with each of the major mechanisms of chronic pain generation: fibromyalgia (a central sensitization cause), OA (a peripheral nociceptive cause), and low back pain (a mixed pain state).

Fibromyalgia: A case of central sensitization

Fibromyalgia is a hallmark diagnosis for those patients in whom central sensitization is the dominant cause of pain. These patients usually present with widespread, diffuse pain, as well as somatic symptoms such as fatigue, memory difficulties, and poor sleep quality.⁸ When explaining the pain mechanism (ie, central sensitization) to patients, it may be useful to use the analogy of a volume control dial that is stuck in the “high” position and can’t be turned down.

Genes, the environment, and neurotransmitters play a role. The origin of the pain amplification process is believed to be multifactorial.

• Genetic factors are thought to contribute to a predisposition for amplification. To date, 5 sets of genes have been implicated in increased sensitivity to pain leading to increased risk of the development of chronic pain during a patient’s lifetime.^14-19
• Environmental factors (eg, early life trauma, physical trauma especially to the trunk, certain infections such as Lyme disease and Epstein-Barr virus, and emotional stress) may trigger or exacerbate symptoms.⁸ Of note: Only about 5% to 10% of people who experience these triggers actually develop a chronic pain state, while the rest regain their baseline health.⁴ This raises the question of whether there is a point during an acute pain episode in which one can intervene and prevent the acute pain from becoming chronic in those at higher risk.⁴
• Imbalances of neurotransmitters (high glutamate;²⁰ low norepinephrine, serotonin,²¹ and gamma-aminobutyric acid [GABA]²²) play a role in central amplification. These substances not only affect sensory transmission, but also control levels of alertness, sleep, mood, and memory.

The diagnostic criteria for fibromyalgia were modified in 2011 to remove the tender point examination and to add in somatic symptoms.⁶ These criteria can be useful in the clinical setting in identifying not only fibromyalgia itself but also the degree of “fibromyalgianess” a patient has, which is an indicator of how large a role the centralization process plays in the maintenance of chronic pain.^23,24

Treatment: Multimodal and patient empowering. Evidence-based treatment options for fibromyalgia, as well as other conditions for which there is a high degree of centralized pain, can be found in TABLE 2.^25-36 Multimodal treatment, with an emphasis on patient knowledge and empowerment, is generally thought to be the most beneficial.^25,37 Treatment should almost always include CBT and exercise/activity therapies,^26,29 which have high degrees of efficacy with few adverse effects.

In terms of medication, centrally-acting agents (tricyclic antidepressants, serotonin norepinephrine reuptake inhibitors [SNRIs], and alpha 2 delta ligands) are the most effective. There is little to no data showing benefit from anti-inflammatories or opioids in the setting of fibromyalgia. There is some data to suggest that combination therapy, for example with an SNRI (milnacipran) and an alpha 2 delta ligand (pregabalin), may provide more benefit than treating with pregabalin alone.³⁸

Identify any factors that might be contributing to your patient's pain, such as co-occurring affect disorders, a history of trauma, poor sleep, or tobacco use.Complementary and alternative therapies (eg, yoga, chiropractic care, acupuncture, massage) are being studied more, and while evidence is only preliminary in terms of efficacy, there is increasing emphasis being placed on the need for patients with chronic pain to shift their treatment expectations to greater acceptance of pain and the need for ongoing self-care.²⁸ (For more advice on managing fibromyalgia, see the related videos at http://bit.ly/2lPEt0f and http://bit.ly/2lmjEcn.)

Osteoarthritis: An example of peripheral nociceptive pain

OA is a condition long thought to be characterized by damage to the cartilage and bone; however, as with many other pain diagnoses, there is frequently little correlation between damage seen on radiographs and the amount of pain that patients experience.

One study analyzed data on almost 7000 patients from the National Health and Nutrition Examination Survey (NHANES I) and found that between 30% and 50% of OA patients with moderate to severe radiographic changes were asymptomatic, and 10% of those with moderate to severe pain had normal radiographs or only mild changes.³⁹ Research is showing that many factors may contribute to this discrepancy, including the typical “wear and tear” of the disease, subacute levels of inflammation that can lead to peripheral sensitization,⁴⁰ and, in some patients, a centralized pain component. The patients with more centralized pain often have pain that is disproportionate to radiographic evidence, as well as more somatic symptoms such as fatigue, sleep disturbance, and memory issues.⁴¹

Treatment should be multimodal and include interventions targeted at halting the progression of damage as well as palliation of pain. All treatment plans for OA should also include exercise, weight reduction, and self-management, in addition to pharmacologic interventions, to reduce both the micro-inflammation and the centralized pain component (when present). Intra-articular injections of various types have been studied with some having more efficacy in pain reduction and functional improvement than others.^42-45 See TABLE 3^42-61 for a summary of evidence-based treatment options.

Low back pain—a mixed pain state

Low back pain (LBP) has been recognized as a mixed pain state for quite some time. While some patients may experience purely nociceptive and/or neuropathic pain, most cases are nonspecific with patients experiencing varying degrees of nociceptive (myofascial low back pain), neuropathic (lumbar radiculopathy), and central sensitization pain.^62,63 Evidence for centralized pain is demonstrated in studies showing hyperalgesia,⁶⁴ augmented central pain processing,⁶⁵ involvement of the emotional brain,⁶⁶ and delayed recovery influenced by poor coping strategies.⁶⁷

When developing a treatment plan for a patient with chronic low back pain, remember that the pain derives from a complex combination of pathophysiologic contributors. Identifying where a patient lies on the pain centralization spectrum can help you tailor treatment.

In one study of 548 patients presenting to a tertiary pain clinic with primary spine pain diagnoses, 42% met diagnostic criteria for fibromyalgia.⁶⁸ Compared to criteria-negative patients, these patients tended to be younger, unemployed, and receiving compensation; they had greater pain intensity, pain interference, and used stronger words to describe their neuropathic pain; they also had higher levels of depression/anxiety and a lower level of physical function.

Because low back pain is a condition with high prevalence and associated disability, many clinical boards have created guidelines for management. These guidelines tend to vary in the strength of evidence used, and the extent to which they are followed in clinical practice remains largely unknown. Recommendations frequently discourage the use of ultrasound/electrotherapy, but many encourage short-term use of medications (see “How effective are opioids for chronic low back pain?” J Fam Pract. 2015;64:584-584), supervised exercise therapy, CBT, and multidisciplinary treatment.

Guidelines tend to differ most widely with regard to recommendations for spinal manipulation and specific drug therapies.⁶⁹ The classes of drugs that may be most useful when centralized pain is present include the SNRIs and the alpha 2 delta calcium channel ligands.⁴ See TABLE 4^70-89 for a summary of evidence-based treatment options.

CASE 1 › Ms. A is started on amitriptyline 25 mg at bedtime, which improves her fatigue and cognitive symptoms. During monthly office visits, her FP educates her about the pathophysiology of fibromyalgia and uses motivational interviewing to get her slowly moving and increasing her activity level. She is weaned off the gabapentin previously prescribed, as her symptoms stabilize and improve.

CASE 2 › Mr. P is sent for a steroid injection, which decreases his pain temporarily. During this time, he begins physical therapy; slowly, with increased movement, his function improves. A trial of duloxetine provides pain relief; that combined with intermittent nonsteroidal anti-inflammatory drugs (NSAIDs) has allowed Mr. P to maintain his function and his job.

CASE 3 › Because Mr. B was only taking the narcotics intermittently and wasn’t certain they were helping, CBT was sufficient to wean Mr. B off the medication without any worsening of his pain in the process. By participating in physical therapy, he has learned how to perform certain tasks at his job without pain or injury. He uses NSAIDs as needed for pain.

CORRESPONDENCE
Jill Schneiderhan, MD, 24 Frank Lloyd Wright Dr., Lobby H, Suite 2300, Ann Arbor, MI 48105; jillsch@med.umich.edu.

ACKNOWLEDGEMENTS
We thank Drs. Daniel Clauw (University of Michigan, Ann Arbor) and Martha Rumschlag (Providence Family Medicine Residency Program, Southfield, Mich), for their valuable contributions to this article.

CASE 1 › Lola A is a 28-year-old woman with a history of muscular aches and joint pain throughout her body, fatigue, and mental fogginess. She has been seen by a rheumatologist and has been given a diagnosis of fibromyalgia, but just moved to your town and is establishing care. She is feeling desperate because her pain has worsened and the medication previously prescribed (gabapentin 300 mg tid) is no longer working. She asks to try oxycodone.

CASE 2 › Matt P is a 59-year-old truck driver with severe hip osteoarthritis (OA). His orthopedist recommended against hip replacement at this time because of his young age and a heart condition that makes him high risk. His pain makes sitting for long periods very difficult. He presents to you for help because he is worried he will be unable to continue working.

CASE 3 › Keith B is a 56-year-old construction worker who has been suffering from bouts of back pain for many years. The pain has become more debilitating over time; currently, it is constant, and Mr. B can hardly make it through his work day. He has been getting hydrocodone/acetaminophen from urgent care centers and emergency rooms, but he isn’t sure it is helping and is coming to you to assume his pain management.

Chronic pain (defined as pain >3 months in duration), is a complex, heterogeneous condition affecting an estimated 116 million US adults.¹ Much of the management of chronic pain occurs in primary care settings, placing family physicians (FPs) on the front lines of 2 epidemics: that of chronic pain itself and that of the abuse and misuse of opioid pain medications.

In an effort to improve communication about the risks and benefits of opioid therapy and the safety and effectiveness of pain treatments in general, many professional organizations, health care institutions, and recently the Centers for Disease Control and Prevention,² have published guidelines on the use of opioids for non-malignant chronic pain. With these guidelines in mind—and in light of the latest evidence—we propose the paradigm that follows for the treatment of chronic pain. A critical aspect of this paradigm is determining the pathophysiology underlying a patient’s pain in order to develop a well-rounded, multimodal, evidence-based treatment plan. Detailed here is the application of this approach to the treatment of 3 common chronic pain diagnoses: fibromyalgia, osteoarthritis, and low back pain.

Look to the central and peripheral nervous system

Acute pain begins with activation of peripheral nociceptors at the site of injury. This causes depolarization up the spinal cord and through the brain stem to higher cortical centers where the pain is perceived and localized. Descending neural pathways transport both excitatory and inhibitory information from the brain to the periphery via the spinal cord, which either increases or decreases the perception of pain.³

When damage/injury doesn’t correlate with the perception of pain

Until recently, it was assumed that chronic pain worked much the same way as acute pain and was caused by ongoing nociceptive input in the periphery, but research has shown us that the central nervous system can play a large role in the modulation of nociception. This new understanding comes from the lack of evidence pointing to any pain state in which the degree of nociceptive input correlates with the degree of pain experienced.

With central sensitization, pain is often accompanied by other systemic symptoms such as fatigue—often in the setting of little to no actual stimulation of the peripheral nociceptors.For most patients with chronic pain, regardless of their diagnosis, there is some degree of alteration in the processing of nociceptive signals by the central nervous system contributing to the experience of pain.⁴ This alteration is thought to be the result of peripheral nociceptive signaling persisting past the point of tissue healing, leading to a hypersensitivity of nerve fibers; the fibers then continue to respond to low, or even absent, sensory stimuli.

Central sensitization is the term used when this hypersensitivity develops in the superficial, deep, and ventral cord nerves. When this happens, pain is often accompanied by other systemic symptoms such as fatigue and slowed cognitive processing, often in the setting of little to no actual stimulation of the peripheral nociceptors.³ (For more on this, see “A new paradigm for pain?” J Fam Pract. 2016;65:598-605 or go to http://www.mdedge.com/jfponline/article/111257/pain/new-paradigm-pain.)

TABLE 1⁴ lists the possible mechanisms of pain, which can be broken down into 4 categories: peripheral nociceptive (inflammatory or mechanical), peripheral neuropathic (underlying damage to a peripheral nerve), central (referring to when the central nervous system is the primary entity involved in maintaining the pain), or any combination of the 3.

As pain becomes chronic, multiple mechanisms overlap

It is important to remember that for any single pain diagnosis, there is likely to be—at least initially—a principle underlying mechanism generating the pain. But as the pain becomes chronic, an overlap of multiple mechanisms develops, with central sensitization often playing a more dominant role than peripheral stimulation (regardless of the diagnosis).

For example, in a patient with rheumatoid arthritis (RA), peripheral nociceptive input (in the form of inflammation) is likely the initial mechanism at work, but as time goes on, central processing becomes more involved. The patient may then begin to experience pain that is disproportional to what is generally expected with RA and may develop other somatic symptoms. The diagnosis then becomes pain primarily related to RA with central sensitization, and both need to be addressed in a treatment plan. In rheumatic conditions, comorbid fibromyalgia (indicative of central sensitization) is thought to occur in 15% to 30% of patients.⁵

FPs can utilize the underlying mechanisms to cut across diagnostic labels and tailor treatments to those that are most likely to be effective. For a patient with more prominent peripheral involvement, a procedural intervention such as injections or surgery alone may suffice, whereas a broader approach including psychotherapy, medications, exercise, and other lifestyle interventions may be necessary for a patient with pain caused predominantly by central sensitization.

Addressing both peripheral and central components is essential. One prospective, observational cohort study of more than 600 patients scheduled for unilateral total knee or total hip arthroplasty found that those patients with a higher degree of centralization of pain (as measured by widespread pain index and modified fibromyalgia screening scales⁶) were less likely to report improvement in the affected body part and in overall body pain following the surgery.⁷

There is a high degree of overlap among many of the chronic pain syndromes (fibromyalgia, irritable bowel syndrome, interstitial cystitis, chronic headaches) that have been found to have a central sensitization component.⁸ Providers of primary care are aptly positioned to recognize central sensitization as the underlying pathology and target treatment effectively.

Tailor the treatment plan to the underlying mechanisms of pain

As with any chronic condition, a thorough work-up (complete with history, physical exam, and diagnostic testing, as appropriate) is indicated. In the setting of chronic pain, it’s important to identify both the primary mechanism, as well as secondary factors that may be contributing to the patient’s pain, before developing your treatment plan. These secondary factors may include co-occurring affect disorders,⁹ a history of trauma,¹⁰ poor sleep,¹¹ and tobacco use,¹² among others. A history of trauma, for example, co-exists with many pain syndromes. For these patients, central sensitization is responsible for much of their pain. As a result, traditional cognitive behavioral therapy (CBT) may not be the best option because of its focus on accepting pain as a chronic diagnosis; more trauma-focused treatments such as those dealing in emotional awareness and understanding of the central nervous system’s role in chronic pain need to be considered.¹³

3 common conditions. Below we present evidence-based treatment approaches for 3 conditions that are typically associated with each of the major mechanisms of chronic pain generation: fibromyalgia (a central sensitization cause), OA (a peripheral nociceptive cause), and low back pain (a mixed pain state).

Fibromyalgia: A case of central sensitization

Fibromyalgia is a hallmark diagnosis for those patients in whom central sensitization is the dominant cause of pain. These patients usually present with widespread, diffuse pain, as well as somatic symptoms such as fatigue, memory difficulties, and poor sleep quality.⁸ When explaining the pain mechanism (ie, central sensitization) to patients, it may be useful to use the analogy of a volume control dial that is stuck in the “high” position and can’t be turned down.

Genes, the environment, and neurotransmitters play a role. The origin of the pain amplification process is believed to be multifactorial.

• Genetic factors are thought to contribute to a predisposition for amplification. To date, 5 sets of genes have been implicated in increased sensitivity to pain leading to increased risk of the development of chronic pain during a patient’s lifetime.^14-19
• Environmental factors (eg, early life trauma, physical trauma especially to the trunk, certain infections such as Lyme disease and Epstein-Barr virus, and emotional stress) may trigger or exacerbate symptoms.⁸ Of note: Only about 5% to 10% of people who experience these triggers actually develop a chronic pain state, while the rest regain their baseline health.⁴ This raises the question of whether there is a point during an acute pain episode in which one can intervene and prevent the acute pain from becoming chronic in those at higher risk.⁴
• Imbalances of neurotransmitters (high glutamate;²⁰ low norepinephrine, serotonin,²¹ and gamma-aminobutyric acid [GABA]²²) play a role in central amplification. These substances not only affect sensory transmission, but also control levels of alertness, sleep, mood, and memory.

The diagnostic criteria for fibromyalgia were modified in 2011 to remove the tender point examination and to add in somatic symptoms.⁶ These criteria can be useful in the clinical setting in identifying not only fibromyalgia itself but also the degree of “fibromyalgianess” a patient has, which is an indicator of how large a role the centralization process plays in the maintenance of chronic pain.^23,24

Treatment: Multimodal and patient empowering. Evidence-based treatment options for fibromyalgia, as well as other conditions for which there is a high degree of centralized pain, can be found in TABLE 2.^25-36 Multimodal treatment, with an emphasis on patient knowledge and empowerment, is generally thought to be the most beneficial.^25,37 Treatment should almost always include CBT and exercise/activity therapies,^26,29 which have high degrees of efficacy with few adverse effects.

In terms of medication, centrally-acting agents (tricyclic antidepressants, serotonin norepinephrine reuptake inhibitors [SNRIs], and alpha 2 delta ligands) are the most effective. There is little to no data showing benefit from anti-inflammatories or opioids in the setting of fibromyalgia. There is some data to suggest that combination therapy, for example with an SNRI (milnacipran) and an alpha 2 delta ligand (pregabalin), may provide more benefit than treating with pregabalin alone.³⁸

Identify any factors that might be contributing to your patient's pain, such as co-occurring affect disorders, a history of trauma, poor sleep, or tobacco use.Complementary and alternative therapies (eg, yoga, chiropractic care, acupuncture, massage) are being studied more, and while evidence is only preliminary in terms of efficacy, there is increasing emphasis being placed on the need for patients with chronic pain to shift their treatment expectations to greater acceptance of pain and the need for ongoing self-care.²⁸ (For more advice on managing fibromyalgia, see the related videos at http://bit.ly/2lPEt0f and http://bit.ly/2lmjEcn.)

Osteoarthritis: An example of peripheral nociceptive pain

OA is a condition long thought to be characterized by damage to the cartilage and bone; however, as with many other pain diagnoses, there is frequently little correlation between damage seen on radiographs and the amount of pain that patients experience.

One study analyzed data on almost 7000 patients from the National Health and Nutrition Examination Survey (NHANES I) and found that between 30% and 50% of OA patients with moderate to severe radiographic changes were asymptomatic, and 10% of those with moderate to severe pain had normal radiographs or only mild changes.³⁹ Research is showing that many factors may contribute to this discrepancy, including the typical “wear and tear” of the disease, subacute levels of inflammation that can lead to peripheral sensitization,⁴⁰ and, in some patients, a centralized pain component. The patients with more centralized pain often have pain that is disproportionate to radiographic evidence, as well as more somatic symptoms such as fatigue, sleep disturbance, and memory issues.⁴¹

Treatment should be multimodal and include interventions targeted at halting the progression of damage as well as palliation of pain. All treatment plans for OA should also include exercise, weight reduction, and self-management, in addition to pharmacologic interventions, to reduce both the micro-inflammation and the centralized pain component (when present). Intra-articular injections of various types have been studied with some having more efficacy in pain reduction and functional improvement than others.^42-45 See TABLE 3^42-61 for a summary of evidence-based treatment options.

Low back pain—a mixed pain state

Low back pain (LBP) has been recognized as a mixed pain state for quite some time. While some patients may experience purely nociceptive and/or neuropathic pain, most cases are nonspecific with patients experiencing varying degrees of nociceptive (myofascial low back pain), neuropathic (lumbar radiculopathy), and central sensitization pain.^62,63 Evidence for centralized pain is demonstrated in studies showing hyperalgesia,⁶⁴ augmented central pain processing,⁶⁵ involvement of the emotional brain,⁶⁶ and delayed recovery influenced by poor coping strategies.⁶⁷

When developing a treatment plan for a patient with chronic low back pain, remember that the pain derives from a complex combination of pathophysiologic contributors. Identifying where a patient lies on the pain centralization spectrum can help you tailor treatment.

In one study of 548 patients presenting to a tertiary pain clinic with primary spine pain diagnoses, 42% met diagnostic criteria for fibromyalgia.⁶⁸ Compared to criteria-negative patients, these patients tended to be younger, unemployed, and receiving compensation; they had greater pain intensity, pain interference, and used stronger words to describe their neuropathic pain; they also had higher levels of depression/anxiety and a lower level of physical function.

Because low back pain is a condition with high prevalence and associated disability, many clinical boards have created guidelines for management. These guidelines tend to vary in the strength of evidence used, and the extent to which they are followed in clinical practice remains largely unknown. Recommendations frequently discourage the use of ultrasound/electrotherapy, but many encourage short-term use of medications (see “How effective are opioids for chronic low back pain?” J Fam Pract. 2015;64:584-584), supervised exercise therapy, CBT, and multidisciplinary treatment.

Guidelines tend to differ most widely with regard to recommendations for spinal manipulation and specific drug therapies.⁶⁹ The classes of drugs that may be most useful when centralized pain is present include the SNRIs and the alpha 2 delta calcium channel ligands.⁴ See TABLE 4^70-89 for a summary of evidence-based treatment options.

CASE 1 › Ms. A is started on amitriptyline 25 mg at bedtime, which improves her fatigue and cognitive symptoms. During monthly office visits, her FP educates her about the pathophysiology of fibromyalgia and uses motivational interviewing to get her slowly moving and increasing her activity level. She is weaned off the gabapentin previously prescribed, as her symptoms stabilize and improve.

CASE 2 › Mr. P is sent for a steroid injection, which decreases his pain temporarily. During this time, he begins physical therapy; slowly, with increased movement, his function improves. A trial of duloxetine provides pain relief; that combined with intermittent nonsteroidal anti-inflammatory drugs (NSAIDs) has allowed Mr. P to maintain his function and his job.

CASE 3 › Because Mr. B was only taking the narcotics intermittently and wasn’t certain they were helping, CBT was sufficient to wean Mr. B off the medication without any worsening of his pain in the process. By participating in physical therapy, he has learned how to perform certain tasks at his job without pain or injury. He uses NSAIDs as needed for pain.

CORRESPONDENCE
Jill Schneiderhan, MD, 24 Frank Lloyd Wright Dr., Lobby H, Suite 2300, Ann Arbor, MI 48105; jillsch@med.umich.edu.

ACKNOWLEDGEMENTS
We thank Drs. Daniel Clauw (University of Michigan, Ann Arbor) and Martha Rumschlag (Providence Family Medicine Residency Program, Southfield, Mich), for their valuable contributions to this article.

CASE 1 › Lola A is a 28-year-old woman with a history of muscular aches and joint pain throughout her body, fatigue, and mental fogginess. She has been seen by a rheumatologist and has been given a diagnosis of fibromyalgia, but just moved to your town and is establishing care. She is feeling desperate because her pain has worsened and the medication previously prescribed (gabapentin 300 mg tid) is no longer working. She asks to try oxycodone.

CASE 2 › Matt P is a 59-year-old truck driver with severe hip osteoarthritis (OA). His orthopedist recommended against hip replacement at this time because of his young age and a heart condition that makes him high risk. His pain makes sitting for long periods very difficult. He presents to you for help because he is worried he will be unable to continue working.

CASE 3 › Keith B is a 56-year-old construction worker who has been suffering from bouts of back pain for many years. The pain has become more debilitating over time; currently, it is constant, and Mr. B can hardly make it through his work day. He has been getting hydrocodone/acetaminophen from urgent care centers and emergency rooms, but he isn’t sure it is helping and is coming to you to assume his pain management.

Chronic pain (defined as pain >3 months in duration), is a complex, heterogeneous condition affecting an estimated 116 million US adults.¹ Much of the management of chronic pain occurs in primary care settings, placing family physicians (FPs) on the front lines of 2 epidemics: that of chronic pain itself and that of the abuse and misuse of opioid pain medications.

In an effort to improve communication about the risks and benefits of opioid therapy and the safety and effectiveness of pain treatments in general, many professional organizations, health care institutions, and recently the Centers for Disease Control and Prevention,² have published guidelines on the use of opioids for non-malignant chronic pain. With these guidelines in mind—and in light of the latest evidence—we propose the paradigm that follows for the treatment of chronic pain. A critical aspect of this paradigm is determining the pathophysiology underlying a patient’s pain in order to develop a well-rounded, multimodal, evidence-based treatment plan. Detailed here is the application of this approach to the treatment of 3 common chronic pain diagnoses: fibromyalgia, osteoarthritis, and low back pain.

Look to the central and peripheral nervous system

Acute pain begins with activation of peripheral nociceptors at the site of injury. This causes depolarization up the spinal cord and through the brain stem to higher cortical centers where the pain is perceived and localized. Descending neural pathways transport both excitatory and inhibitory information from the brain to the periphery via the spinal cord, which either increases or decreases the perception of pain.³

When damage/injury doesn’t correlate with the perception of pain

Until recently, it was assumed that chronic pain worked much the same way as acute pain and was caused by ongoing nociceptive input in the periphery, but research has shown us that the central nervous system can play a large role in the modulation of nociception. This new understanding comes from the lack of evidence pointing to any pain state in which the degree of nociceptive input correlates with the degree of pain experienced.

With central sensitization, pain is often accompanied by other systemic symptoms such as fatigue—often in the setting of little to no actual stimulation of the peripheral nociceptors.For most patients with chronic pain, regardless of their diagnosis, there is some degree of alteration in the processing of nociceptive signals by the central nervous system contributing to the experience of pain.⁴ This alteration is thought to be the result of peripheral nociceptive signaling persisting past the point of tissue healing, leading to a hypersensitivity of nerve fibers; the fibers then continue to respond to low, or even absent, sensory stimuli.

Central sensitization is the term used when this hypersensitivity develops in the superficial, deep, and ventral cord nerves. When this happens, pain is often accompanied by other systemic symptoms such as fatigue and slowed cognitive processing, often in the setting of little to no actual stimulation of the peripheral nociceptors.³ (For more on this, see “A new paradigm for pain?” J Fam Pract. 2016;65:598-605 or go to http://www.mdedge.com/jfponline/article/111257/pain/new-paradigm-pain.)

TABLE 1⁴ lists the possible mechanisms of pain, which can be broken down into 4 categories: peripheral nociceptive (inflammatory or mechanical), peripheral neuropathic (underlying damage to a peripheral nerve), central (referring to when the central nervous system is the primary entity involved in maintaining the pain), or any combination of the 3.

As pain becomes chronic, multiple mechanisms overlap

It is important to remember that for any single pain diagnosis, there is likely to be—at least initially—a principle underlying mechanism generating the pain. But as the pain becomes chronic, an overlap of multiple mechanisms develops, with central sensitization often playing a more dominant role than peripheral stimulation (regardless of the diagnosis).

For example, in a patient with rheumatoid arthritis (RA), peripheral nociceptive input (in the form of inflammation) is likely the initial mechanism at work, but as time goes on, central processing becomes more involved. The patient may then begin to experience pain that is disproportional to what is generally expected with RA and may develop other somatic symptoms. The diagnosis then becomes pain primarily related to RA with central sensitization, and both need to be addressed in a treatment plan. In rheumatic conditions, comorbid fibromyalgia (indicative of central sensitization) is thought to occur in 15% to 30% of patients.⁵

FPs can utilize the underlying mechanisms to cut across diagnostic labels and tailor treatments to those that are most likely to be effective. For a patient with more prominent peripheral involvement, a procedural intervention such as injections or surgery alone may suffice, whereas a broader approach including psychotherapy, medications, exercise, and other lifestyle interventions may be necessary for a patient with pain caused predominantly by central sensitization.

Addressing both peripheral and central components is essential. One prospective, observational cohort study of more than 600 patients scheduled for unilateral total knee or total hip arthroplasty found that those patients with a higher degree of centralization of pain (as measured by widespread pain index and modified fibromyalgia screening scales⁶) were less likely to report improvement in the affected body part and in overall body pain following the surgery.⁷

There is a high degree of overlap among many of the chronic pain syndromes (fibromyalgia, irritable bowel syndrome, interstitial cystitis, chronic headaches) that have been found to have a central sensitization component.⁸ Providers of primary care are aptly positioned to recognize central sensitization as the underlying pathology and target treatment effectively.

Tailor the treatment plan to the underlying mechanisms of pain

As with any chronic condition, a thorough work-up (complete with history, physical exam, and diagnostic testing, as appropriate) is indicated. In the setting of chronic pain, it’s important to identify both the primary mechanism, as well as secondary factors that may be contributing to the patient’s pain, before developing your treatment plan. These secondary factors may include co-occurring affect disorders,⁹ a history of trauma,¹⁰ poor sleep,¹¹ and tobacco use,¹² among others. A history of trauma, for example, co-exists with many pain syndromes. For these patients, central sensitization is responsible for much of their pain. As a result, traditional cognitive behavioral therapy (CBT) may not be the best option because of its focus on accepting pain as a chronic diagnosis; more trauma-focused treatments such as those dealing in emotional awareness and understanding of the central nervous system’s role in chronic pain need to be considered.¹³

3 common conditions. Below we present evidence-based treatment approaches for 3 conditions that are typically associated with each of the major mechanisms of chronic pain generation: fibromyalgia (a central sensitization cause), OA (a peripheral nociceptive cause), and low back pain (a mixed pain state).

Fibromyalgia: A case of central sensitization

Fibromyalgia is a hallmark diagnosis for those patients in whom central sensitization is the dominant cause of pain. These patients usually present with widespread, diffuse pain, as well as somatic symptoms such as fatigue, memory difficulties, and poor sleep quality.⁸ When explaining the pain mechanism (ie, central sensitization) to patients, it may be useful to use the analogy of a volume control dial that is stuck in the “high” position and can’t be turned down.

Genes, the environment, and neurotransmitters play a role. The origin of the pain amplification process is believed to be multifactorial.

• Genetic factors are thought to contribute to a predisposition for amplification. To date, 5 sets of genes have been implicated in increased sensitivity to pain leading to increased risk of the development of chronic pain during a patient’s lifetime.^14-19
• Environmental factors (eg, early life trauma, physical trauma especially to the trunk, certain infections such as Lyme disease and Epstein-Barr virus, and emotional stress) may trigger or exacerbate symptoms.⁸ Of note: Only about 5% to 10% of people who experience these triggers actually develop a chronic pain state, while the rest regain their baseline health.⁴ This raises the question of whether there is a point during an acute pain episode in which one can intervene and prevent the acute pain from becoming chronic in those at higher risk.⁴
• Imbalances of neurotransmitters (high glutamate;²⁰ low norepinephrine, serotonin,²¹ and gamma-aminobutyric acid [GABA]²²) play a role in central amplification. These substances not only affect sensory transmission, but also control levels of alertness, sleep, mood, and memory.

The diagnostic criteria for fibromyalgia were modified in 2011 to remove the tender point examination and to add in somatic symptoms.⁶ These criteria can be useful in the clinical setting in identifying not only fibromyalgia itself but also the degree of “fibromyalgianess” a patient has, which is an indicator of how large a role the centralization process plays in the maintenance of chronic pain.^23,24

Treatment: Multimodal and patient empowering. Evidence-based treatment options for fibromyalgia, as well as other conditions for which there is a high degree of centralized pain, can be found in TABLE 2.^25-36 Multimodal treatment, with an emphasis on patient knowledge and empowerment, is generally thought to be the most beneficial.^25,37 Treatment should almost always include CBT and exercise/activity therapies,^26,29 which have high degrees of efficacy with few adverse effects.

In terms of medication, centrally-acting agents (tricyclic antidepressants, serotonin norepinephrine reuptake inhibitors [SNRIs], and alpha 2 delta ligands) are the most effective. There is little to no data showing benefit from anti-inflammatories or opioids in the setting of fibromyalgia. There is some data to suggest that combination therapy, for example with an SNRI (milnacipran) and an alpha 2 delta ligand (pregabalin), may provide more benefit than treating with pregabalin alone.³⁸

Identify any factors that might be contributing to your patient's pain, such as co-occurring affect disorders, a history of trauma, poor sleep, or tobacco use.Complementary and alternative therapies (eg, yoga, chiropractic care, acupuncture, massage) are being studied more, and while evidence is only preliminary in terms of efficacy, there is increasing emphasis being placed on the need for patients with chronic pain to shift their treatment expectations to greater acceptance of pain and the need for ongoing self-care.²⁸ (For more advice on managing fibromyalgia, see the related videos at http://bit.ly/2lPEt0f and http://bit.ly/2lmjEcn.)

Osteoarthritis: An example of peripheral nociceptive pain

OA is a condition long thought to be characterized by damage to the cartilage and bone; however, as with many other pain diagnoses, there is frequently little correlation between damage seen on radiographs and the amount of pain that patients experience.

One study analyzed data on almost 7000 patients from the National Health and Nutrition Examination Survey (NHANES I) and found that between 30% and 50% of OA patients with moderate to severe radiographic changes were asymptomatic, and 10% of those with moderate to severe pain had normal radiographs or only mild changes.³⁹ Research is showing that many factors may contribute to this discrepancy, including the typical “wear and tear” of the disease, subacute levels of inflammation that can lead to peripheral sensitization,⁴⁰ and, in some patients, a centralized pain component. The patients with more centralized pain often have pain that is disproportionate to radiographic evidence, as well as more somatic symptoms such as fatigue, sleep disturbance, and memory issues.⁴¹

Treatment should be multimodal and include interventions targeted at halting the progression of damage as well as palliation of pain. All treatment plans for OA should also include exercise, weight reduction, and self-management, in addition to pharmacologic interventions, to reduce both the micro-inflammation and the centralized pain component (when present). Intra-articular injections of various types have been studied with some having more efficacy in pain reduction and functional improvement than others.^42-45 See TABLE 3^42-61 for a summary of evidence-based treatment options.

Low back pain—a mixed pain state

Low back pain (LBP) has been recognized as a mixed pain state for quite some time. While some patients may experience purely nociceptive and/or neuropathic pain, most cases are nonspecific with patients experiencing varying degrees of nociceptive (myofascial low back pain), neuropathic (lumbar radiculopathy), and central sensitization pain.^62,63 Evidence for centralized pain is demonstrated in studies showing hyperalgesia,⁶⁴ augmented central pain processing,⁶⁵ involvement of the emotional brain,⁶⁶ and delayed recovery influenced by poor coping strategies.⁶⁷

When developing a treatment plan for a patient with chronic low back pain, remember that the pain derives from a complex combination of pathophysiologic contributors. Identifying where a patient lies on the pain centralization spectrum can help you tailor treatment.

In one study of 548 patients presenting to a tertiary pain clinic with primary spine pain diagnoses, 42% met diagnostic criteria for fibromyalgia.⁶⁸ Compared to criteria-negative patients, these patients tended to be younger, unemployed, and receiving compensation; they had greater pain intensity, pain interference, and used stronger words to describe their neuropathic pain; they also had higher levels of depression/anxiety and a lower level of physical function.

Because low back pain is a condition with high prevalence and associated disability, many clinical boards have created guidelines for management. These guidelines tend to vary in the strength of evidence used, and the extent to which they are followed in clinical practice remains largely unknown. Recommendations frequently discourage the use of ultrasound/electrotherapy, but many encourage short-term use of medications (see “How effective are opioids for chronic low back pain?” J Fam Pract. 2015;64:584-584), supervised exercise therapy, CBT, and multidisciplinary treatment.

Guidelines tend to differ most widely with regard to recommendations for spinal manipulation and specific drug therapies.⁶⁹ The classes of drugs that may be most useful when centralized pain is present include the SNRIs and the alpha 2 delta calcium channel ligands.⁴ See TABLE 4^70-89 for a summary of evidence-based treatment options.

CASE 1 › Ms. A is started on amitriptyline 25 mg at bedtime, which improves her fatigue and cognitive symptoms. During monthly office visits, her FP educates her about the pathophysiology of fibromyalgia and uses motivational interviewing to get her slowly moving and increasing her activity level. She is weaned off the gabapentin previously prescribed, as her symptoms stabilize and improve.

CASE 2 › Mr. P is sent for a steroid injection, which decreases his pain temporarily. During this time, he begins physical therapy; slowly, with increased movement, his function improves. A trial of duloxetine provides pain relief; that combined with intermittent nonsteroidal anti-inflammatory drugs (NSAIDs) has allowed Mr. P to maintain his function and his job.

CASE 3 › Because Mr. B was only taking the narcotics intermittently and wasn’t certain they were helping, CBT was sufficient to wean Mr. B off the medication without any worsening of his pain in the process. By participating in physical therapy, he has learned how to perform certain tasks at his job without pain or injury. He uses NSAIDs as needed for pain.

CORRESPONDENCE
Jill Schneiderhan, MD, 24 Frank Lloyd Wright Dr., Lobby H, Suite 2300, Ann Arbor, MI 48105; jillsch@med.umich.edu.

ACKNOWLEDGEMENTS
We thank Drs. Daniel Clauw (University of Michigan, Ann Arbor) and Martha Rumschlag (Providence Family Medicine Residency Program, Southfield, Mich), for their valuable contributions to this article.

New clinical practice advice has been issued for use of the functional lumen imaging probe (FLIP) to assess disorders of the upper gastrointestinal tract, with the main takeaway being the device’s potency in diagnosing achalasia.

“Although the strongest data appear to be focused on the management of achalasia, emerging evidence supports the clinical relevance of FLIP in the assessment of disease severity and as an outcome measure in [eosinophilic esophagitis (EoE)] intervention trials,” wrote the authors of the update, led by John E. Pandolfino, MD, of Northwestern University, Chicago. The report is in the March issue of Clinical Gastroenterology and Hepatology (doi: 10.1016/j.cgh.2016.
10.022).

*This story updated on 3/9/2017.

dchitnis@frontlinemedcom.com

New clinical practice advice has been issued for use of the functional lumen imaging probe (FLIP) to assess disorders of the upper gastrointestinal tract, with the main takeaway being the device’s potency in diagnosing achalasia.

“Although the strongest data appear to be focused on the management of achalasia, emerging evidence supports the clinical relevance of FLIP in the assessment of disease severity and as an outcome measure in [eosinophilic esophagitis (EoE)] intervention trials,” wrote the authors of the update, led by John E. Pandolfino, MD, of Northwestern University, Chicago. The report is in the March issue of Clinical Gastroenterology and Hepatology (doi: 10.1016/j.cgh.2016.
10.022).

*This story updated on 3/9/2017.

dchitnis@frontlinemedcom.com

New clinical practice advice has been issued for use of the functional lumen imaging probe (FLIP) to assess disorders of the upper gastrointestinal tract, with the main takeaway being the device’s potency in diagnosing achalasia.

“Although the strongest data appear to be focused on the management of achalasia, emerging evidence supports the clinical relevance of FLIP in the assessment of disease severity and as an outcome measure in [eosinophilic esophagitis (EoE)] intervention trials,” wrote the authors of the update, led by John E. Pandolfino, MD, of Northwestern University, Chicago. The report is in the March issue of Clinical Gastroenterology and Hepatology (doi: 10.1016/j.cgh.2016.
10.022).

*This story updated on 3/9/2017.

dchitnis@frontlinemedcom.com

The AGA Institute has released a series of new best practice statements that gastroenterologists should use when considering a patient for endoscopic bariatric treatments or surgeries (EBTs).

“There is a need for less-invasive weight loss therapies that are more effective and durable than lifestyle interventions alone, less invasive and risky than bariatric surgery, and easily performed at a lower expense than that of surgery, thereby allowing improved access and application to a larger segment of the population with moderate obesity,” wrote the authors of the expert review, led by Barham K. Abu Dayyeh, MD of the Mayo Clinic in Rochester, Minn. The report is in the March issue of Gastroenterology (doi: 10.1053/j.gastro.2017.01.035). “[EBTs] potentially meet these criteria and may provide an effective treatment approach to obesity in selected patients.”

copyright kikkerdirk/Thinkstock

dchitnis@frontlinemedcom.com

The AGA Institute has released a series of new best practice statements that gastroenterologists should use when considering a patient for endoscopic bariatric treatments or surgeries (EBTs).

“There is a need for less-invasive weight loss therapies that are more effective and durable than lifestyle interventions alone, less invasive and risky than bariatric surgery, and easily performed at a lower expense than that of surgery, thereby allowing improved access and application to a larger segment of the population with moderate obesity,” wrote the authors of the expert review, led by Barham K. Abu Dayyeh, MD of the Mayo Clinic in Rochester, Minn. The report is in the March issue of Gastroenterology (doi: 10.1053/j.gastro.2017.01.035). “[EBTs] potentially meet these criteria and may provide an effective treatment approach to obesity in selected patients.”

copyright kikkerdirk/Thinkstock

dchitnis@frontlinemedcom.com

The AGA Institute has released a series of new best practice statements that gastroenterologists should use when considering a patient for endoscopic bariatric treatments or surgeries (EBTs).

“There is a need for less-invasive weight loss therapies that are more effective and durable than lifestyle interventions alone, less invasive and risky than bariatric surgery, and easily performed at a lower expense than that of surgery, thereby allowing improved access and application to a larger segment of the population with moderate obesity,” wrote the authors of the expert review, led by Barham K. Abu Dayyeh, MD of the Mayo Clinic in Rochester, Minn. The report is in the March issue of Gastroenterology (doi: 10.1053/j.gastro.2017.01.035). “[EBTs] potentially meet these criteria and may provide an effective treatment approach to obesity in selected patients.”

copyright kikkerdirk/Thinkstock

dchitnis@frontlinemedcom.com

Updated best practice statements regarding the use of proton pump inhibitors first detail what types of patients should be using short and long-term PPIs.

“When PPIs are appropriately prescribed, their benefits are likely to outweigh their risks [but] when PPIs are inappropriately prescribed, modest risks become important because there is no potential benefit,” wrote the authors of the updated guidance, published in the March issue of Gastroenterology.

“There is currently insufficient evidence to recommend specific strategies for mitigating PPI adverse effects,” noted Daniel E. Freedberg, MD, of Columbia University, New York, and his colleagues.

PPIs should be used on a short-term basis for individuals with gastroesophageal reflux disease (GERD) or conditions such as erosive esophagitis. These patients can also use PPIs for maintenance and occasional symptom management, but those with uncomplicated GERD should be weaned off PPIs if they respond favorably to them.

If a patient is unable to be weaned off PPIs, then ambulatory esophageal pH and impedance monitoring should be done, as this will allow clinicians to determine if the patient has a functional syndrome or GERD. Lifelong PPI treatment should not be considered until this step is taken, according to the new best practice statements.

“Short-term PPIs are highly effective for uncomplicated GERD [but] because patients who cannot reduce PPIs face lifelong therapy, we would consider testing for an acid-related disorder in this situation,” the authors explained. “However, there is no high-quality evidence on which to base this recommendation.”

Patients who have symptomatic GERD or Barrett’s esophagus, either symptomatic or asymptomatic, should be on long-term PPI treatment. Patients who are at a higher risk for NSAID-induced ulcer bleeding should be taking PPIs if they continue to take NSAIDs.

When recommending long-term PPI treatment for a patient, the patient need not use probiotics on a regular basis; there appears to be no need to routinely check the patient’s bone mineral density, serum creatinine, magnesium, or vitamin B₁₂ level on a regular basis. In addition, they need not consume more than the Recommended Dietary Allowance of calcium, magnesium, or vitamin B₁₂.

Finally, the authors state that “specific PPI formulations should not be selected based on potential risks.” This is because no evidence has been found indicating that PPI formulations can be ranked in any way based on risk.

These recommendations come from the AGA’s Clinical Practice Updates Committee, which pored through studies published through July 2016 in the PubMed, EMbase, and Cochrane library databases. Expert opinions and quality assessments on each study contributed to forming these best practice statements.

“In sum, the best current strategies for mitigating the potential risks of long-term PPIs are to avoid prescribing them when they are not indicated and to reduce them to their minimum dose when they are indicated,” Dr. Freedberg and his colleagues concluded.

The researchers did not report any relevant financial disclosures.

Updated best practice statements regarding the use of proton pump inhibitors first detail what types of patients should be using short and long-term PPIs.

“When PPIs are appropriately prescribed, their benefits are likely to outweigh their risks [but] when PPIs are inappropriately prescribed, modest risks become important because there is no potential benefit,” wrote the authors of the updated guidance, published in the March issue of Gastroenterology.

“There is currently insufficient evidence to recommend specific strategies for mitigating PPI adverse effects,” noted Daniel E. Freedberg, MD, of Columbia University, New York, and his colleagues.

PPIs should be used on a short-term basis for individuals with gastroesophageal reflux disease (GERD) or conditions such as erosive esophagitis. These patients can also use PPIs for maintenance and occasional symptom management, but those with uncomplicated GERD should be weaned off PPIs if they respond favorably to them.

If a patient is unable to be weaned off PPIs, then ambulatory esophageal pH and impedance monitoring should be done, as this will allow clinicians to determine if the patient has a functional syndrome or GERD. Lifelong PPI treatment should not be considered until this step is taken, according to the new best practice statements.

“Short-term PPIs are highly effective for uncomplicated GERD [but] because patients who cannot reduce PPIs face lifelong therapy, we would consider testing for an acid-related disorder in this situation,” the authors explained. “However, there is no high-quality evidence on which to base this recommendation.”

Patients who have symptomatic GERD or Barrett’s esophagus, either symptomatic or asymptomatic, should be on long-term PPI treatment. Patients who are at a higher risk for NSAID-induced ulcer bleeding should be taking PPIs if they continue to take NSAIDs.

When recommending long-term PPI treatment for a patient, the patient need not use probiotics on a regular basis; there appears to be no need to routinely check the patient’s bone mineral density, serum creatinine, magnesium, or vitamin B₁₂ level on a regular basis. In addition, they need not consume more than the Recommended Dietary Allowance of calcium, magnesium, or vitamin B₁₂.

Finally, the authors state that “specific PPI formulations should not be selected based on potential risks.” This is because no evidence has been found indicating that PPI formulations can be ranked in any way based on risk.

These recommendations come from the AGA’s Clinical Practice Updates Committee, which pored through studies published through July 2016 in the PubMed, EMbase, and Cochrane library databases. Expert opinions and quality assessments on each study contributed to forming these best practice statements.

“In sum, the best current strategies for mitigating the potential risks of long-term PPIs are to avoid prescribing them when they are not indicated and to reduce them to their minimum dose when they are indicated,” Dr. Freedberg and his colleagues concluded.

The researchers did not report any relevant financial disclosures.

Updated best practice statements regarding the use of proton pump inhibitors first detail what types of patients should be using short and long-term PPIs.

“When PPIs are appropriately prescribed, their benefits are likely to outweigh their risks [but] when PPIs are inappropriately prescribed, modest risks become important because there is no potential benefit,” wrote the authors of the updated guidance, published in the March issue of Gastroenterology.

“There is currently insufficient evidence to recommend specific strategies for mitigating PPI adverse effects,” noted Daniel E. Freedberg, MD, of Columbia University, New York, and his colleagues.

PPIs should be used on a short-term basis for individuals with gastroesophageal reflux disease (GERD) or conditions such as erosive esophagitis. These patients can also use PPIs for maintenance and occasional symptom management, but those with uncomplicated GERD should be weaned off PPIs if they respond favorably to them.

If a patient is unable to be weaned off PPIs, then ambulatory esophageal pH and impedance monitoring should be done, as this will allow clinicians to determine if the patient has a functional syndrome or GERD. Lifelong PPI treatment should not be considered until this step is taken, according to the new best practice statements.

“Short-term PPIs are highly effective for uncomplicated GERD [but] because patients who cannot reduce PPIs face lifelong therapy, we would consider testing for an acid-related disorder in this situation,” the authors explained. “However, there is no high-quality evidence on which to base this recommendation.”

Patients who have symptomatic GERD or Barrett’s esophagus, either symptomatic or asymptomatic, should be on long-term PPI treatment. Patients who are at a higher risk for NSAID-induced ulcer bleeding should be taking PPIs if they continue to take NSAIDs.

When recommending long-term PPI treatment for a patient, the patient need not use probiotics on a regular basis; there appears to be no need to routinely check the patient’s bone mineral density, serum creatinine, magnesium, or vitamin B₁₂ level on a regular basis. In addition, they need not consume more than the Recommended Dietary Allowance of calcium, magnesium, or vitamin B₁₂.

Finally, the authors state that “specific PPI formulations should not be selected based on potential risks.” This is because no evidence has been found indicating that PPI formulations can be ranked in any way based on risk.

These recommendations come from the AGA’s Clinical Practice Updates Committee, which pored through studies published through July 2016 in the PubMed, EMbase, and Cochrane library databases. Expert opinions and quality assessments on each study contributed to forming these best practice statements.

“In sum, the best current strategies for mitigating the potential risks of long-term PPIs are to avoid prescribing them when they are not indicated and to reduce them to their minimum dose when they are indicated,” Dr. Freedberg and his colleagues concluded.

The researchers did not report any relevant financial disclosures.

Q2: Answer: B

This patient, with no imaging or laboratory findings to suggest cirrhosis, most likely has noncirrhotic portal hypertension (NCPH). There is now a well-described association between HIV and NCPH with the prevalence of NCPH in HIV estimated to be –0.5% to 1%. Patients typically are unaware of any underlying liver disease until presentation with variceal bleeding. Variceal bleeding is a much more common manifestation of NCPH than ascites. Clinical presentation with normal hepatic enzymes and normal hepatic synthetic function is a very typical feature in these patients.  Although the exact etiology is not fully understood, NCPH in HIV is likely related to HAART, particularly didanosine use, hypercoagulability, microbial translocation from the gut, and direct effects of HIV. NCPH is a presinusoidal lesion, and liver biopsy may reveal paucity of portal vasculature and focal obliteration of small portal veins. Portal vein thrombosis in patients with HIV and NCPH is common and has been observed in 25%-75% of patients.  
 

Reference

1. Vispo E., Morello J., Rodriguez-Novoa S., Soriano V. Noncirrhotic portal hypertension in HIV infection. Curr Opin Infect Dis. 2011;24:12-8.
2. Khanna R., Sarin S.K. Noncirrhotic portal hypertension – Diagnosis and management. J Hepatol. 2014;60:421-41. 
 

Q2: Answer: B

This patient, with no imaging or laboratory findings to suggest cirrhosis, most likely has noncirrhotic portal hypertension (NCPH). There is now a well-described association between HIV and NCPH with the prevalence of NCPH in HIV estimated to be –0.5% to 1%. Patients typically are unaware of any underlying liver disease until presentation with variceal bleeding. Variceal bleeding is a much more common manifestation of NCPH than ascites. Clinical presentation with normal hepatic enzymes and normal hepatic synthetic function is a very typical feature in these patients.  Although the exact etiology is not fully understood, NCPH in HIV is likely related to HAART, particularly didanosine use, hypercoagulability, microbial translocation from the gut, and direct effects of HIV. NCPH is a presinusoidal lesion, and liver biopsy may reveal paucity of portal vasculature and focal obliteration of small portal veins. Portal vein thrombosis in patients with HIV and NCPH is common and has been observed in 25%-75% of patients.  
 

Reference

1. Vispo E., Morello J., Rodriguez-Novoa S., Soriano V. Noncirrhotic portal hypertension in HIV infection. Curr Opin Infect Dis. 2011;24:12-8.
2. Khanna R., Sarin S.K. Noncirrhotic portal hypertension – Diagnosis and management. J Hepatol. 2014;60:421-41. 
 

Q2: Answer: B

This patient, with no imaging or laboratory findings to suggest cirrhosis, most likely has noncirrhotic portal hypertension (NCPH). There is now a well-described association between HIV and NCPH with the prevalence of NCPH in HIV estimated to be –0.5% to 1%. Patients typically are unaware of any underlying liver disease until presentation with variceal bleeding. Variceal bleeding is a much more common manifestation of NCPH than ascites. Clinical presentation with normal hepatic enzymes and normal hepatic synthetic function is a very typical feature in these patients.  Although the exact etiology is not fully understood, NCPH in HIV is likely related to HAART, particularly didanosine use, hypercoagulability, microbial translocation from the gut, and direct effects of HIV. NCPH is a presinusoidal lesion, and liver biopsy may reveal paucity of portal vasculature and focal obliteration of small portal veins. Portal vein thrombosis in patients with HIV and NCPH is common and has been observed in 25%-75% of patients.  
 

Reference

1. Vispo E., Morello J., Rodriguez-Novoa S., Soriano V. Noncirrhotic portal hypertension in HIV infection. Curr Opin Infect Dis. 2011;24:12-8.
2. Khanna R., Sarin S.K. Noncirrhotic portal hypertension – Diagnosis and management. J Hepatol. 2014;60:421-41. 
 

Q1: Answer: A

Critique: This is a classic presentation of eosinophilic esophagitis (EoE). As many as half of older children with food impactions suffer from EoE. EoE is characterized by a severe, eosinophilic infiltration of the esophagus that may respond to acid inhibition, systemic or topical steroid therapy, or removal of dietary allergens. Epidemiologic studies suggest a rising incidence in the United States in both children and adults, with at least one case occurring in every 10,000 children each year. Treatment is aimed at alleviating symptoms and healing esophageal inflammation. Allergy testing should be performed at the time of diagnosis; however, radioallergosorbent  tests and skin-prick tests are often negative, and only half of affected children have a antecedent history of other allergic symptoms. 

A five-food elimination diet can be helpful for many affected children and adults, although adherence to the diet can be difficult. There is a group of affected children who respond to high doses of proton pump inhibitors, and most patients respond to either systemic or topical steroid therapy. Even with therapy, some patients go on to develop esophageal strictures and may need serial or repeated dilatations.  

While eosinophilic infiltration and inflammation may be present with gastroesophageal reflux disease and associated esophagitis, the number of eosinophils seen in this boy’s biopsies is much more consistent with EoE. Moreover, stricture formation as a result of peptic esophagitis in a child this age would be extremely rare. While inflammatory bowel disease may be associated with eosinophilic infiltration of the intestinal tract, isolated esophageal Crohn’s disease would be extraordinarily rare.Our patient has no history of any immune deficiency or steroid use that would predispose to fungal esophagitis. Achalasia typically presents with gradually worsening symptoms, and the obstruction would be at the lower esophageal sphincter, not in the mid-esophagus.  
 

Reference

<sup>1. Liacouras C., Furuta G., Hirano I., et al. Eosinophilic esophagitis: updated consensus recommendations for children and adults. J Allergy Clin Immunol. 2011;128:3-20. 
2. Furuta G., Liacouras C., Collins M., et al. Eosinophilic esophagitis in children and adults: A systematic review and consensus recommendations for diagnosis and treatment. Gastroenterology. 2007;133:1342-63.</sup>

Q1: Answer: A

Critique: This is a classic presentation of eosinophilic esophagitis (EoE). As many as half of older children with food impactions suffer from EoE. EoE is characterized by a severe, eosinophilic infiltration of the esophagus that may respond to acid inhibition, systemic or topical steroid therapy, or removal of dietary allergens. Epidemiologic studies suggest a rising incidence in the United States in both children and adults, with at least one case occurring in every 10,000 children each year. Treatment is aimed at alleviating symptoms and healing esophageal inflammation. Allergy testing should be performed at the time of diagnosis; however, radioallergosorbent  tests and skin-prick tests are often negative, and only half of affected children have a antecedent history of other allergic symptoms. 

A five-food elimination diet can be helpful for many affected children and adults, although adherence to the diet can be difficult. There is a group of affected children who respond to high doses of proton pump inhibitors, and most patients respond to either systemic or topical steroid therapy. Even with therapy, some patients go on to develop esophageal strictures and may need serial or repeated dilatations.  

While eosinophilic infiltration and inflammation may be present with gastroesophageal reflux disease and associated esophagitis, the number of eosinophils seen in this boy’s biopsies is much more consistent with EoE. Moreover, stricture formation as a result of peptic esophagitis in a child this age would be extremely rare. While inflammatory bowel disease may be associated with eosinophilic infiltration of the intestinal tract, isolated esophageal Crohn’s disease would be extraordinarily rare.Our patient has no history of any immune deficiency or steroid use that would predispose to fungal esophagitis. Achalasia typically presents with gradually worsening symptoms, and the obstruction would be at the lower esophageal sphincter, not in the mid-esophagus.  
 

Reference

<sup>1. Liacouras C., Furuta G., Hirano I., et al. Eosinophilic esophagitis: updated consensus recommendations for children and adults. J Allergy Clin Immunol. 2011;128:3-20. 
2. Furuta G., Liacouras C., Collins M., et al. Eosinophilic esophagitis in children and adults: A systematic review and consensus recommendations for diagnosis and treatment. Gastroenterology. 2007;133:1342-63.</sup>

Q1: Answer: A

Critique: This is a classic presentation of eosinophilic esophagitis (EoE). As many as half of older children with food impactions suffer from EoE. EoE is characterized by a severe, eosinophilic infiltration of the esophagus that may respond to acid inhibition, systemic or topical steroid therapy, or removal of dietary allergens. Epidemiologic studies suggest a rising incidence in the United States in both children and adults, with at least one case occurring in every 10,000 children each year. Treatment is aimed at alleviating symptoms and healing esophageal inflammation. Allergy testing should be performed at the time of diagnosis; however, radioallergosorbent  tests and skin-prick tests are often negative, and only half of affected children have a antecedent history of other allergic symptoms. 

A five-food elimination diet can be helpful for many affected children and adults, although adherence to the diet can be difficult. There is a group of affected children who respond to high doses of proton pump inhibitors, and most patients respond to either systemic or topical steroid therapy. Even with therapy, some patients go on to develop esophageal strictures and may need serial or repeated dilatations.  

While eosinophilic infiltration and inflammation may be present with gastroesophageal reflux disease and associated esophagitis, the number of eosinophils seen in this boy’s biopsies is much more consistent with EoE. Moreover, stricture formation as a result of peptic esophagitis in a child this age would be extremely rare. While inflammatory bowel disease may be associated with eosinophilic infiltration of the intestinal tract, isolated esophageal Crohn’s disease would be extraordinarily rare.Our patient has no history of any immune deficiency or steroid use that would predispose to fungal esophagitis. Achalasia typically presents with gradually worsening symptoms, and the obstruction would be at the lower esophageal sphincter, not in the mid-esophagus.  
 

Reference

<sup>1. Liacouras C., Furuta G., Hirano I., et al. Eosinophilic esophagitis: updated consensus recommendations for children and adults. J Allergy Clin Immunol. 2011;128:3-20. 
2. Furuta G., Liacouras C., Collins M., et al. Eosinophilic esophagitis in children and adults: A systematic review and consensus recommendations for diagnosis and treatment. Gastroenterology. 2007;133:1342-63.</sup>

The Diagnosis

Answer: Gastrocardiac fistula with active bleeding

Active bleeding from a fistula between the right ventricle and reconstructed gastric conduit was identified after opening the gastric conduit (Figure B, black arrow). The surgeon decided to resect the gastric tube, create an esophagotomy and

Only seven cases of fistula between postesophagectomy gastric conduits and cardiac chambers, including this case, have been reported in English literature. The disease mortality rate is as high as 60%.¹ Several predisposing risk factors exist for gastrocardiac fistula, including malignancy, radiation, ischemia, and peptic ulcer disease.¹ We surmised that the previous pericardiectomy was the predisposing factor in this case.

Fistula rarely develops between the upper gastrointestinal tract and adjacent structures, including the trachea, bronchi, pleura, aorta, pericardium, and heart.^2,3 The symptoms differ depending on the location of the fistula, and recurrent bronchopneumonia, pleuritis, mediastinitis, pericarditis, and upper gastrointestinal bleeding may be present. Because of the high mortality rate, physicians should be alert to these fatal fistula. If fistula is suspected, a contrast radiological study and direct endoscopic visualization can be employed to establish a diagnosis.
Gastrocardiac fistula is a rare cause of upper gastrointestinal bleeding. The majority of diagnoses were made at autopsy. Only aggressive and emergent operative intervention can offer patients a chance of survival because they tend to deteriorate rapidly.¹ This case of gastrocardiac fistula occurred after esophagectomy with gastric conduit reconstruction and a pericardiectomy. Immediate surgery is required for life-threatening upper gastrointestinal bleeding if gastrocardiac fistula is suspected. Patient survival is likely after immediate operation.
 

References

1. Pentiak, P., Seder, C.W., Chmielewski, G.W., et al. Benign post-esophagectomy gastrocardiac fistula. Interact Cardiovasc Thorac Surg. 2011;13(4):447-9.
2. Schouten van der Velden, A.P., Ruers, T.J., Bonenkamp, J.J. A cardiogastric fistula after gastric tube interposition (A case report and review of literature). J Surg Oncol. 2007;95(1):79-82.
3. Rana, Z.A., Hosmane, V.R., Rana, N.R., et al. Gastro-right ventricular fistula: a deadly complication of a gastric pull-through. Ann Thorac Surg. 2010;90(1):297-9.

The Diagnosis

Answer: Gastrocardiac fistula with active bleeding

Active bleeding from a fistula between the right ventricle and reconstructed gastric conduit was identified after opening the gastric conduit (Figure B, black arrow). The surgeon decided to resect the gastric tube, create an esophagotomy and

Only seven cases of fistula between postesophagectomy gastric conduits and cardiac chambers, including this case, have been reported in English literature. The disease mortality rate is as high as 60%.¹ Several predisposing risk factors exist for gastrocardiac fistula, including malignancy, radiation, ischemia, and peptic ulcer disease.¹ We surmised that the previous pericardiectomy was the predisposing factor in this case.

Fistula rarely develops between the upper gastrointestinal tract and adjacent structures, including the trachea, bronchi, pleura, aorta, pericardium, and heart.^2,3 The symptoms differ depending on the location of the fistula, and recurrent bronchopneumonia, pleuritis, mediastinitis, pericarditis, and upper gastrointestinal bleeding may be present. Because of the high mortality rate, physicians should be alert to these fatal fistula. If fistula is suspected, a contrast radiological study and direct endoscopic visualization can be employed to establish a diagnosis.
Gastrocardiac fistula is a rare cause of upper gastrointestinal bleeding. The majority of diagnoses were made at autopsy. Only aggressive and emergent operative intervention can offer patients a chance of survival because they tend to deteriorate rapidly.¹ This case of gastrocardiac fistula occurred after esophagectomy with gastric conduit reconstruction and a pericardiectomy. Immediate surgery is required for life-threatening upper gastrointestinal bleeding if gastrocardiac fistula is suspected. Patient survival is likely after immediate operation.
 

References

1. Pentiak, P., Seder, C.W., Chmielewski, G.W., et al. Benign post-esophagectomy gastrocardiac fistula. Interact Cardiovasc Thorac Surg. 2011;13(4):447-9.
2. Schouten van der Velden, A.P., Ruers, T.J., Bonenkamp, J.J. A cardiogastric fistula after gastric tube interposition (A case report and review of literature). J Surg Oncol. 2007;95(1):79-82.
3. Rana, Z.A., Hosmane, V.R., Rana, N.R., et al. Gastro-right ventricular fistula: a deadly complication of a gastric pull-through. Ann Thorac Surg. 2010;90(1):297-9.

The Diagnosis

Answer: Gastrocardiac fistula with active bleeding

Active bleeding from a fistula between the right ventricle and reconstructed gastric conduit was identified after opening the gastric conduit (Figure B, black arrow). The surgeon decided to resect the gastric tube, create an esophagotomy and

Only seven cases of fistula between postesophagectomy gastric conduits and cardiac chambers, including this case, have been reported in English literature. The disease mortality rate is as high as 60%.¹ Several predisposing risk factors exist for gastrocardiac fistula, including malignancy, radiation, ischemia, and peptic ulcer disease.¹ We surmised that the previous pericardiectomy was the predisposing factor in this case.

Fistula rarely develops between the upper gastrointestinal tract and adjacent structures, including the trachea, bronchi, pleura, aorta, pericardium, and heart.^2,3 The symptoms differ depending on the location of the fistula, and recurrent bronchopneumonia, pleuritis, mediastinitis, pericarditis, and upper gastrointestinal bleeding may be present. Because of the high mortality rate, physicians should be alert to these fatal fistula. If fistula is suspected, a contrast radiological study and direct endoscopic visualization can be employed to establish a diagnosis.
Gastrocardiac fistula is a rare cause of upper gastrointestinal bleeding. The majority of diagnoses were made at autopsy. Only aggressive and emergent operative intervention can offer patients a chance of survival because they tend to deteriorate rapidly.¹ This case of gastrocardiac fistula occurred after esophagectomy with gastric conduit reconstruction and a pericardiectomy. Immediate surgery is required for life-threatening upper gastrointestinal bleeding if gastrocardiac fistula is suspected. Patient survival is likely after immediate operation.
 

References

1. Pentiak, P., Seder, C.W., Chmielewski, G.W., et al. Benign post-esophagectomy gastrocardiac fistula. Interact Cardiovasc Thorac Surg. 2011;13(4):447-9.
2. Schouten van der Velden, A.P., Ruers, T.J., Bonenkamp, J.J. A cardiogastric fistula after gastric tube interposition (A case report and review of literature). J Surg Oncol. 2007;95(1):79-82.
3. Rana, Z.A., Hosmane, V.R., Rana, N.R., et al. Gastro-right ventricular fistula: a deadly complication of a gastric pull-through. Ann Thorac Surg. 2010;90(1):297-9.

We are a group of six adult Inflammatory bowel disease (IBD) patients who serve as the Patient Governance Committee for CCFA Partners – a patient powered research network that assists IBD patients, researchers, and healthcare providers to partner in finding the answers to questions patients care about and improving the health and lives of patients living with these conditions. To find out more about us, please visit our website at https://ccfa.med.unc.edu/ or send an email to info@ccfapartners.org.

monkeybusinessimages/Thinkstock

Open communication between patient and physician

Perhaps the single most important quality of a physician is a willingness to listen. IBD patients often don’t feel like they are being heard. Starting with a conversation about the patient’s goals in terms of managing the disease as well as their goals in life will help the physician understand the patient’s unique situation and concerns. This is really a twofold proposition: what are the patient’s short-term and long-term goals? What is the most effective treatment plan to help them? How do the physician and the patient define treatment success?

Coordinating care and transitions

When a patient needs to transfer to a new physician it’s important to help them find the right fit for their particular circumstances. Ask what is most important to patients. Is it the distance between their residence and their provider? Is it ability to manage complex disease? Is the physician in-network? All of these are important factors in helping the patient find the right care.

Holistic approach to treatment

Treating an IBD patient means treating the patient as a whole, not only their symptoms. IBD can lead to many challenges for patients and that is why treatment plans must consider not only physical, but also emotional and mental health, needs. One underserved area is pain management. While the dangers of opiates have been well documented, it seems the pendulum has swung too far in the opposite direction: some doctors are ignoring the topic of pain management altogether or establishing policies against prescribing any narcotic pain medications. This trend is troubling. Pain management is not an issue that goes away by ignoring it and remains a very important part of overall care needs. Doctors should be encouraged to take the time to learn about the many different approaches to pain management, including nonnarcotic and nonmedication therapies.

Conclusion

The mark of a high-functioning patient/physician relationship is that the patient feels empowered to be engaged with the management of their disease. An empowered patient is one who feels comfortable asking about new therapeutic options, explores new approaches to managing their disease without fear of being judged, and sticks with a treatment plan. By treating patients as partners in the fight against IBD, you can help patients accomplish their goals through a relationship based on mutual trust.

Patient Accounts

Since my diagnosis 15 years ago, the gastroenterologists who have cared for me were all effective clinicians who improved my quality of life. However, the best physicians asked me directly what aspects of my life I found most important.

My answer to this “life priority” question has changed over time. As a teenager, I wanted to fit in with my peer group as much as I could. In my early 20s, I wanted to take part in physical activity and reduce my pain as much as possible. Today, I prioritize being mentally sharp and reliable for those who depend on me professionally and maintaining empathy for those who depend on me emotionally.

I can imagine that my priorities are more easily relatable to an adult physician now than when I was in my teens, but the best gastroenterologists have empathetically listened and respected my wishes, within reason, throughout my entire experience of illness.

To me, what makes an excellent gastroenterologist is the ability to understand a patient’s greatest priorities, the activities or feelings or connections that make that person feel most whole, and, whenever possible, to direct treatment strategy according to these priorities.

– Jessica Burris
 

As young physicians, you may feel the need to know the answers to all our questions or a thorny diagnostic problem we present. The truth is we don’t expect you to know all the answers in the moment, it’s OK to stay you don’t know, but stay curious in finding a solution.

Also, at times there is a third presence in the room with you and your patient: the electronic medical record. It can be easy to become distracted and not make eye contact with us, which can seem as if you aren’t paying attention. Remember to always be fully present with your patient. Your patient will truly appreciate it.

– David Walter
 

We are a group of six adult Inflammatory bowel disease (IBD) patients who serve as the Patient Governance Committee for CCFA Partners – a patient powered research network that assists IBD patients, researchers, and healthcare providers to partner in finding the answers to questions patients care about and improving the health and lives of patients living with these conditions. To find out more about us, please visit our website at https://ccfa.med.unc.edu/ or send an email to info@ccfapartners.org.

monkeybusinessimages/Thinkstock

Open communication between patient and physician

Perhaps the single most important quality of a physician is a willingness to listen. IBD patients often don’t feel like they are being heard. Starting with a conversation about the patient’s goals in terms of managing the disease as well as their goals in life will help the physician understand the patient’s unique situation and concerns. This is really a twofold proposition: what are the patient’s short-term and long-term goals? What is the most effective treatment plan to help them? How do the physician and the patient define treatment success?

Coordinating care and transitions

When a patient needs to transfer to a new physician it’s important to help them find the right fit for their particular circumstances. Ask what is most important to patients. Is it the distance between their residence and their provider? Is it ability to manage complex disease? Is the physician in-network? All of these are important factors in helping the patient find the right care.

Holistic approach to treatment

Treating an IBD patient means treating the patient as a whole, not only their symptoms. IBD can lead to many challenges for patients and that is why treatment plans must consider not only physical, but also emotional and mental health, needs. One underserved area is pain management. While the dangers of opiates have been well documented, it seems the pendulum has swung too far in the opposite direction: some doctors are ignoring the topic of pain management altogether or establishing policies against prescribing any narcotic pain medications. This trend is troubling. Pain management is not an issue that goes away by ignoring it and remains a very important part of overall care needs. Doctors should be encouraged to take the time to learn about the many different approaches to pain management, including nonnarcotic and nonmedication therapies.

Conclusion

The mark of a high-functioning patient/physician relationship is that the patient feels empowered to be engaged with the management of their disease. An empowered patient is one who feels comfortable asking about new therapeutic options, explores new approaches to managing their disease without fear of being judged, and sticks with a treatment plan. By treating patients as partners in the fight against IBD, you can help patients accomplish their goals through a relationship based on mutual trust.

Patient Accounts

Since my diagnosis 15 years ago, the gastroenterologists who have cared for me were all effective clinicians who improved my quality of life. However, the best physicians asked me directly what aspects of my life I found most important.

My answer to this “life priority” question has changed over time. As a teenager, I wanted to fit in with my peer group as much as I could. In my early 20s, I wanted to take part in physical activity and reduce my pain as much as possible. Today, I prioritize being mentally sharp and reliable for those who depend on me professionally and maintaining empathy for those who depend on me emotionally.

I can imagine that my priorities are more easily relatable to an adult physician now than when I was in my teens, but the best gastroenterologists have empathetically listened and respected my wishes, within reason, throughout my entire experience of illness.

To me, what makes an excellent gastroenterologist is the ability to understand a patient’s greatest priorities, the activities or feelings or connections that make that person feel most whole, and, whenever possible, to direct treatment strategy according to these priorities.

– Jessica Burris
 

As young physicians, you may feel the need to know the answers to all our questions or a thorny diagnostic problem we present. The truth is we don’t expect you to know all the answers in the moment, it’s OK to stay you don’t know, but stay curious in finding a solution.

Also, at times there is a third presence in the room with you and your patient: the electronic medical record. It can be easy to become distracted and not make eye contact with us, which can seem as if you aren’t paying attention. Remember to always be fully present with your patient. Your patient will truly appreciate it.

– David Walter
 

We are a group of six adult Inflammatory bowel disease (IBD) patients who serve as the Patient Governance Committee for CCFA Partners – a patient powered research network that assists IBD patients, researchers, and healthcare providers to partner in finding the answers to questions patients care about and improving the health and lives of patients living with these conditions. To find out more about us, please visit our website at https://ccfa.med.unc.edu/ or send an email to info@ccfapartners.org.

monkeybusinessimages/Thinkstock

Open communication between patient and physician

Perhaps the single most important quality of a physician is a willingness to listen. IBD patients often don’t feel like they are being heard. Starting with a conversation about the patient’s goals in terms of managing the disease as well as their goals in life will help the physician understand the patient’s unique situation and concerns. This is really a twofold proposition: what are the patient’s short-term and long-term goals? What is the most effective treatment plan to help them? How do the physician and the patient define treatment success?

Coordinating care and transitions

When a patient needs to transfer to a new physician it’s important to help them find the right fit for their particular circumstances. Ask what is most important to patients. Is it the distance between their residence and their provider? Is it ability to manage complex disease? Is the physician in-network? All of these are important factors in helping the patient find the right care.

Holistic approach to treatment

Treating an IBD patient means treating the patient as a whole, not only their symptoms. IBD can lead to many challenges for patients and that is why treatment plans must consider not only physical, but also emotional and mental health, needs. One underserved area is pain management. While the dangers of opiates have been well documented, it seems the pendulum has swung too far in the opposite direction: some doctors are ignoring the topic of pain management altogether or establishing policies against prescribing any narcotic pain medications. This trend is troubling. Pain management is not an issue that goes away by ignoring it and remains a very important part of overall care needs. Doctors should be encouraged to take the time to learn about the many different approaches to pain management, including nonnarcotic and nonmedication therapies.

Conclusion

The mark of a high-functioning patient/physician relationship is that the patient feels empowered to be engaged with the management of their disease. An empowered patient is one who feels comfortable asking about new therapeutic options, explores new approaches to managing their disease without fear of being judged, and sticks with a treatment plan. By treating patients as partners in the fight against IBD, you can help patients accomplish their goals through a relationship based on mutual trust.

Patient Accounts

Since my diagnosis 15 years ago, the gastroenterologists who have cared for me were all effective clinicians who improved my quality of life. However, the best physicians asked me directly what aspects of my life I found most important.

My answer to this “life priority” question has changed over time. As a teenager, I wanted to fit in with my peer group as much as I could. In my early 20s, I wanted to take part in physical activity and reduce my pain as much as possible. Today, I prioritize being mentally sharp and reliable for those who depend on me professionally and maintaining empathy for those who depend on me emotionally.

I can imagine that my priorities are more easily relatable to an adult physician now than when I was in my teens, but the best gastroenterologists have empathetically listened and respected my wishes, within reason, throughout my entire experience of illness.

To me, what makes an excellent gastroenterologist is the ability to understand a patient’s greatest priorities, the activities or feelings or connections that make that person feel most whole, and, whenever possible, to direct treatment strategy according to these priorities.

– Jessica Burris
 

As young physicians, you may feel the need to know the answers to all our questions or a thorny diagnostic problem we present. The truth is we don’t expect you to know all the answers in the moment, it’s OK to stay you don’t know, but stay curious in finding a solution.

Also, at times there is a third presence in the room with you and your patient: the electronic medical record. It can be easy to become distracted and not make eye contact with us, which can seem as if you aren’t paying attention. Remember to always be fully present with your patient. Your patient will truly appreciate it.

– David Walter
 

Your next patient is a 67-year-old Medicare beneficiary with corticosteroid-dependent ulcerative colitis. Despite 4 months of maximally dosed mesalamine, his colitis flares with prednisone taper below 20 mg daily. Hepatitis B serologies and tuberculin skin test were negative 10 months ago. Which of the following do you recommend?

A. Steroid-sparing therapy initiation

B. Repeat latent tuberculosis screening in anticipation of anti–tumor necrosis factor (TNF) therapy

C. Bone loss assessment

D. Pneumococcal vaccination

E. Tobacco use screening

Why are IBD quality measures needed?

What makes a good quality measure?

Quality must be defined and measured before it can be improved. This is easier said than done, especially for IBD where a gold standard in “ideal care” is ill defined and continually evolving as new research emerges. Nonetheless, hundreds of health care quality measures have been proposed. Desirable quality measure attributes should satisfy three broad categories: importance, scientific soundness, and feasibility.10 Quality measures should address relevant and important aspects of health that are highly prevalent and for which evidence indicates a need for improvement. There should be strong evidence supporting the beneficial impact of adhering to a given measure.

What IBD quality measures already exist?

Expert panels from the AGA and the Crohn’s & Colitis Foundation of America (CCFA) produced IBD quality measure sets comprising mostly process measures (Table 1). The original 10 AGA measures released in 2011 address aspects of disease assessment, treatment, complication prevention, and health care maintenance.12 They include seven IBD-specific measures, three cross-cutting measures – defined by Centers for Medicare & Medicaid Services (CMS) as being broadly applicable across multiple clinical settings – and two inpatient measures. A major goal of the AGA measures was to facilitate quality reporting to the former PQRS program.

What are some quality measure limitations?

Quality measure development has an evidence base but designing an optimal measure and demonstrating impact can be challenging. Few IBD process measures are validated and thus there is often logic but not data linking process measure adherence to improved outcomes. The denominator (number of eligible patients) and potential impact of broad adherence vary for each quality measure. For example, only a small fraction of IBD patients are infected with hepatitis B and fewer than 10% will experience viral reactivation during anti-TNF therapy.17,18 Even with optimal adherence to the hepatitis B measure, few reactivations will be prevented. The wording of some measures lacks precision, allowing physicians to potentially claim credit without improving care. For example, ordering a bone density scan satisfies the bone loss assessment measure, even if osteoporosis goes unrecognized and untreated. Finally, some measures relate to actions that may not be under the control of the gastroenterologist whose performance is being measured (e.g., administering vaccinations).

IBD quality measures under MIPS

Table 1 depicts the evolution of IBD process measures from 2011 to 2017. Rather than building upon initial experience to revise and refine IBD quality measures, the measures have instead been progressively culled with the changing pay-for-performance landscape. In 2016, AGA eliminated the two inpatient measures.19 Seven of the remaining eight measures formed the IBD Measures Group which was reportable under PQRS. In 2017, MIPS brought a seismic shift in quality measure focus. The PQRS IBD Measures Group was abolished – as were all Measures Groups – and replaced by a 16-item GI Measures Set. Although AGA advocated for all of the IBD measures to be included, the new GI Measures Set deemphasized the IBD-specific measures in favor of expanded cross-cutting measures (e.g., screening for abnormal body mass index, documenting current medications, sending specialist report to referring provider).20 This reflected a previously observed trend that gastroenterologists more often reported on cross-cutting measures than specialist-specific measures.21 However, there was no evidence-based justification for dropping certain IBD-specific measures (especially the steroid-sparing therapy measure) in favor of retaining the two chosen IBD-specific measures – bone loss assessment and hepatitis B screening – which apply to only a subset of IBD patients and have limited potential to impact clinical outcomes. Although it is not mandatory to report using the GI Measures Set, we suspect that many gastroenterologists will use this set to guide their initial reporting.

AGA Institute

A word about Alternative Payment Models (APMs)

APMs represent the non-MIPS pathway for participating in the QPP. APMs focus on chronic disease care coordination and qualify for lump-sum incentive payments by adhering to stringent standards and financial risk-sharing requirements. A detailed overview of APMs is beyond the scope of this discussion, as the vast majority of MACRA-eligible gastroenterologists will participate in MIPS and there are currently no GI-specific APMs. However, this is an evolving area and Project Sonar has been submitted to the Physician-Focused Payment Model Technical Advisory Committee for consideration as an APM for Crohn’s disease.23

Conclusion

Quality measurement and reporting are at a crossroads. Ideally, performance improvement should be an internally driven process that addresses specific local priorities and needs. Most medical practices (73%) believe that current externally driven quality measures do not represent care quality and only 28% use their quality scores to focus their internal quality improvement activities.2 The burden and cost of external quality reporting demand better alignment with local priorities as resources are currently being diverted away from internally driven efforts that might have the greatest potential to improve patient outcomes.24 The dawn of the MACRA era presents an opportunity to shape the future of the IBD quality movement. Through validating and prioritizing existing measures and developing novel, precisely stated, and high-value metrics, there remains vast (and measurable) potential to enhance patient outcomes.

Dr. McConnell is a fellow in gastroenterology and advanced inflammatory bowel disease, division of gastroenterology, University of California, San Francisco. Dr. Velayos is professor of medicine, co–medical director, Center for Crohn’s and Colitis, University of California, San Francisco.

References

1. September 2016 Medscape survey summary. Available at http://www.healthcaredive.com/news/survey-29-of-physicians-still-havent-heard-of-macra/429322/. Accessed March 23, 2017.

2. Casalino L.P., et al. Health Aff. 2016;35:401-6.

3. Rubin D.T., et al. Curr Med Res Opin. 2017;33:529-36.

4. David G., et al. Gastroenterology. 2013;144:S-647.

5. Nguyen G.C., et al. Clin Gastroenterol Hepatol. 2006;4:1507-13.

6. Esrailian E., et al. Aliment Pharmacol Ther. 2007;26:1005-18.

7. Spiegel B.M., et al. Clin Gastroenterol Hepatol. 2009;7:68-74.

8. Kappelman M.D., et al. Inflamm Bowel Dis. 2010;16:125-133.

9. Reddy S.I., et al. Am J Gastroenterol. 2005;100:1357-61.

10. National Quality Measures Clearinghouse. Available at https://www.qualitymeasures.ahrq.gov/help-and-about/quality-measure-tutorials/desirable-attributes-of-a-quality-measure. Accessed March 23, 2017.

11. McGlynn E.A. Med Care. 2003;41(1 Suppl):139-47.

12. American Gastroenterological Association. Available at https://www.gastro.org/practice/quality-initiatives/IBD_Measures.pdf. Accessed March 23, 2017.

13. Melmed G.Y., et al. Inflamm Bowel Dis. 2013;19:662-8.

14. Feuerstein J.D., et al. Clin Gastroenterol Hepatol. 2016;14:421-8.

15. Sapir T., et al. Dig Dis Sci. 2016;61:1862-9.

16. Crohn’s & Colitis Foundation of America. IBD Qorus. Available at http://www.ccfa.org/science-and-professionals/ibdqorus/. Accessed March 23, 2017.

17. Hou J.K., et al. Gastroenterology. 2015;148(Suppl 1):S-61.

18. Reddy K.R., et al. Gastroenterology. 2015;48:215-9.

19. American Gastroenterological Association. Available at http://www.gastro.org/practice-management/measures/2016_AGA_Measures_-_IBD.pdf. Accessed March 23, 2017.

20. American Gastroenterological Association. Available at http://www.gastro.org/news_items/gi-quality-measures-for-2017-are-released-in-macra-final-rule. Accessed March 23, 2017.

21. Centers for Medicare & Medicaid Services. Available at https://www.cms.gov/Medicare/Quality-Initiatives-Patient-Assessment-Instruments/PQRS/Downloads/2014_PQRS_Experience_Rpt.pdf. Accessed March 23, 2017.

22. Dahlhamer J.M., et al. MMWR. 2016;65:1166-9.

23. U.S. Department of Health & Human Services Office of the Assistant Secretary for Planning and Evaluation. Available at https://aspe.hhs.gov/system/files/pdf/253406/ProjectSonarSonarMD.pdf. Accessed March 23, 2017.

24. Meyer G.S., et al. BMJ Qual Saf. 2012;21:964-8.

Your next patient is a 67-year-old Medicare beneficiary with corticosteroid-dependent ulcerative colitis. Despite 4 months of maximally dosed mesalamine, his colitis flares with prednisone taper below 20 mg daily. Hepatitis B serologies and tuberculin skin test were negative 10 months ago. Which of the following do you recommend?

A. Steroid-sparing therapy initiation

B. Repeat latent tuberculosis screening in anticipation of anti–tumor necrosis factor (TNF) therapy

C. Bone loss assessment

D. Pneumococcal vaccination

E. Tobacco use screening

Why are IBD quality measures needed?

What makes a good quality measure?

Quality must be defined and measured before it can be improved. This is easier said than done, especially for IBD where a gold standard in “ideal care” is ill defined and continually evolving as new research emerges. Nonetheless, hundreds of health care quality measures have been proposed. Desirable quality measure attributes should satisfy three broad categories: importance, scientific soundness, and feasibility.10 Quality measures should address relevant and important aspects of health that are highly prevalent and for which evidence indicates a need for improvement. There should be strong evidence supporting the beneficial impact of adhering to a given measure.

What IBD quality measures already exist?

Expert panels from the AGA and the Crohn’s & Colitis Foundation of America (CCFA) produced IBD quality measure sets comprising mostly process measures (Table 1). The original 10 AGA measures released in 2011 address aspects of disease assessment, treatment, complication prevention, and health care maintenance.12 They include seven IBD-specific measures, three cross-cutting measures – defined by Centers for Medicare & Medicaid Services (CMS) as being broadly applicable across multiple clinical settings – and two inpatient measures. A major goal of the AGA measures was to facilitate quality reporting to the former PQRS program.

What are some quality measure limitations?

Quality measure development has an evidence base but designing an optimal measure and demonstrating impact can be challenging. Few IBD process measures are validated and thus there is often logic but not data linking process measure adherence to improved outcomes. The denominator (number of eligible patients) and potential impact of broad adherence vary for each quality measure. For example, only a small fraction of IBD patients are infected with hepatitis B and fewer than 10% will experience viral reactivation during anti-TNF therapy.17,18 Even with optimal adherence to the hepatitis B measure, few reactivations will be prevented. The wording of some measures lacks precision, allowing physicians to potentially claim credit without improving care. For example, ordering a bone density scan satisfies the bone loss assessment measure, even if osteoporosis goes unrecognized and untreated. Finally, some measures relate to actions that may not be under the control of the gastroenterologist whose performance is being measured (e.g., administering vaccinations).

IBD quality measures under MIPS

Table 1 depicts the evolution of IBD process measures from 2011 to 2017. Rather than building upon initial experience to revise and refine IBD quality measures, the measures have instead been progressively culled with the changing pay-for-performance landscape. In 2016, AGA eliminated the two inpatient measures.19 Seven of the remaining eight measures formed the IBD Measures Group which was reportable under PQRS. In 2017, MIPS brought a seismic shift in quality measure focus. The PQRS IBD Measures Group was abolished – as were all Measures Groups – and replaced by a 16-item GI Measures Set. Although AGA advocated for all of the IBD measures to be included, the new GI Measures Set deemphasized the IBD-specific measures in favor of expanded cross-cutting measures (e.g., screening for abnormal body mass index, documenting current medications, sending specialist report to referring provider).20 This reflected a previously observed trend that gastroenterologists more often reported on cross-cutting measures than specialist-specific measures.21 However, there was no evidence-based justification for dropping certain IBD-specific measures (especially the steroid-sparing therapy measure) in favor of retaining the two chosen IBD-specific measures – bone loss assessment and hepatitis B screening – which apply to only a subset of IBD patients and have limited potential to impact clinical outcomes. Although it is not mandatory to report using the GI Measures Set, we suspect that many gastroenterologists will use this set to guide their initial reporting.

AGA Institute

A word about Alternative Payment Models (APMs)

APMs represent the non-MIPS pathway for participating in the QPP. APMs focus on chronic disease care coordination and qualify for lump-sum incentive payments by adhering to stringent standards and financial risk-sharing requirements. A detailed overview of APMs is beyond the scope of this discussion, as the vast majority of MACRA-eligible gastroenterologists will participate in MIPS and there are currently no GI-specific APMs. However, this is an evolving area and Project Sonar has been submitted to the Physician-Focused Payment Model Technical Advisory Committee for consideration as an APM for Crohn’s disease.23

Conclusion

Quality measurement and reporting are at a crossroads. Ideally, performance improvement should be an internally driven process that addresses specific local priorities and needs. Most medical practices (73%) believe that current externally driven quality measures do not represent care quality and only 28% use their quality scores to focus their internal quality improvement activities.2 The burden and cost of external quality reporting demand better alignment with local priorities as resources are currently being diverted away from internally driven efforts that might have the greatest potential to improve patient outcomes.24 The dawn of the MACRA era presents an opportunity to shape the future of the IBD quality movement. Through validating and prioritizing existing measures and developing novel, precisely stated, and high-value metrics, there remains vast (and measurable) potential to enhance patient outcomes.

Dr. McConnell is a fellow in gastroenterology and advanced inflammatory bowel disease, division of gastroenterology, University of California, San Francisco. Dr. Velayos is professor of medicine, co–medical director, Center for Crohn’s and Colitis, University of California, San Francisco.

References

1. September 2016 Medscape survey summary. Available at http://www.healthcaredive.com/news/survey-29-of-physicians-still-havent-heard-of-macra/429322/. Accessed March 23, 2017.

2. Casalino L.P., et al. Health Aff. 2016;35:401-6.

3. Rubin D.T., et al. Curr Med Res Opin. 2017;33:529-36.

4. David G., et al. Gastroenterology. 2013;144:S-647.

5. Nguyen G.C., et al. Clin Gastroenterol Hepatol. 2006;4:1507-13.

6. Esrailian E., et al. Aliment Pharmacol Ther. 2007;26:1005-18.

7. Spiegel B.M., et al. Clin Gastroenterol Hepatol. 2009;7:68-74.

8. Kappelman M.D., et al. Inflamm Bowel Dis. 2010;16:125-133.

9. Reddy S.I., et al. Am J Gastroenterol. 2005;100:1357-61.

10. National Quality Measures Clearinghouse. Available at https://www.qualitymeasures.ahrq.gov/help-and-about/quality-measure-tutorials/desirable-attributes-of-a-quality-measure. Accessed March 23, 2017.

11. McGlynn E.A. Med Care. 2003;41(1 Suppl):139-47.

12. American Gastroenterological Association. Available at https://www.gastro.org/practice/quality-initiatives/IBD_Measures.pdf. Accessed March 23, 2017.

13. Melmed G.Y., et al. Inflamm Bowel Dis. 2013;19:662-8.

14. Feuerstein J.D., et al. Clin Gastroenterol Hepatol. 2016;14:421-8.

15. Sapir T., et al. Dig Dis Sci. 2016;61:1862-9.

16. Crohn’s & Colitis Foundation of America. IBD Qorus. Available at http://www.ccfa.org/science-and-professionals/ibdqorus/. Accessed March 23, 2017.

17. Hou J.K., et al. Gastroenterology. 2015;148(Suppl 1):S-61.

18. Reddy K.R., et al. Gastroenterology. 2015;48:215-9.

19. American Gastroenterological Association. Available at http://www.gastro.org/practice-management/measures/2016_AGA_Measures_-_IBD.pdf. Accessed March 23, 2017.

20. American Gastroenterological Association. Available at http://www.gastro.org/news_items/gi-quality-measures-for-2017-are-released-in-macra-final-rule. Accessed March 23, 2017.

21. Centers for Medicare & Medicaid Services. Available at https://www.cms.gov/Medicare/Quality-Initiatives-Patient-Assessment-Instruments/PQRS/Downloads/2014_PQRS_Experience_Rpt.pdf. Accessed March 23, 2017.

22. Dahlhamer J.M., et al. MMWR. 2016;65:1166-9.

23. U.S. Department of Health & Human Services Office of the Assistant Secretary for Planning and Evaluation. Available at https://aspe.hhs.gov/system/files/pdf/253406/ProjectSonarSonarMD.pdf. Accessed March 23, 2017.

24. Meyer G.S., et al. BMJ Qual Saf. 2012;21:964-8.

Your next patient is a 67-year-old Medicare beneficiary with corticosteroid-dependent ulcerative colitis. Despite 4 months of maximally dosed mesalamine, his colitis flares with prednisone taper below 20 mg daily. Hepatitis B serologies and tuberculin skin test were negative 10 months ago. Which of the following do you recommend?

A. Steroid-sparing therapy initiation

B. Repeat latent tuberculosis screening in anticipation of anti–tumor necrosis factor (TNF) therapy

C. Bone loss assessment

D. Pneumococcal vaccination

E. Tobacco use screening

Why are IBD quality measures needed?

What makes a good quality measure?

Quality must be defined and measured before it can be improved. This is easier said than done, especially for IBD where a gold standard in “ideal care” is ill defined and continually evolving as new research emerges. Nonetheless, hundreds of health care quality measures have been proposed. Desirable quality measure attributes should satisfy three broad categories: importance, scientific soundness, and feasibility.10 Quality measures should address relevant and important aspects of health that are highly prevalent and for which evidence indicates a need for improvement. There should be strong evidence supporting the beneficial impact of adhering to a given measure.

What IBD quality measures already exist?

Expert panels from the AGA and the Crohn’s & Colitis Foundation of America (CCFA) produced IBD quality measure sets comprising mostly process measures (Table 1). The original 10 AGA measures released in 2011 address aspects of disease assessment, treatment, complication prevention, and health care maintenance.12 They include seven IBD-specific measures, three cross-cutting measures – defined by Centers for Medicare & Medicaid Services (CMS) as being broadly applicable across multiple clinical settings – and two inpatient measures. A major goal of the AGA measures was to facilitate quality reporting to the former PQRS program.

What are some quality measure limitations?

Quality measure development has an evidence base but designing an optimal measure and demonstrating impact can be challenging. Few IBD process measures are validated and thus there is often logic but not data linking process measure adherence to improved outcomes. The denominator (number of eligible patients) and potential impact of broad adherence vary for each quality measure. For example, only a small fraction of IBD patients are infected with hepatitis B and fewer than 10% will experience viral reactivation during anti-TNF therapy.17,18 Even with optimal adherence to the hepatitis B measure, few reactivations will be prevented. The wording of some measures lacks precision, allowing physicians to potentially claim credit without improving care. For example, ordering a bone density scan satisfies the bone loss assessment measure, even if osteoporosis goes unrecognized and untreated. Finally, some measures relate to actions that may not be under the control of the gastroenterologist whose performance is being measured (e.g., administering vaccinations).

IBD quality measures under MIPS

Table 1 depicts the evolution of IBD process measures from 2011 to 2017. Rather than building upon initial experience to revise and refine IBD quality measures, the measures have instead been progressively culled with the changing pay-for-performance landscape. In 2016, AGA eliminated the two inpatient measures.19 Seven of the remaining eight measures formed the IBD Measures Group which was reportable under PQRS. In 2017, MIPS brought a seismic shift in quality measure focus. The PQRS IBD Measures Group was abolished – as were all Measures Groups – and replaced by a 16-item GI Measures Set. Although AGA advocated for all of the IBD measures to be included, the new GI Measures Set deemphasized the IBD-specific measures in favor of expanded cross-cutting measures (e.g., screening for abnormal body mass index, documenting current medications, sending specialist report to referring provider).20 This reflected a previously observed trend that gastroenterologists more often reported on cross-cutting measures than specialist-specific measures.21 However, there was no evidence-based justification for dropping certain IBD-specific measures (especially the steroid-sparing therapy measure) in favor of retaining the two chosen IBD-specific measures – bone loss assessment and hepatitis B screening – which apply to only a subset of IBD patients and have limited potential to impact clinical outcomes. Although it is not mandatory to report using the GI Measures Set, we suspect that many gastroenterologists will use this set to guide their initial reporting.

AGA Institute

A word about Alternative Payment Models (APMs)

APMs represent the non-MIPS pathway for participating in the QPP. APMs focus on chronic disease care coordination and qualify for lump-sum incentive payments by adhering to stringent standards and financial risk-sharing requirements. A detailed overview of APMs is beyond the scope of this discussion, as the vast majority of MACRA-eligible gastroenterologists will participate in MIPS and there are currently no GI-specific APMs. However, this is an evolving area and Project Sonar has been submitted to the Physician-Focused Payment Model Technical Advisory Committee for consideration as an APM for Crohn’s disease.23

Conclusion

Quality measurement and reporting are at a crossroads. Ideally, performance improvement should be an internally driven process that addresses specific local priorities and needs. Most medical practices (73%) believe that current externally driven quality measures do not represent care quality and only 28% use their quality scores to focus their internal quality improvement activities.2 The burden and cost of external quality reporting demand better alignment with local priorities as resources are currently being diverted away from internally driven efforts that might have the greatest potential to improve patient outcomes.24 The dawn of the MACRA era presents an opportunity to shape the future of the IBD quality movement. Through validating and prioritizing existing measures and developing novel, precisely stated, and high-value metrics, there remains vast (and measurable) potential to enhance patient outcomes.

Dr. McConnell is a fellow in gastroenterology and advanced inflammatory bowel disease, division of gastroenterology, University of California, San Francisco. Dr. Velayos is professor of medicine, co–medical director, Center for Crohn’s and Colitis, University of California, San Francisco.

References

1. September 2016 Medscape survey summary. Available at http://www.healthcaredive.com/news/survey-29-of-physicians-still-havent-heard-of-macra/429322/. Accessed March 23, 2017.

2. Casalino L.P., et al. Health Aff. 2016;35:401-6.

3. Rubin D.T., et al. Curr Med Res Opin. 2017;33:529-36.

4. David G., et al. Gastroenterology. 2013;144:S-647.

5. Nguyen G.C., et al. Clin Gastroenterol Hepatol. 2006;4:1507-13.

6. Esrailian E., et al. Aliment Pharmacol Ther. 2007;26:1005-18.

7. Spiegel B.M., et al. Clin Gastroenterol Hepatol. 2009;7:68-74.

8. Kappelman M.D., et al. Inflamm Bowel Dis. 2010;16:125-133.

9. Reddy S.I., et al. Am J Gastroenterol. 2005;100:1357-61.

10. National Quality Measures Clearinghouse. Available at https://www.qualitymeasures.ahrq.gov/help-and-about/quality-measure-tutorials/desirable-attributes-of-a-quality-measure. Accessed March 23, 2017.

11. McGlynn E.A. Med Care. 2003;41(1 Suppl):139-47.

12. American Gastroenterological Association. Available at https://www.gastro.org/practice/quality-initiatives/IBD_Measures.pdf. Accessed March 23, 2017.

13. Melmed G.Y., et al. Inflamm Bowel Dis. 2013;19:662-8.

14. Feuerstein J.D., et al. Clin Gastroenterol Hepatol. 2016;14:421-8.

15. Sapir T., et al. Dig Dis Sci. 2016;61:1862-9.

16. Crohn’s & Colitis Foundation of America. IBD Qorus. Available at http://www.ccfa.org/science-and-professionals/ibdqorus/. Accessed March 23, 2017.

17. Hou J.K., et al. Gastroenterology. 2015;148(Suppl 1):S-61.

18. Reddy K.R., et al. Gastroenterology. 2015;48:215-9.

19. American Gastroenterological Association. Available at http://www.gastro.org/practice-management/measures/2016_AGA_Measures_-_IBD.pdf. Accessed March 23, 2017.

20. American Gastroenterological Association. Available at http://www.gastro.org/news_items/gi-quality-measures-for-2017-are-released-in-macra-final-rule. Accessed March 23, 2017.

21. Centers for Medicare & Medicaid Services. Available at https://www.cms.gov/Medicare/Quality-Initiatives-Patient-Assessment-Instruments/PQRS/Downloads/2014_PQRS_Experience_Rpt.pdf. Accessed March 23, 2017.

22. Dahlhamer J.M., et al. MMWR. 2016;65:1166-9.

23. U.S. Department of Health & Human Services Office of the Assistant Secretary for Planning and Evaluation. Available at https://aspe.hhs.gov/system/files/pdf/253406/ProjectSonarSonarMD.pdf. Accessed March 23, 2017.

24. Meyer G.S., et al. BMJ Qual Saf. 2012;21:964-8.