Pain

The mainstay of treatment for many musculoskeletal (MSK) complaints is physical or occupational therapy. But often an individual’s underlying biomechanical issue is one that can be easily addressed with a home exercise plan, and, in light of the COVID-19 pandemic, patients may wish to avoid in-person physical therapy. This article describes the rationale for, and methods of providing, home exercises for several MSK conditions commonly seen in the primary care setting.

General rehabilitation principles: First things first

With basic MSK complaints, focus on controlling pain and swelling before undertaking restoration of function. Tailor pharmacologic and nonpharmacologic options to the patient’s needs, using first-line modalities such as ice and compression to reduce inflammation, and prescribing scheduled doses of an anti-inflammatory medication to help with both pain and inflammation.

Once pain is sufficiently controlled, have patients begin basic rehabilitation with simple range-of-motion exercises that move the injured region through normal patterns, as tolerated. Later, the patient can progress through more specific exercises to return the injured region to full functional capacity.

Explain to patients that it takes about 7 to 10 days of consistent care to decrease inflammation, but that they should begin prescribed exercises once they are able to tolerate them. Plan a follow-up visit in 2 to 3 weeks to check on the patient’s response to prescribed care.

Which is better, ice or heat?

Ice and heat are both commonly used to treat MSK injuries and pain, although scrutiny of the use of either intervention has increased. Despite the widespread use of these modalities, there is little evidence to support their effect on patient outcomes. The historical consensus has been that ice decreases pain, inflammation, and edema,while heat can facilitate movement in rehabilitation by improving blood flow and decreasing stiffness.^1-3 In our practice, we encourage use of both topical modalities as a way to start exercise therapy when pain from the acute injury limits participation. Patients often ask which modality they should use. Ice is generally applied in the acute injury phase (48-72 hours after injury), while heat has been thought to be more beneficial in the chronic stages.

Ccontinue to: When and how to apply ice

When and how to apply ice. Applying an ice pack or a bag of frozen vegetables directly to the affected area will help control pain and swelling. Ice should be applied for 15 to 20 minutes at a time, once an hour. If a patient has sensitivity to cold or if the ice pack is a gel-type, have the patient place a layer (eg, towel) between the ice and skin to avoid injury to the skin. Additional caution should be exercised in patients with peripheral vascular disease, cryoglobulinemia, Raynaud disease, or a history of frostbite at the site.⁴

An alternative method we sometimes recommend is ice-cup massage. The patient can fill a small paper cup with water and freeze it. The cup is then used to massage the injured area, providing a more active method of icing whereby the cold can penetrate more quickly. Ice-cup massage should be done for 5 to 10 minutes, 3 to 4 times a day.

When and how to apply heat. Heat will help relax and loosen muscles and is a preferred treatment for older injuries, chronic pain, muscle tension, and spasms.⁵ Because heat can increase blood flow and, likely, inflammation, it should not be used in the acute injury phase. A heating pad or a warm, wet towel can be applied for up to 20 minutes at a time to help relieve pain and tension. Heat is also beneficial before participating in rehab activities as a method of “warming up” a recently injured area.⁶ However, ice should still be used following activity to prevent any new inflammation.

Anti-inflammatory medications

For an acute injury, nonsteroidal anti-­inflammatory drugs (NSAIDs) not only can decrease inflammation and aid in healing but can alleviate pain. We typically start with over-the-counter (OTC) NSAIDs taken on a schedule. A good suggestion is to have the patient take the scheduled NSAID with food for 7 to 10 days or until symptoms subside.

Topical analgesics

Because oral medications can occasionally cause adverse effects or be contraindicated in some patients, topical analgesics can be a good substitute due to their minimal adverse effects. Acceptable topical medications include NSAIDs, lidocaine, menthol, and arnica. Other than prescribed topical NSAIDs, these products can be applied directly to the painful area on an as-needed basis. Often, a topical patch is a nice option to recommend for use during work or school, and a topical cream or ointment can be used at bedtime.

Continue to: Graduated rehabilitation

Graduated rehabilitation

The following 4 common MSK injuries are ones that can benefit from a graduated approach to rehabilitation at home.

Lateral ankle sprain

Lateral ankle sprain, usually resulting from an inversion mechanism, is the most common type of acute ankle sprain seen in primary care and sports medicine settings.^7-9 The injury causes lateral ankle pain and swelling, decreased range of motion and strength, and pain with weight-bearing activities.

Have patients avoid using heat in the acute injury phase because it can increase inflammation due to increased blood flow.

Treatment and rehabilitation after this type of injury are critical to restoring normal function and increasing the likelihood of returning to pre-injury levels of activity.^9,10 Goals for an acute ankle sprain include controlling swelling, regaining full range of motion, increasing muscle strength and power, and improving balance.

Phase 1: Immediately following injury, have the patient protect the injured area with rest, ice, compression, and elevation (RICE). This will help to decrease swelling and pain. Exercises to regain range of motion, such as stretching and doing ankle “ABCs,” should begin within 48 to 72 hours of the initial injury (TABLE 1).^9-11

Continue to: Phase 2

Phase 2: Once the patient has achieved full range of motion and pain is controlled, begin the process of regaining strength. The 4-way ankle exercise program (with elastic tubing) is an easy at-home exercise that has been shown to improve strength in plantar flexion, dorsiflexion, eversion, and inversion (TABLE 1).^9-11

Phase 3: Once your patient is able to bear full weight with little to no pain, begin a balance program (TABLE 1^9-11). This is the most frequently neglected component of rehabilitation and the most common reason patients return with chronic ankle pain or repeat ankle injuries. Deficits in postural stability and balance have been reported in unstable ankles following acute ankle sprains,^10,12-15 and studies have shown that individuals with poor stability are at a greater risk of injury.^13-16

For most lateral ankle sprains, patients can expect time to recovery to range from 2 to 8 weeks. Longer recoveries are associated with more severe injuries or those that involve the syndesmosis.

Plantar fasciitis

Plantar fasciitis (PF) of the foot can be frustrating for a patient due to its chronic nature. Most patients will present with pain in the heel that is aggravated by weight-bearing activities. A conservative management program that focuses on reducing pain and inflammation, reducing tissue stress, and restoring strength and flexibility has been shown to be effective for this type of injury.^17,18

Step 1: Reduce pain and inflammation. Deep-tissue massage and cryotherapy are easy ways to help with pain and inflammation. Deep-tissue massage can be accomplished by rolling the bottom of the foot on a golf or lacrosse ball. A favorite recommendation of ours to reduce inflammation is to use the ice-cup massage, mentioned earlier, for 5 minutes. Or rolling the bottom of the foot on a frozen water bottle will accomplish both tasks at once (TABLE 2^17,18).

Step 2: Reduce tissue stress. Management tools commonly used to reduce tissue stress are OTC orthotics and night splints. The night splint has been shown to improve symptoms,but patients often stop using it due to discomfort.¹⁹ Many kinds of night splints are available, but we have found that the sock variety with a strap to keep the foot in dorsiflexion is best tolerated, and it should be covered by most care plans.

Continue to: Step 3

Step 3: Restore muscle strength and flexibility. Restoring flexibility of the gastrocnemius and soleus is most frequently recommended for treating PF. Strengthening exercises that involve intrinsic and extrinsic muscles of the foot and ankle are also essential.^17,18 Helpful exercises include those listed in TABLE 1.^9-11 Additionally, an eccentric heel stretch can help to alleviate PF symptoms (TABLE 2^17,18).

A reasonable timeline for follow-up on newly diagnosed PF is 4 to 6 weeks. While many patients will not have recovered in that time, the goal is to document progress in recovery. If no progress is made, consider other treatment modalities.

Patellofemoral pain syndrome

Patellofemoral pain syndrome (PFPS) is one of the most common orthopedic complaints, estimated to comprise 7.3% of all orthopedic visits.²⁰ Commonly called “runner’s knee,” PFPS is the leading cause of anterior knee pain in active individuals. Studies suggest a gender bias, with PFPS being diagnosed more frequently in females than in males, particularly between the ages of 10 and 19.²⁰ Often, there is vague anterior knee pain, or pain that worsens with activities such as climbing hills or stairs, or with long sitting or when fatigued.

In general, unbalanced patellar tracking within the trochlear groove likely leads to this pain. Multiple contributory factors have been described; however, evidence increasingly has shown that deficiencies in hip strength may contribute significantly to maltracking of the patella with resultant pain. Specifically, weakness in hip external rotators and abductors is associated with abnormal lower extremity mechanics.²¹ One randomized controlled trial by Ferber et al found that therapy protocols directed at hip and core strength showed earlier resolution of pain and greater strength when compared with knee protocols alone.²²

We routinely talk to patients about how the knee is the “victim” caught between weak hips and/or flat feet. It is prudent to look for both in the office visit. This can be done with one simple maneuver: Ask your patient to do a squat followed by 3 or 4 single-leg squats on each side. This will often reveal dysfunction at the foot/ankle or weakness in the hips/core as demonstrated by pronated feet (along with valgus tracking of the knees inward) or loss of balance upon squatting.

There is general consensus that a nonsurgical approach is the mainstay of treatment for PFPS.²³ Pelvic stabilization and hip strengthening are standard components along with treatment protocols of exercises tailored to one’s individual weaknesses.

Numerous types of exercises do not require specialized equipment and can be taught in the office (TABLE 3²⁴). Explain to patients that the recovery process may take several months. Monthly follow-up to document progress is essential and helps to ensure compliance with one’s home program.

Continue to : Neck pain

Neck pain

The annual prevalence of nonspecific neck pain ranges from 27% to 48%, with 70% of individuals being afflicted at some time in their lives.²⁵ First rule out any neurologic factors that might suggest cervical disc disease or spinal stenosis. If a patient describes weakness or sensory changes along one or both upper extremities, obtain imaging and consider more formalized therapy with a physical therapist.

In patients without any red flags, investigate possible biomechanical causes. It is essential to review the patient’s work and home habits, particularly in light of COVID-19, to determine if adjustments may be needed. Factors to consider are desk and computer setups at work or home, reading or laptop use in bed, sleep habits, and frequency of cellular phone calls/texting.²⁶ A formal ergonomic assessment of the patient’s workplace may be helpful.

A mainstay in treating mechanical neck pain is alleviating trapezial tightness or spasm. Manipulative therapies such as osteopathic manipulation, massage, and chiropractic care can provide pain relief in the acute setting as well as help with control of chronic symptoms.²⁷ A simple self-care tool is using a tennis ball to massage the trapezial muscles. This can be accomplished by having the patient position the tennis ball along the upper trapezial muscles, holding it in place by leaning against a wall, and initiating self-massage. Another method of self-massage is to put 2 tennis balls in an athletic tube sock and tie off the end, place the sock on the floor, and lie on it in the supine position.

There is also evidence that exercise of any kind can help control neck pain.^28,29 The easiest exercises one can offer a patient with neck stiffness, or even mild cervical strains, is self-directed stretching through gentle pressure applied in all 4 directions on the neck. This technique can be repeated hourly both at work and at home (TABLE 4).

Reminders that can help ensure success

You can use the approaches described here for numerous other MSK conditions in helping patients on the road to recovery.

After the acute phase, advise patients to

• apply heat to the affected area before exercising. This can help bring blood flow to the region and promote ease of movement.

• continue icing the area following rehabilitation exercises in order to control exercise-induced inflammation.

• report any changing symptoms such as worsening pain, numbness, or weakness.


These techniques are one step in the recovery process. A home program can benefit the patient either alone or in combination with more advanced techniques that are best accomplished under the watchful eye of a physical or occupational therapist.
 

CORRESPONDENCE

Carrie A. Jaworski, MD, FAAFP, FACSM, 2180 Pfingsten Road, Suite 3100, Glenview, IL 60026; [email protected]

The mainstay of treatment for many musculoskeletal (MSK) complaints is physical or occupational therapy. But often an individual’s underlying biomechanical issue is one that can be easily addressed with a home exercise plan, and, in light of the COVID-19 pandemic, patients may wish to avoid in-person physical therapy. This article describes the rationale for, and methods of providing, home exercises for several MSK conditions commonly seen in the primary care setting.

General rehabilitation principles: First things first

With basic MSK complaints, focus on controlling pain and swelling before undertaking restoration of function. Tailor pharmacologic and nonpharmacologic options to the patient’s needs, using first-line modalities such as ice and compression to reduce inflammation, and prescribing scheduled doses of an anti-inflammatory medication to help with both pain and inflammation.

Once pain is sufficiently controlled, have patients begin basic rehabilitation with simple range-of-motion exercises that move the injured region through normal patterns, as tolerated. Later, the patient can progress through more specific exercises to return the injured region to full functional capacity.

Explain to patients that it takes about 7 to 10 days of consistent care to decrease inflammation, but that they should begin prescribed exercises once they are able to tolerate them. Plan a follow-up visit in 2 to 3 weeks to check on the patient’s response to prescribed care.

Which is better, ice or heat?

Ice and heat are both commonly used to treat MSK injuries and pain, although scrutiny of the use of either intervention has increased. Despite the widespread use of these modalities, there is little evidence to support their effect on patient outcomes. The historical consensus has been that ice decreases pain, inflammation, and edema,while heat can facilitate movement in rehabilitation by improving blood flow and decreasing stiffness.^1-3 In our practice, we encourage use of both topical modalities as a way to start exercise therapy when pain from the acute injury limits participation. Patients often ask which modality they should use. Ice is generally applied in the acute injury phase (48-72 hours after injury), while heat has been thought to be more beneficial in the chronic stages.

Ccontinue to: When and how to apply ice

When and how to apply ice. Applying an ice pack or a bag of frozen vegetables directly to the affected area will help control pain and swelling. Ice should be applied for 15 to 20 minutes at a time, once an hour. If a patient has sensitivity to cold or if the ice pack is a gel-type, have the patient place a layer (eg, towel) between the ice and skin to avoid injury to the skin. Additional caution should be exercised in patients with peripheral vascular disease, cryoglobulinemia, Raynaud disease, or a history of frostbite at the site.⁴

An alternative method we sometimes recommend is ice-cup massage. The patient can fill a small paper cup with water and freeze it. The cup is then used to massage the injured area, providing a more active method of icing whereby the cold can penetrate more quickly. Ice-cup massage should be done for 5 to 10 minutes, 3 to 4 times a day.

When and how to apply heat. Heat will help relax and loosen muscles and is a preferred treatment for older injuries, chronic pain, muscle tension, and spasms.⁵ Because heat can increase blood flow and, likely, inflammation, it should not be used in the acute injury phase. A heating pad or a warm, wet towel can be applied for up to 20 minutes at a time to help relieve pain and tension. Heat is also beneficial before participating in rehab activities as a method of “warming up” a recently injured area.⁶ However, ice should still be used following activity to prevent any new inflammation.

Anti-inflammatory medications

For an acute injury, nonsteroidal anti-­inflammatory drugs (NSAIDs) not only can decrease inflammation and aid in healing but can alleviate pain. We typically start with over-the-counter (OTC) NSAIDs taken on a schedule. A good suggestion is to have the patient take the scheduled NSAID with food for 7 to 10 days or until symptoms subside.

Topical analgesics

Because oral medications can occasionally cause adverse effects or be contraindicated in some patients, topical analgesics can be a good substitute due to their minimal adverse effects. Acceptable topical medications include NSAIDs, lidocaine, menthol, and arnica. Other than prescribed topical NSAIDs, these products can be applied directly to the painful area on an as-needed basis. Often, a topical patch is a nice option to recommend for use during work or school, and a topical cream or ointment can be used at bedtime.

Continue to: Graduated rehabilitation

Graduated rehabilitation

The following 4 common MSK injuries are ones that can benefit from a graduated approach to rehabilitation at home.

Lateral ankle sprain

Lateral ankle sprain, usually resulting from an inversion mechanism, is the most common type of acute ankle sprain seen in primary care and sports medicine settings.^7-9 The injury causes lateral ankle pain and swelling, decreased range of motion and strength, and pain with weight-bearing activities.

Have patients avoid using heat in the acute injury phase because it can increase inflammation due to increased blood flow.

Treatment and rehabilitation after this type of injury are critical to restoring normal function and increasing the likelihood of returning to pre-injury levels of activity.^9,10 Goals for an acute ankle sprain include controlling swelling, regaining full range of motion, increasing muscle strength and power, and improving balance.

Phase 1: Immediately following injury, have the patient protect the injured area with rest, ice, compression, and elevation (RICE). This will help to decrease swelling and pain. Exercises to regain range of motion, such as stretching and doing ankle “ABCs,” should begin within 48 to 72 hours of the initial injury (TABLE 1).^9-11

Continue to: Phase 2

Phase 2: Once the patient has achieved full range of motion and pain is controlled, begin the process of regaining strength. The 4-way ankle exercise program (with elastic tubing) is an easy at-home exercise that has been shown to improve strength in plantar flexion, dorsiflexion, eversion, and inversion (TABLE 1).^9-11

Phase 3: Once your patient is able to bear full weight with little to no pain, begin a balance program (TABLE 1^9-11). This is the most frequently neglected component of rehabilitation and the most common reason patients return with chronic ankle pain or repeat ankle injuries. Deficits in postural stability and balance have been reported in unstable ankles following acute ankle sprains,^10,12-15 and studies have shown that individuals with poor stability are at a greater risk of injury.^13-16

For most lateral ankle sprains, patients can expect time to recovery to range from 2 to 8 weeks. Longer recoveries are associated with more severe injuries or those that involve the syndesmosis.

Plantar fasciitis

Plantar fasciitis (PF) of the foot can be frustrating for a patient due to its chronic nature. Most patients will present with pain in the heel that is aggravated by weight-bearing activities. A conservative management program that focuses on reducing pain and inflammation, reducing tissue stress, and restoring strength and flexibility has been shown to be effective for this type of injury.^17,18

Step 1: Reduce pain and inflammation. Deep-tissue massage and cryotherapy are easy ways to help with pain and inflammation. Deep-tissue massage can be accomplished by rolling the bottom of the foot on a golf or lacrosse ball. A favorite recommendation of ours to reduce inflammation is to use the ice-cup massage, mentioned earlier, for 5 minutes. Or rolling the bottom of the foot on a frozen water bottle will accomplish both tasks at once (TABLE 2^17,18).

Step 2: Reduce tissue stress. Management tools commonly used to reduce tissue stress are OTC orthotics and night splints. The night splint has been shown to improve symptoms,but patients often stop using it due to discomfort.¹⁹ Many kinds of night splints are available, but we have found that the sock variety with a strap to keep the foot in dorsiflexion is best tolerated, and it should be covered by most care plans.

Continue to: Step 3

Step 3: Restore muscle strength and flexibility. Restoring flexibility of the gastrocnemius and soleus is most frequently recommended for treating PF. Strengthening exercises that involve intrinsic and extrinsic muscles of the foot and ankle are also essential.^17,18 Helpful exercises include those listed in TABLE 1.^9-11 Additionally, an eccentric heel stretch can help to alleviate PF symptoms (TABLE 2^17,18).

A reasonable timeline for follow-up on newly diagnosed PF is 4 to 6 weeks. While many patients will not have recovered in that time, the goal is to document progress in recovery. If no progress is made, consider other treatment modalities.

Patellofemoral pain syndrome

Patellofemoral pain syndrome (PFPS) is one of the most common orthopedic complaints, estimated to comprise 7.3% of all orthopedic visits.²⁰ Commonly called “runner’s knee,” PFPS is the leading cause of anterior knee pain in active individuals. Studies suggest a gender bias, with PFPS being diagnosed more frequently in females than in males, particularly between the ages of 10 and 19.²⁰ Often, there is vague anterior knee pain, or pain that worsens with activities such as climbing hills or stairs, or with long sitting or when fatigued.

In general, unbalanced patellar tracking within the trochlear groove likely leads to this pain. Multiple contributory factors have been described; however, evidence increasingly has shown that deficiencies in hip strength may contribute significantly to maltracking of the patella with resultant pain. Specifically, weakness in hip external rotators and abductors is associated with abnormal lower extremity mechanics.²¹ One randomized controlled trial by Ferber et al found that therapy protocols directed at hip and core strength showed earlier resolution of pain and greater strength when compared with knee protocols alone.²²

We routinely talk to patients about how the knee is the “victim” caught between weak hips and/or flat feet. It is prudent to look for both in the office visit. This can be done with one simple maneuver: Ask your patient to do a squat followed by 3 or 4 single-leg squats on each side. This will often reveal dysfunction at the foot/ankle or weakness in the hips/core as demonstrated by pronated feet (along with valgus tracking of the knees inward) or loss of balance upon squatting.

There is general consensus that a nonsurgical approach is the mainstay of treatment for PFPS.²³ Pelvic stabilization and hip strengthening are standard components along with treatment protocols of exercises tailored to one’s individual weaknesses.

Numerous types of exercises do not require specialized equipment and can be taught in the office (TABLE 3²⁴). Explain to patients that the recovery process may take several months. Monthly follow-up to document progress is essential and helps to ensure compliance with one’s home program.

Continue to : Neck pain

Neck pain

The annual prevalence of nonspecific neck pain ranges from 27% to 48%, with 70% of individuals being afflicted at some time in their lives.²⁵ First rule out any neurologic factors that might suggest cervical disc disease or spinal stenosis. If a patient describes weakness or sensory changes along one or both upper extremities, obtain imaging and consider more formalized therapy with a physical therapist.

In patients without any red flags, investigate possible biomechanical causes. It is essential to review the patient’s work and home habits, particularly in light of COVID-19, to determine if adjustments may be needed. Factors to consider are desk and computer setups at work or home, reading or laptop use in bed, sleep habits, and frequency of cellular phone calls/texting.²⁶ A formal ergonomic assessment of the patient’s workplace may be helpful.

A mainstay in treating mechanical neck pain is alleviating trapezial tightness or spasm. Manipulative therapies such as osteopathic manipulation, massage, and chiropractic care can provide pain relief in the acute setting as well as help with control of chronic symptoms.²⁷ A simple self-care tool is using a tennis ball to massage the trapezial muscles. This can be accomplished by having the patient position the tennis ball along the upper trapezial muscles, holding it in place by leaning against a wall, and initiating self-massage. Another method of self-massage is to put 2 tennis balls in an athletic tube sock and tie off the end, place the sock on the floor, and lie on it in the supine position.

There is also evidence that exercise of any kind can help control neck pain.^28,29 The easiest exercises one can offer a patient with neck stiffness, or even mild cervical strains, is self-directed stretching through gentle pressure applied in all 4 directions on the neck. This technique can be repeated hourly both at work and at home (TABLE 4).

Reminders that can help ensure success

You can use the approaches described here for numerous other MSK conditions in helping patients on the road to recovery.

After the acute phase, advise patients to

• apply heat to the affected area before exercising. This can help bring blood flow to the region and promote ease of movement.

• continue icing the area following rehabilitation exercises in order to control exercise-induced inflammation.

• report any changing symptoms such as worsening pain, numbness, or weakness.


These techniques are one step in the recovery process. A home program can benefit the patient either alone or in combination with more advanced techniques that are best accomplished under the watchful eye of a physical or occupational therapist.
 

CORRESPONDENCE

Carrie A. Jaworski, MD, FAAFP, FACSM, 2180 Pfingsten Road, Suite 3100, Glenview, IL 60026; [email protected]

The mainstay of treatment for many musculoskeletal (MSK) complaints is physical or occupational therapy. But often an individual’s underlying biomechanical issue is one that can be easily addressed with a home exercise plan, and, in light of the COVID-19 pandemic, patients may wish to avoid in-person physical therapy. This article describes the rationale for, and methods of providing, home exercises for several MSK conditions commonly seen in the primary care setting.

General rehabilitation principles: First things first

With basic MSK complaints, focus on controlling pain and swelling before undertaking restoration of function. Tailor pharmacologic and nonpharmacologic options to the patient’s needs, using first-line modalities such as ice and compression to reduce inflammation, and prescribing scheduled doses of an anti-inflammatory medication to help with both pain and inflammation.

Once pain is sufficiently controlled, have patients begin basic rehabilitation with simple range-of-motion exercises that move the injured region through normal patterns, as tolerated. Later, the patient can progress through more specific exercises to return the injured region to full functional capacity.

Explain to patients that it takes about 7 to 10 days of consistent care to decrease inflammation, but that they should begin prescribed exercises once they are able to tolerate them. Plan a follow-up visit in 2 to 3 weeks to check on the patient’s response to prescribed care.

Which is better, ice or heat?

Ice and heat are both commonly used to treat MSK injuries and pain, although scrutiny of the use of either intervention has increased. Despite the widespread use of these modalities, there is little evidence to support their effect on patient outcomes. The historical consensus has been that ice decreases pain, inflammation, and edema,while heat can facilitate movement in rehabilitation by improving blood flow and decreasing stiffness.^1-3 In our practice, we encourage use of both topical modalities as a way to start exercise therapy when pain from the acute injury limits participation. Patients often ask which modality they should use. Ice is generally applied in the acute injury phase (48-72 hours after injury), while heat has been thought to be more beneficial in the chronic stages.

Ccontinue to: When and how to apply ice

When and how to apply ice. Applying an ice pack or a bag of frozen vegetables directly to the affected area will help control pain and swelling. Ice should be applied for 15 to 20 minutes at a time, once an hour. If a patient has sensitivity to cold or if the ice pack is a gel-type, have the patient place a layer (eg, towel) between the ice and skin to avoid injury to the skin. Additional caution should be exercised in patients with peripheral vascular disease, cryoglobulinemia, Raynaud disease, or a history of frostbite at the site.⁴

An alternative method we sometimes recommend is ice-cup massage. The patient can fill a small paper cup with water and freeze it. The cup is then used to massage the injured area, providing a more active method of icing whereby the cold can penetrate more quickly. Ice-cup massage should be done for 5 to 10 minutes, 3 to 4 times a day.

When and how to apply heat. Heat will help relax and loosen muscles and is a preferred treatment for older injuries, chronic pain, muscle tension, and spasms.⁵ Because heat can increase blood flow and, likely, inflammation, it should not be used in the acute injury phase. A heating pad or a warm, wet towel can be applied for up to 20 minutes at a time to help relieve pain and tension. Heat is also beneficial before participating in rehab activities as a method of “warming up” a recently injured area.⁶ However, ice should still be used following activity to prevent any new inflammation.

Anti-inflammatory medications

For an acute injury, nonsteroidal anti-­inflammatory drugs (NSAIDs) not only can decrease inflammation and aid in healing but can alleviate pain. We typically start with over-the-counter (OTC) NSAIDs taken on a schedule. A good suggestion is to have the patient take the scheduled NSAID with food for 7 to 10 days or until symptoms subside.

Topical analgesics

Because oral medications can occasionally cause adverse effects or be contraindicated in some patients, topical analgesics can be a good substitute due to their minimal adverse effects. Acceptable topical medications include NSAIDs, lidocaine, menthol, and arnica. Other than prescribed topical NSAIDs, these products can be applied directly to the painful area on an as-needed basis. Often, a topical patch is a nice option to recommend for use during work or school, and a topical cream or ointment can be used at bedtime.

Continue to: Graduated rehabilitation

Graduated rehabilitation

The following 4 common MSK injuries are ones that can benefit from a graduated approach to rehabilitation at home.

Lateral ankle sprain

Lateral ankle sprain, usually resulting from an inversion mechanism, is the most common type of acute ankle sprain seen in primary care and sports medicine settings.^7-9 The injury causes lateral ankle pain and swelling, decreased range of motion and strength, and pain with weight-bearing activities.

Have patients avoid using heat in the acute injury phase because it can increase inflammation due to increased blood flow.

Treatment and rehabilitation after this type of injury are critical to restoring normal function and increasing the likelihood of returning to pre-injury levels of activity.^9,10 Goals for an acute ankle sprain include controlling swelling, regaining full range of motion, increasing muscle strength and power, and improving balance.

Phase 1: Immediately following injury, have the patient protect the injured area with rest, ice, compression, and elevation (RICE). This will help to decrease swelling and pain. Exercises to regain range of motion, such as stretching and doing ankle “ABCs,” should begin within 48 to 72 hours of the initial injury (TABLE 1).^9-11

Continue to: Phase 2

Phase 2: Once the patient has achieved full range of motion and pain is controlled, begin the process of regaining strength. The 4-way ankle exercise program (with elastic tubing) is an easy at-home exercise that has been shown to improve strength in plantar flexion, dorsiflexion, eversion, and inversion (TABLE 1).^9-11

Phase 3: Once your patient is able to bear full weight with little to no pain, begin a balance program (TABLE 1^9-11). This is the most frequently neglected component of rehabilitation and the most common reason patients return with chronic ankle pain or repeat ankle injuries. Deficits in postural stability and balance have been reported in unstable ankles following acute ankle sprains,^10,12-15 and studies have shown that individuals with poor stability are at a greater risk of injury.^13-16

For most lateral ankle sprains, patients can expect time to recovery to range from 2 to 8 weeks. Longer recoveries are associated with more severe injuries or those that involve the syndesmosis.

Plantar fasciitis

Plantar fasciitis (PF) of the foot can be frustrating for a patient due to its chronic nature. Most patients will present with pain in the heel that is aggravated by weight-bearing activities. A conservative management program that focuses on reducing pain and inflammation, reducing tissue stress, and restoring strength and flexibility has been shown to be effective for this type of injury.^17,18

Step 1: Reduce pain and inflammation. Deep-tissue massage and cryotherapy are easy ways to help with pain and inflammation. Deep-tissue massage can be accomplished by rolling the bottom of the foot on a golf or lacrosse ball. A favorite recommendation of ours to reduce inflammation is to use the ice-cup massage, mentioned earlier, for 5 minutes. Or rolling the bottom of the foot on a frozen water bottle will accomplish both tasks at once (TABLE 2^17,18).

Step 2: Reduce tissue stress. Management tools commonly used to reduce tissue stress are OTC orthotics and night splints. The night splint has been shown to improve symptoms,but patients often stop using it due to discomfort.¹⁹ Many kinds of night splints are available, but we have found that the sock variety with a strap to keep the foot in dorsiflexion is best tolerated, and it should be covered by most care plans.

Continue to: Step 3

Step 3: Restore muscle strength and flexibility. Restoring flexibility of the gastrocnemius and soleus is most frequently recommended for treating PF. Strengthening exercises that involve intrinsic and extrinsic muscles of the foot and ankle are also essential.^17,18 Helpful exercises include those listed in TABLE 1.^9-11 Additionally, an eccentric heel stretch can help to alleviate PF symptoms (TABLE 2^17,18).

A reasonable timeline for follow-up on newly diagnosed PF is 4 to 6 weeks. While many patients will not have recovered in that time, the goal is to document progress in recovery. If no progress is made, consider other treatment modalities.

Patellofemoral pain syndrome

Patellofemoral pain syndrome (PFPS) is one of the most common orthopedic complaints, estimated to comprise 7.3% of all orthopedic visits.²⁰ Commonly called “runner’s knee,” PFPS is the leading cause of anterior knee pain in active individuals. Studies suggest a gender bias, with PFPS being diagnosed more frequently in females than in males, particularly between the ages of 10 and 19.²⁰ Often, there is vague anterior knee pain, or pain that worsens with activities such as climbing hills or stairs, or with long sitting or when fatigued.

In general, unbalanced patellar tracking within the trochlear groove likely leads to this pain. Multiple contributory factors have been described; however, evidence increasingly has shown that deficiencies in hip strength may contribute significantly to maltracking of the patella with resultant pain. Specifically, weakness in hip external rotators and abductors is associated with abnormal lower extremity mechanics.²¹ One randomized controlled trial by Ferber et al found that therapy protocols directed at hip and core strength showed earlier resolution of pain and greater strength when compared with knee protocols alone.²²

We routinely talk to patients about how the knee is the “victim” caught between weak hips and/or flat feet. It is prudent to look for both in the office visit. This can be done with one simple maneuver: Ask your patient to do a squat followed by 3 or 4 single-leg squats on each side. This will often reveal dysfunction at the foot/ankle or weakness in the hips/core as demonstrated by pronated feet (along with valgus tracking of the knees inward) or loss of balance upon squatting.

There is general consensus that a nonsurgical approach is the mainstay of treatment for PFPS.²³ Pelvic stabilization and hip strengthening are standard components along with treatment protocols of exercises tailored to one’s individual weaknesses.

Numerous types of exercises do not require specialized equipment and can be taught in the office (TABLE 3²⁴). Explain to patients that the recovery process may take several months. Monthly follow-up to document progress is essential and helps to ensure compliance with one’s home program.

Continue to : Neck pain

Neck pain

The annual prevalence of nonspecific neck pain ranges from 27% to 48%, with 70% of individuals being afflicted at some time in their lives.²⁵ First rule out any neurologic factors that might suggest cervical disc disease or spinal stenosis. If a patient describes weakness or sensory changes along one or both upper extremities, obtain imaging and consider more formalized therapy with a physical therapist.

In patients without any red flags, investigate possible biomechanical causes. It is essential to review the patient’s work and home habits, particularly in light of COVID-19, to determine if adjustments may be needed. Factors to consider are desk and computer setups at work or home, reading or laptop use in bed, sleep habits, and frequency of cellular phone calls/texting.²⁶ A formal ergonomic assessment of the patient’s workplace may be helpful.

A mainstay in treating mechanical neck pain is alleviating trapezial tightness or spasm. Manipulative therapies such as osteopathic manipulation, massage, and chiropractic care can provide pain relief in the acute setting as well as help with control of chronic symptoms.²⁷ A simple self-care tool is using a tennis ball to massage the trapezial muscles. This can be accomplished by having the patient position the tennis ball along the upper trapezial muscles, holding it in place by leaning against a wall, and initiating self-massage. Another method of self-massage is to put 2 tennis balls in an athletic tube sock and tie off the end, place the sock on the floor, and lie on it in the supine position.

There is also evidence that exercise of any kind can help control neck pain.^28,29 The easiest exercises one can offer a patient with neck stiffness, or even mild cervical strains, is self-directed stretching through gentle pressure applied in all 4 directions on the neck. This technique can be repeated hourly both at work and at home (TABLE 4).

Reminders that can help ensure success

You can use the approaches described here for numerous other MSK conditions in helping patients on the road to recovery.

After the acute phase, advise patients to

• apply heat to the affected area before exercising. This can help bring blood flow to the region and promote ease of movement.

• continue icing the area following rehabilitation exercises in order to control exercise-induced inflammation.

• report any changing symptoms such as worsening pain, numbness, or weakness.


These techniques are one step in the recovery process. A home program can benefit the patient either alone or in combination with more advanced techniques that are best accomplished under the watchful eye of a physical or occupational therapist.
 

CORRESPONDENCE

Carrie A. Jaworski, MD, FAAFP, FACSM, 2180 Pfingsten Road, Suite 3100, Glenview, IL 60026; [email protected]

Peripheral arterial disease (PAD), the progressive disorder that results in ischemia to distal vascular territories as a result of atherosclerosis, spans a wide range of presentations, from minimally symptomatic disease to limb ischemia secondary to acute or chronic occlusion.

The prevalence of PAD is variable, due to differing diagnostic criteria used in studies, but PAD appears to affect 1 in every 22 people older than age 40.¹ However, since PAD incidence increases with age, it is increasing in prevalence as the US population ages.^1-3

PAD is associated with increased hospitalizations and decreased quality of life.⁴ Patients with PAD have an estimated 30% 5-year risk for myocardial infarction, stroke, or death from a vascular cause.³

Screening. Although PAD is underdiagnosed and appears to be undertreated,³ population-based screening for PAD in asymptomatic patients is not recommended. A Cochrane review found no studies evaluating the benefit of ­asymptomatic population-based screening.⁵ Similarly, in 2018, the USPSTF performed a comprehensive review and found no studies to support routine screening and determined there was insufficient evidence to recommend it.^6,7

Risk factors and associated comorbidities

PAD risk factors, like the ones detailed below, have a potentiating effect. The presence of 2 risk factors doubles PAD risk, while 3 or more risk factors increase PAD risk by a factor of 10.¹

Increasing age is the greatest single risk factor for PAD.^1,2,8,9 Researchers using data from the National Health and Nutrition Examination Survey (NHANES) found that the prevalence of PAD increased from 1.4% in individuals ages 40 to 49 years to almost 17% in those age 70 or older.¹

© kostudios

Patients with PAD have an estimated 30% 5-year risk for myocardial infarction, stroke, or death from a vascular cause.

Demographic characteristics. Most studies demonstrate a higher risk for PAD in men.^1-3,10 African-American patients have more than twice the risk for PAD, compared with Whites, even after adjustment for the increased prevalence of associated diseases such as hypertension and diabetes in this population.^1-3,10

Continue to: Genetics...

Genetics. A study performed by the National Heart Lung and Blood Institute suggested that genetic correlations between twins were more important than environmental factors in the development of PAD.¹¹

Smoking. Most population studies show smoking to be the greatest modifiable risk factor for PAD. An analysis of the NHANES data yielded an odds ratio (OR) of 4.1 for current smokers and of 1.8 for former smokers.¹ Risk increases linearly with cumulative years of smoking.^1,2,9,10

Diabetes is another significant modifiable risk factor, increasing PAD risk by 2.5 times.² Diabetes is also associated with increases in functional limitation from claudication, risk for acute coronary syndrome, and progression to amputation.¹

Hypertension nearly doubles the risk for PAD, and poor control further increases this risk.^2,9,10

Chronic kidney disease (CKD). Patients with CKD have a progressively higher prevalence of PAD with worsening renal function.¹ There is also an association between CKD and increased morbidity, revascularization failure, and increased mortality.¹

Two additional risk factors that are less well understood are dyslipidemia and chronic inflammation. There is conflicting data regarding the role of individual components of cholesterol and their effect on PAD, although lipoprotein (a) has been shown to be an independent risk factor for both the development and progression of PAD.¹² Similarly, chronic inflammation has been shown to play a role in the initiation and progression of the disease, although the role of inflammatory markers in evaluation and treatment is unclear and assessment for these purposes is not currently recommended.^12,13

Continue to: Diagnosis...

Diagnosis

Clinical presentation

Lower extremity pain is the hallmark symptom of PAD, but presentation varies. The classic presentation is claudication, pain within a defined muscle group that occurs with exertion and is relieved by rest. Claudication is most common in the calf but also occurs in the buttock/thigh and the foot.

African- American patients have more than twice the risk for PAD, compared with Whites, even after adjustment for the increased prevalence of associated diseases in this population.

However, most patients with PAD present with pain that does not fit the definition of claudication. Patients with comorbidities, physical inactivity, and neuropathy are more likely to present with atypical pain.¹⁴ These patients may demonstrate critical or acute limb ischemia, characterized by pain at rest and most often localized to the forefoot and toes. Patients with critical limb ischemia may also present with nonhealing wounds/ulcers or gangrene.¹⁵

Physical exam findings can support the diagnosis of PAD, but none are reliable enough to rule the diagnosis in or out. Findings suggestive of PAD include cool skin, presence of a bruit (iliac, femoral, or popliteal), and palpable pulse abnormality. Multiple abnormal physical exam findings increase the likelihood of PAD, while the absence of a bruit or palpable pulse abnormality makes PAD less likely.¹⁶ In patients with PAD, an associated wound/ulcer is most often distal in the foot and usually appears dry.¹⁷

The differential diagnosis for intermittent leg pain is broad and includes neurologic, musculoskeletal, and venous etiologies. Table 1¹⁸ lists some common alternate diagnoses for patients presenting with leg pain or claudication.

Continue to: Diagnostic testing...

Diagnostic testing

An ankle-brachial index (ABI) test should be performed in patients with history or physical exam findings suggestive of PAD. A resting ABI is performed with the patient in the supine position, with measurement of systolic blood pressure in both arms and ankles using a Doppler ultrasound device. Table 2¹³ outlines ABI scoring and interpretation.

An ABI > 1.4 is an invalid measurement, indicating that the arteries are too calcified to be compressed. These highly elevated ABI measurements are common in patients with diabetes and/or advanced CKD. In these patients, a toe-brachial index (TBI) test should be performed, because the digital arteries are almost always compressible.¹³

Patients with symptomatic PAD who are under consideration for revascularization may benefit from radiologic imaging of the lower extremities with duplex ultrasound, computed tomography angiography, or magnetic resonance angiography to determine the anatomic location and severity of stenosis.¹³

Management of PAD

Lifestyle interventions

For patients with PAD, lifestyle modifications are an essential—but challenging—component of disease management.

Continue to: Smoking cessation...

Smoking cessation. As with other atherosclerotic diseases, PAD progression is strongly correlated with smoking. A trial involving 204 active smokers with PAD showed that 5-year mortality and amputation rates dropped by more than half in those who quit smoking within a year, with numbers needed to treat (NNT) of 6 for mortality and 5 for amputation.¹⁹ Because of this dramatic effect, American College of Cardiology/American Heart Association (ACC/AHA) guidelines encourage providers to address smoking at every visit and use cessation programs and medication to increase quit rates.¹³

Exercise may be the most important intervention for PAD. A 2017 Cochrane review found that supervised, structured exercise programs increase pain-free and maximal walking distances by at least 20% and also improve physical and mental quality of life.²⁰ In a trial involving 111 patients with aortoiliac PAD, supervised exercise plus medical care led to greater functional improvement than either revascularization plus medical care or medical care alone.²¹ In a 2018 Cochrane review, neither revascularization or revascularization added to supervised exercise were better than supervised exercise alone.²² ACC/AHA guidelines recommend supervised exercise programs for claudication prior to considering revascularization.¹³TABLE 3¹³ outlines the components of a structured exercise program.

Unfortunately, the benefit of these programs has been difficult to reproduce without supervision. Another 2018 Cochrane review demonstrated significant improvement with supervised exercise and no clear improvement in patients given home exercise or advice to walk.²³ A recent study examined the effect of having patients use a wearable fitness tracker for home exercise and demonstrated no benefit over usual care.²⁴

Diet. There is some evidence that dietary interventions can prevent and possibly improve PAD. A large randomized controlled trial showed that a Mediterranean diet lowered rates of PAD over 1 year compared to a low-fat diet, with an NNT of 336 if supplemented with extra-virgin olive oil and 448 if supplemented with nuts.²⁵ A small trial of 25 patients who consumed non-soy legumes daily for 8 weeks showed average ABI improvement of 6%, although there was no control group.²⁶

Medical therapy to address peripheral and cardiovascular events

Standard medical therapy for coronary artery disease (CAD) is recommended for patients with PAD to reduce cardiovascular and limb events. For example, treatment of hypertension reduces cardiovascular and cerebrovascular events, and studies verify that lowering blood pressure does not worsen claudication or limb perfusion.

A trial involving 204 active smokers with PAD showed that 5-year mortality and amputation rates dropped by more than half in those who quit smoking within a year.

¹³TABLE 4^13,27-30 outlines the options for medical therapy.

Continue to: Statins...

Statins reduce cardiovascular events in PAD patients. A large study demonstrated that 40 mg of simvastatin has an NNT of 21 to prevent a coronary or cerebrovascular event in PAD, similar to the NNT of 23 seen in treatment of CAD.²⁷ Statins also reduce adverse limb outcomes. A registry of atherosclerosis patients showed that statins have an NNT of 56 to prevent amputation in PAD and an NNT of 28 to prevent worsening claudication, critical limb ischemia, revascularization, or amputation.²⁸

Antiplatelet therapy with low-dose aspirin or clopidogrel is recommended for symptomatic patients and for asymptomatic patients with an ABI ≤ 0.9.¹³ A Cochrane review demonstrated significantly reduced mortality with nonaspirin antiplatelet agents vs aspirin (NNT = 94) without increase in major bleeding.²⁹ Only British guidelines specifically recommend clopidogrel over aspirin.³¹

Dual antiplatelet therapy has not shown consistent benefits over aspirin alone. ACC/AHA guidelines state that dual antiplatelet therapy is not well established for PAD but may be reasonable after revascularization.¹³

Voraxapar is a novel antiplatelet agent that targets the thrombin-binding receptor on platelets. However, trials show no significant coronary benefit, and slight reductions in acute limb ischemia are offset by increases in major bleeding.¹³

For patients receiving medical therapy, ongoing evaluation and treatment should be based on claudication symptoms and clinical assessment.

Medical therapy for claudication

Several medications have been proposed for symptomatic treatment of intermittent claudication. Cilostazol is a phosphodiesterase inhibitor with the best risk-benefit ratio. A Cochrane review showed improvements in maximal and pain-free walking distances compared to placebo and improvements in quality of life with cilostazol 100 mg taken twice daily.³² Adverse effects included headache, dizziness, palpitations, and diarrhea.²⁹

Continue to: Pentoxifylline...

Pentoxifylline is another phosphodiesterase inhibitor with less evidence of improvement, higher adverse effect rates, and more frequent dosing. It is not recommended for treatment of intermittent claudication.^13,33

Supplements. Padma 28, a Tibetan herbal formulation, appears to improve maximal walking distance with adverse effect rates similar to placebo.³⁴ Other supplements, including vitamin E, ginkgo biloba, and omega-3 fatty acids, have no evidence of benefit.^35-37

When revascularizationis needed

Patients who develop limb ischemia or lifestyle-limiting claudication despite conservative therapy are candidates for revascularization. Endovascular techniques include angioplasty, stenting, atherectomy, and precise medication delivery. Surgical approaches mainly consist of thrombectomy and bypass grafting. For intermittent claudication despite conservative care, ACC/AHA guidelines state endovascular procedures are appropriate for aortoiliac disease and reasonable for femoropopliteal disease, but unproven for infrapopliteal disease.¹³

Acute limb ischemia is an emergency requiring immediate intervention. Two trials revealed identical overall and amputation-free survival rates for percutaneous thrombolysis and surgical thrombectomy.^38,39 ACC/AHA guidelines recommend anticoagulation with heparin followed by the revascularization technique that will most rapidly restore arterial flow.¹³

For chronic limb ischemia, a large trial showed angioplasty had lower initial morbidity, length of hospitalization, and cost than surgical repair. However, surgical mortality was lower after 2 years.⁴⁰ ACC/AHA guidelines recommend either surgery or endovascular procedures and propose initial endovascular treatment followed by surgery if needed.¹³ After revascularization, the patient should be followed periodically with a clinical evaluation and ABI measurement with further consideration for routine duplex ultrasound surveillance.¹³

For chronic limb ischemia, a large trial showed angioplasty had lower initial morbidity, length of hospitalization, and cost than surgical repair. Surgical mortality was lower after 2 years.

Outcomes

Patients with PAD have variable outcomes. About 70% to 80% of patients with this diagnosis will have a stable disease process with no worsening of symptoms, 10% to 20% will experience worsening symptoms over time, 5% to 10% will require revascularization within 5 years of diagnosis, and 1% to 5% will progress to critical limb ischemia, which has a 5-year amputation rate of 1% to 4%.² Patients who require amputation have poor outcomes: Within 2 years, 30% are dead and 15% have had further amputations.¹⁸

In addition to the morbidity and mortality from its own progression, PAD is an important predictor of CAD and is associated with a significant elevation in morbidity and mortality from CAD. One small but well-designed prospective cohort study found that patients with PAD had a more than 6-fold increased risk of death from CAD than did patients without PAD.⁴¹

Acknowledgement
The authors thank Francesca Cimino, MD, FAAFP, for her help in reviewing this manuscript.

CORRESPONDENCE
Dustin K. Smith, DO, 2080 Child Street, Jacksonville, FL 32214; [email protected]

Peripheral arterial disease (PAD), the progressive disorder that results in ischemia to distal vascular territories as a result of atherosclerosis, spans a wide range of presentations, from minimally symptomatic disease to limb ischemia secondary to acute or chronic occlusion.

The prevalence of PAD is variable, due to differing diagnostic criteria used in studies, but PAD appears to affect 1 in every 22 people older than age 40.¹ However, since PAD incidence increases with age, it is increasing in prevalence as the US population ages.^1-3

PAD is associated with increased hospitalizations and decreased quality of life.⁴ Patients with PAD have an estimated 30% 5-year risk for myocardial infarction, stroke, or death from a vascular cause.³

Screening. Although PAD is underdiagnosed and appears to be undertreated,³ population-based screening for PAD in asymptomatic patients is not recommended. A Cochrane review found no studies evaluating the benefit of ­asymptomatic population-based screening.⁵ Similarly, in 2018, the USPSTF performed a comprehensive review and found no studies to support routine screening and determined there was insufficient evidence to recommend it.^6,7

Risk factors and associated comorbidities

PAD risk factors, like the ones detailed below, have a potentiating effect. The presence of 2 risk factors doubles PAD risk, while 3 or more risk factors increase PAD risk by a factor of 10.¹

Increasing age is the greatest single risk factor for PAD.^1,2,8,9 Researchers using data from the National Health and Nutrition Examination Survey (NHANES) found that the prevalence of PAD increased from 1.4% in individuals ages 40 to 49 years to almost 17% in those age 70 or older.¹

© kostudios

Patients with PAD have an estimated 30% 5-year risk for myocardial infarction, stroke, or death from a vascular cause.

Demographic characteristics. Most studies demonstrate a higher risk for PAD in men.^1-3,10 African-American patients have more than twice the risk for PAD, compared with Whites, even after adjustment for the increased prevalence of associated diseases such as hypertension and diabetes in this population.^1-3,10

Continue to: Genetics...

Genetics. A study performed by the National Heart Lung and Blood Institute suggested that genetic correlations between twins were more important than environmental factors in the development of PAD.¹¹

Smoking. Most population studies show smoking to be the greatest modifiable risk factor for PAD. An analysis of the NHANES data yielded an odds ratio (OR) of 4.1 for current smokers and of 1.8 for former smokers.¹ Risk increases linearly with cumulative years of smoking.^1,2,9,10

Diabetes is another significant modifiable risk factor, increasing PAD risk by 2.5 times.² Diabetes is also associated with increases in functional limitation from claudication, risk for acute coronary syndrome, and progression to amputation.¹

Hypertension nearly doubles the risk for PAD, and poor control further increases this risk.^2,9,10

Chronic kidney disease (CKD). Patients with CKD have a progressively higher prevalence of PAD with worsening renal function.¹ There is also an association between CKD and increased morbidity, revascularization failure, and increased mortality.¹

Two additional risk factors that are less well understood are dyslipidemia and chronic inflammation. There is conflicting data regarding the role of individual components of cholesterol and their effect on PAD, although lipoprotein (a) has been shown to be an independent risk factor for both the development and progression of PAD.¹² Similarly, chronic inflammation has been shown to play a role in the initiation and progression of the disease, although the role of inflammatory markers in evaluation and treatment is unclear and assessment for these purposes is not currently recommended.^12,13

Continue to: Diagnosis...

Diagnosis

Clinical presentation

Lower extremity pain is the hallmark symptom of PAD, but presentation varies. The classic presentation is claudication, pain within a defined muscle group that occurs with exertion and is relieved by rest. Claudication is most common in the calf but also occurs in the buttock/thigh and the foot.

African- American patients have more than twice the risk for PAD, compared with Whites, even after adjustment for the increased prevalence of associated diseases in this population.

However, most patients with PAD present with pain that does not fit the definition of claudication. Patients with comorbidities, physical inactivity, and neuropathy are more likely to present with atypical pain.¹⁴ These patients may demonstrate critical or acute limb ischemia, characterized by pain at rest and most often localized to the forefoot and toes. Patients with critical limb ischemia may also present with nonhealing wounds/ulcers or gangrene.¹⁵

Physical exam findings can support the diagnosis of PAD, but none are reliable enough to rule the diagnosis in or out. Findings suggestive of PAD include cool skin, presence of a bruit (iliac, femoral, or popliteal), and palpable pulse abnormality. Multiple abnormal physical exam findings increase the likelihood of PAD, while the absence of a bruit or palpable pulse abnormality makes PAD less likely.¹⁶ In patients with PAD, an associated wound/ulcer is most often distal in the foot and usually appears dry.¹⁷

The differential diagnosis for intermittent leg pain is broad and includes neurologic, musculoskeletal, and venous etiologies. Table 1¹⁸ lists some common alternate diagnoses for patients presenting with leg pain or claudication.

Continue to: Diagnostic testing...

Diagnostic testing

An ankle-brachial index (ABI) test should be performed in patients with history or physical exam findings suggestive of PAD. A resting ABI is performed with the patient in the supine position, with measurement of systolic blood pressure in both arms and ankles using a Doppler ultrasound device. Table 2¹³ outlines ABI scoring and interpretation.

An ABI > 1.4 is an invalid measurement, indicating that the arteries are too calcified to be compressed. These highly elevated ABI measurements are common in patients with diabetes and/or advanced CKD. In these patients, a toe-brachial index (TBI) test should be performed, because the digital arteries are almost always compressible.¹³

Patients with symptomatic PAD who are under consideration for revascularization may benefit from radiologic imaging of the lower extremities with duplex ultrasound, computed tomography angiography, or magnetic resonance angiography to determine the anatomic location and severity of stenosis.¹³

Management of PAD

Lifestyle interventions

For patients with PAD, lifestyle modifications are an essential—but challenging—component of disease management.

Continue to: Smoking cessation...

Smoking cessation. As with other atherosclerotic diseases, PAD progression is strongly correlated with smoking. A trial involving 204 active smokers with PAD showed that 5-year mortality and amputation rates dropped by more than half in those who quit smoking within a year, with numbers needed to treat (NNT) of 6 for mortality and 5 for amputation.¹⁹ Because of this dramatic effect, American College of Cardiology/American Heart Association (ACC/AHA) guidelines encourage providers to address smoking at every visit and use cessation programs and medication to increase quit rates.¹³

Exercise may be the most important intervention for PAD. A 2017 Cochrane review found that supervised, structured exercise programs increase pain-free and maximal walking distances by at least 20% and also improve physical and mental quality of life.²⁰ In a trial involving 111 patients with aortoiliac PAD, supervised exercise plus medical care led to greater functional improvement than either revascularization plus medical care or medical care alone.²¹ In a 2018 Cochrane review, neither revascularization or revascularization added to supervised exercise were better than supervised exercise alone.²² ACC/AHA guidelines recommend supervised exercise programs for claudication prior to considering revascularization.¹³TABLE 3¹³ outlines the components of a structured exercise program.

Unfortunately, the benefit of these programs has been difficult to reproduce without supervision. Another 2018 Cochrane review demonstrated significant improvement with supervised exercise and no clear improvement in patients given home exercise or advice to walk.²³ A recent study examined the effect of having patients use a wearable fitness tracker for home exercise and demonstrated no benefit over usual care.²⁴

Diet. There is some evidence that dietary interventions can prevent and possibly improve PAD. A large randomized controlled trial showed that a Mediterranean diet lowered rates of PAD over 1 year compared to a low-fat diet, with an NNT of 336 if supplemented with extra-virgin olive oil and 448 if supplemented with nuts.²⁵ A small trial of 25 patients who consumed non-soy legumes daily for 8 weeks showed average ABI improvement of 6%, although there was no control group.²⁶

Medical therapy to address peripheral and cardiovascular events

Standard medical therapy for coronary artery disease (CAD) is recommended for patients with PAD to reduce cardiovascular and limb events. For example, treatment of hypertension reduces cardiovascular and cerebrovascular events, and studies verify that lowering blood pressure does not worsen claudication or limb perfusion.

A trial involving 204 active smokers with PAD showed that 5-year mortality and amputation rates dropped by more than half in those who quit smoking within a year.

¹³TABLE 4^13,27-30 outlines the options for medical therapy.

Continue to: Statins...

Statins reduce cardiovascular events in PAD patients. A large study demonstrated that 40 mg of simvastatin has an NNT of 21 to prevent a coronary or cerebrovascular event in PAD, similar to the NNT of 23 seen in treatment of CAD.²⁷ Statins also reduce adverse limb outcomes. A registry of atherosclerosis patients showed that statins have an NNT of 56 to prevent amputation in PAD and an NNT of 28 to prevent worsening claudication, critical limb ischemia, revascularization, or amputation.²⁸

Antiplatelet therapy with low-dose aspirin or clopidogrel is recommended for symptomatic patients and for asymptomatic patients with an ABI ≤ 0.9.¹³ A Cochrane review demonstrated significantly reduced mortality with nonaspirin antiplatelet agents vs aspirin (NNT = 94) without increase in major bleeding.²⁹ Only British guidelines specifically recommend clopidogrel over aspirin.³¹

Dual antiplatelet therapy has not shown consistent benefits over aspirin alone. ACC/AHA guidelines state that dual antiplatelet therapy is not well established for PAD but may be reasonable after revascularization.¹³

Voraxapar is a novel antiplatelet agent that targets the thrombin-binding receptor on platelets. However, trials show no significant coronary benefit, and slight reductions in acute limb ischemia are offset by increases in major bleeding.¹³

For patients receiving medical therapy, ongoing evaluation and treatment should be based on claudication symptoms and clinical assessment.

Medical therapy for claudication

Several medications have been proposed for symptomatic treatment of intermittent claudication. Cilostazol is a phosphodiesterase inhibitor with the best risk-benefit ratio. A Cochrane review showed improvements in maximal and pain-free walking distances compared to placebo and improvements in quality of life with cilostazol 100 mg taken twice daily.³² Adverse effects included headache, dizziness, palpitations, and diarrhea.²⁹

Continue to: Pentoxifylline...

Pentoxifylline is another phosphodiesterase inhibitor with less evidence of improvement, higher adverse effect rates, and more frequent dosing. It is not recommended for treatment of intermittent claudication.^13,33

Supplements. Padma 28, a Tibetan herbal formulation, appears to improve maximal walking distance with adverse effect rates similar to placebo.³⁴ Other supplements, including vitamin E, ginkgo biloba, and omega-3 fatty acids, have no evidence of benefit.^35-37

When revascularizationis needed

Patients who develop limb ischemia or lifestyle-limiting claudication despite conservative therapy are candidates for revascularization. Endovascular techniques include angioplasty, stenting, atherectomy, and precise medication delivery. Surgical approaches mainly consist of thrombectomy and bypass grafting. For intermittent claudication despite conservative care, ACC/AHA guidelines state endovascular procedures are appropriate for aortoiliac disease and reasonable for femoropopliteal disease, but unproven for infrapopliteal disease.¹³

Acute limb ischemia is an emergency requiring immediate intervention. Two trials revealed identical overall and amputation-free survival rates for percutaneous thrombolysis and surgical thrombectomy.^38,39 ACC/AHA guidelines recommend anticoagulation with heparin followed by the revascularization technique that will most rapidly restore arterial flow.¹³

For chronic limb ischemia, a large trial showed angioplasty had lower initial morbidity, length of hospitalization, and cost than surgical repair. However, surgical mortality was lower after 2 years.⁴⁰ ACC/AHA guidelines recommend either surgery or endovascular procedures and propose initial endovascular treatment followed by surgery if needed.¹³ After revascularization, the patient should be followed periodically with a clinical evaluation and ABI measurement with further consideration for routine duplex ultrasound surveillance.¹³

For chronic limb ischemia, a large trial showed angioplasty had lower initial morbidity, length of hospitalization, and cost than surgical repair. Surgical mortality was lower after 2 years.

Outcomes

Patients with PAD have variable outcomes. About 70% to 80% of patients with this diagnosis will have a stable disease process with no worsening of symptoms, 10% to 20% will experience worsening symptoms over time, 5% to 10% will require revascularization within 5 years of diagnosis, and 1% to 5% will progress to critical limb ischemia, which has a 5-year amputation rate of 1% to 4%.² Patients who require amputation have poor outcomes: Within 2 years, 30% are dead and 15% have had further amputations.¹⁸

In addition to the morbidity and mortality from its own progression, PAD is an important predictor of CAD and is associated with a significant elevation in morbidity and mortality from CAD. One small but well-designed prospective cohort study found that patients with PAD had a more than 6-fold increased risk of death from CAD than did patients without PAD.⁴¹

Acknowledgement
The authors thank Francesca Cimino, MD, FAAFP, for her help in reviewing this manuscript.

CORRESPONDENCE
Dustin K. Smith, DO, 2080 Child Street, Jacksonville, FL 32214; [email protected]

Peripheral arterial disease (PAD), the progressive disorder that results in ischemia to distal vascular territories as a result of atherosclerosis, spans a wide range of presentations, from minimally symptomatic disease to limb ischemia secondary to acute or chronic occlusion.

The prevalence of PAD is variable, due to differing diagnostic criteria used in studies, but PAD appears to affect 1 in every 22 people older than age 40.¹ However, since PAD incidence increases with age, it is increasing in prevalence as the US population ages.^1-3

PAD is associated with increased hospitalizations and decreased quality of life.⁴ Patients with PAD have an estimated 30% 5-year risk for myocardial infarction, stroke, or death from a vascular cause.³

Screening. Although PAD is underdiagnosed and appears to be undertreated,³ population-based screening for PAD in asymptomatic patients is not recommended. A Cochrane review found no studies evaluating the benefit of ­asymptomatic population-based screening.⁵ Similarly, in 2018, the USPSTF performed a comprehensive review and found no studies to support routine screening and determined there was insufficient evidence to recommend it.^6,7

Risk factors and associated comorbidities

PAD risk factors, like the ones detailed below, have a potentiating effect. The presence of 2 risk factors doubles PAD risk, while 3 or more risk factors increase PAD risk by a factor of 10.¹

Increasing age is the greatest single risk factor for PAD.^1,2,8,9 Researchers using data from the National Health and Nutrition Examination Survey (NHANES) found that the prevalence of PAD increased from 1.4% in individuals ages 40 to 49 years to almost 17% in those age 70 or older.¹

© kostudios

Patients with PAD have an estimated 30% 5-year risk for myocardial infarction, stroke, or death from a vascular cause.

Demographic characteristics. Most studies demonstrate a higher risk for PAD in men.^1-3,10 African-American patients have more than twice the risk for PAD, compared with Whites, even after adjustment for the increased prevalence of associated diseases such as hypertension and diabetes in this population.^1-3,10

Continue to: Genetics...

Genetics. A study performed by the National Heart Lung and Blood Institute suggested that genetic correlations between twins were more important than environmental factors in the development of PAD.¹¹

Smoking. Most population studies show smoking to be the greatest modifiable risk factor for PAD. An analysis of the NHANES data yielded an odds ratio (OR) of 4.1 for current smokers and of 1.8 for former smokers.¹ Risk increases linearly with cumulative years of smoking.^1,2,9,10

Diabetes is another significant modifiable risk factor, increasing PAD risk by 2.5 times.² Diabetes is also associated with increases in functional limitation from claudication, risk for acute coronary syndrome, and progression to amputation.¹

Hypertension nearly doubles the risk for PAD, and poor control further increases this risk.^2,9,10

Chronic kidney disease (CKD). Patients with CKD have a progressively higher prevalence of PAD with worsening renal function.¹ There is also an association between CKD and increased morbidity, revascularization failure, and increased mortality.¹

Two additional risk factors that are less well understood are dyslipidemia and chronic inflammation. There is conflicting data regarding the role of individual components of cholesterol and their effect on PAD, although lipoprotein (a) has been shown to be an independent risk factor for both the development and progression of PAD.¹² Similarly, chronic inflammation has been shown to play a role in the initiation and progression of the disease, although the role of inflammatory markers in evaluation and treatment is unclear and assessment for these purposes is not currently recommended.^12,13

Continue to: Diagnosis...

Diagnosis

Clinical presentation

Lower extremity pain is the hallmark symptom of PAD, but presentation varies. The classic presentation is claudication, pain within a defined muscle group that occurs with exertion and is relieved by rest. Claudication is most common in the calf but also occurs in the buttock/thigh and the foot.

African- American patients have more than twice the risk for PAD, compared with Whites, even after adjustment for the increased prevalence of associated diseases in this population.

However, most patients with PAD present with pain that does not fit the definition of claudication. Patients with comorbidities, physical inactivity, and neuropathy are more likely to present with atypical pain.¹⁴ These patients may demonstrate critical or acute limb ischemia, characterized by pain at rest and most often localized to the forefoot and toes. Patients with critical limb ischemia may also present with nonhealing wounds/ulcers or gangrene.¹⁵

Physical exam findings can support the diagnosis of PAD, but none are reliable enough to rule the diagnosis in or out. Findings suggestive of PAD include cool skin, presence of a bruit (iliac, femoral, or popliteal), and palpable pulse abnormality. Multiple abnormal physical exam findings increase the likelihood of PAD, while the absence of a bruit or palpable pulse abnormality makes PAD less likely.¹⁶ In patients with PAD, an associated wound/ulcer is most often distal in the foot and usually appears dry.¹⁷

The differential diagnosis for intermittent leg pain is broad and includes neurologic, musculoskeletal, and venous etiologies. Table 1¹⁸ lists some common alternate diagnoses for patients presenting with leg pain or claudication.

Continue to: Diagnostic testing...

Diagnostic testing

An ankle-brachial index (ABI) test should be performed in patients with history or physical exam findings suggestive of PAD. A resting ABI is performed with the patient in the supine position, with measurement of systolic blood pressure in both arms and ankles using a Doppler ultrasound device. Table 2¹³ outlines ABI scoring and interpretation.

An ABI > 1.4 is an invalid measurement, indicating that the arteries are too calcified to be compressed. These highly elevated ABI measurements are common in patients with diabetes and/or advanced CKD. In these patients, a toe-brachial index (TBI) test should be performed, because the digital arteries are almost always compressible.¹³

Patients with symptomatic PAD who are under consideration for revascularization may benefit from radiologic imaging of the lower extremities with duplex ultrasound, computed tomography angiography, or magnetic resonance angiography to determine the anatomic location and severity of stenosis.¹³

Management of PAD

Lifestyle interventions

For patients with PAD, lifestyle modifications are an essential—but challenging—component of disease management.

Continue to: Smoking cessation...

Smoking cessation. As with other atherosclerotic diseases, PAD progression is strongly correlated with smoking. A trial involving 204 active smokers with PAD showed that 5-year mortality and amputation rates dropped by more than half in those who quit smoking within a year, with numbers needed to treat (NNT) of 6 for mortality and 5 for amputation.¹⁹ Because of this dramatic effect, American College of Cardiology/American Heart Association (ACC/AHA) guidelines encourage providers to address smoking at every visit and use cessation programs and medication to increase quit rates.¹³

Exercise may be the most important intervention for PAD. A 2017 Cochrane review found that supervised, structured exercise programs increase pain-free and maximal walking distances by at least 20% and also improve physical and mental quality of life.²⁰ In a trial involving 111 patients with aortoiliac PAD, supervised exercise plus medical care led to greater functional improvement than either revascularization plus medical care or medical care alone.²¹ In a 2018 Cochrane review, neither revascularization or revascularization added to supervised exercise were better than supervised exercise alone.²² ACC/AHA guidelines recommend supervised exercise programs for claudication prior to considering revascularization.¹³TABLE 3¹³ outlines the components of a structured exercise program.

Unfortunately, the benefit of these programs has been difficult to reproduce without supervision. Another 2018 Cochrane review demonstrated significant improvement with supervised exercise and no clear improvement in patients given home exercise or advice to walk.²³ A recent study examined the effect of having patients use a wearable fitness tracker for home exercise and demonstrated no benefit over usual care.²⁴

Diet. There is some evidence that dietary interventions can prevent and possibly improve PAD. A large randomized controlled trial showed that a Mediterranean diet lowered rates of PAD over 1 year compared to a low-fat diet, with an NNT of 336 if supplemented with extra-virgin olive oil and 448 if supplemented with nuts.²⁵ A small trial of 25 patients who consumed non-soy legumes daily for 8 weeks showed average ABI improvement of 6%, although there was no control group.²⁶

Medical therapy to address peripheral and cardiovascular events

Standard medical therapy for coronary artery disease (CAD) is recommended for patients with PAD to reduce cardiovascular and limb events. For example, treatment of hypertension reduces cardiovascular and cerebrovascular events, and studies verify that lowering blood pressure does not worsen claudication or limb perfusion.

A trial involving 204 active smokers with PAD showed that 5-year mortality and amputation rates dropped by more than half in those who quit smoking within a year.

¹³TABLE 4^13,27-30 outlines the options for medical therapy.

Continue to: Statins...

Statins reduce cardiovascular events in PAD patients. A large study demonstrated that 40 mg of simvastatin has an NNT of 21 to prevent a coronary or cerebrovascular event in PAD, similar to the NNT of 23 seen in treatment of CAD.²⁷ Statins also reduce adverse limb outcomes. A registry of atherosclerosis patients showed that statins have an NNT of 56 to prevent amputation in PAD and an NNT of 28 to prevent worsening claudication, critical limb ischemia, revascularization, or amputation.²⁸

Antiplatelet therapy with low-dose aspirin or clopidogrel is recommended for symptomatic patients and for asymptomatic patients with an ABI ≤ 0.9.¹³ A Cochrane review demonstrated significantly reduced mortality with nonaspirin antiplatelet agents vs aspirin (NNT = 94) without increase in major bleeding.²⁹ Only British guidelines specifically recommend clopidogrel over aspirin.³¹

Dual antiplatelet therapy has not shown consistent benefits over aspirin alone. ACC/AHA guidelines state that dual antiplatelet therapy is not well established for PAD but may be reasonable after revascularization.¹³

Voraxapar is a novel antiplatelet agent that targets the thrombin-binding receptor on platelets. However, trials show no significant coronary benefit, and slight reductions in acute limb ischemia are offset by increases in major bleeding.¹³

For patients receiving medical therapy, ongoing evaluation and treatment should be based on claudication symptoms and clinical assessment.

Medical therapy for claudication

Several medications have been proposed for symptomatic treatment of intermittent claudication. Cilostazol is a phosphodiesterase inhibitor with the best risk-benefit ratio. A Cochrane review showed improvements in maximal and pain-free walking distances compared to placebo and improvements in quality of life with cilostazol 100 mg taken twice daily.³² Adverse effects included headache, dizziness, palpitations, and diarrhea.²⁹

Continue to: Pentoxifylline...

Pentoxifylline is another phosphodiesterase inhibitor with less evidence of improvement, higher adverse effect rates, and more frequent dosing. It is not recommended for treatment of intermittent claudication.^13,33

Supplements. Padma 28, a Tibetan herbal formulation, appears to improve maximal walking distance with adverse effect rates similar to placebo.³⁴ Other supplements, including vitamin E, ginkgo biloba, and omega-3 fatty acids, have no evidence of benefit.^35-37

When revascularizationis needed

Patients who develop limb ischemia or lifestyle-limiting claudication despite conservative therapy are candidates for revascularization. Endovascular techniques include angioplasty, stenting, atherectomy, and precise medication delivery. Surgical approaches mainly consist of thrombectomy and bypass grafting. For intermittent claudication despite conservative care, ACC/AHA guidelines state endovascular procedures are appropriate for aortoiliac disease and reasonable for femoropopliteal disease, but unproven for infrapopliteal disease.¹³

Acute limb ischemia is an emergency requiring immediate intervention. Two trials revealed identical overall and amputation-free survival rates for percutaneous thrombolysis and surgical thrombectomy.^38,39 ACC/AHA guidelines recommend anticoagulation with heparin followed by the revascularization technique that will most rapidly restore arterial flow.¹³

For chronic limb ischemia, a large trial showed angioplasty had lower initial morbidity, length of hospitalization, and cost than surgical repair. However, surgical mortality was lower after 2 years.⁴⁰ ACC/AHA guidelines recommend either surgery or endovascular procedures and propose initial endovascular treatment followed by surgery if needed.¹³ After revascularization, the patient should be followed periodically with a clinical evaluation and ABI measurement with further consideration for routine duplex ultrasound surveillance.¹³

For chronic limb ischemia, a large trial showed angioplasty had lower initial morbidity, length of hospitalization, and cost than surgical repair. Surgical mortality was lower after 2 years.

Outcomes

Patients with PAD have variable outcomes. About 70% to 80% of patients with this diagnosis will have a stable disease process with no worsening of symptoms, 10% to 20% will experience worsening symptoms over time, 5% to 10% will require revascularization within 5 years of diagnosis, and 1% to 5% will progress to critical limb ischemia, which has a 5-year amputation rate of 1% to 4%.² Patients who require amputation have poor outcomes: Within 2 years, 30% are dead and 15% have had further amputations.¹⁸

In addition to the morbidity and mortality from its own progression, PAD is an important predictor of CAD and is associated with a significant elevation in morbidity and mortality from CAD. One small but well-designed prospective cohort study found that patients with PAD had a more than 6-fold increased risk of death from CAD than did patients without PAD.⁴¹

Acknowledgement
The authors thank Francesca Cimino, MD, FAAFP, for her help in reviewing this manuscript.

CORRESPONDENCE
Dustin K. Smith, DO, 2080 Child Street, Jacksonville, FL 32214; [email protected]

Here is our problem: Family medicine has allowed itself, and its patients, to be picked apart by the forces of reductionism and a system that profits from the sick and suffering. We have lost sight of our purpose and our vision to care for the whole person. We have lost our way as healers.

The result is not only a decline in the specialty of family medicine as a leader in primary care but declining value and worsening outcomes in health care overall. We need to get our mojo back. We can do this by focusing less on trying to be all things to all people at all times, and more on creating better models for preventing, managing, and reversing chronic disease. This means providing health care that is person centered, relationship based, recovery focused, and paid for comprehensively.

I call this model Advanced Primary Care, or APC ­(FIGURE). In this article, I describe exemplars of APC from across the United States. I also provide tools to help you recover its central feature, holism—care of the whole person in mind, body, community, and spirit—in your practice, thus returning us to the core purpose of family medicine.

Holism is central to family medicine

More than 40 years ago, psychiatrist George Engel, MD, published a seminal article in Science that inspired a radical vision of how health care should be practiced.¹ Called the biopsychosocial model, it stated what, in some ways, is obvious: Human beings are complex organisms embedded in complex environments made up of distinct, yet interacting, dimensions. These dimensions included physical, psychological, and social components. Engel’s radical proposition was that these dimensions are definable and measurable and that good medicine cannot afford to ignore any of them.

Engel’s assertion that good medicine requires holism was a clarion call during a time of rapidly expanding knowledge and subspecialization. That call was the inspiration for a new medical specialty called family medicine, which dared to proclaim that the best way to heal was to care for the whole person within the context of that person’s emotional and social environment. Family medicine reinvigorated primary care and grew rapidly, becoming a preeminent primary care specialty in the United States.

Continue to : Reductionism is relentless

Reductionism is relentless

But the forces of medicine were—and still are—driving relentlessly the other way. The science of the small and particular (reductionism), with dazzling technology and exploding subspecialty knowledge, and backed by powerful economic drivers, rewards health care for pulling the patient and the medical profession apart. We pay more to those who treat small parts of a person over a short period than to those who attend to the whole person over the lifetime.

Today, family medicine—for all of its common sense, scientific soundness, connectedness to patients, and demonstrated value—struggles to survive.^2-6 The holistic vision of Engel is declining. The struggle in primary care is that its holistic vision gets co-opted by specialized medical science—and then it desperately attempts to apply those small and specialized tools to the care of patients in their wholeness. Holism is largely dead in health care, and everyone pays the consequences.⁷

Health care is losing its value

The damage from this decline in holism is not just to primary care but to the value of health care in general. Most medical care being delivered today—comprising diagnosis, treatment, and payment (the innermost circle of the FIGURE)—is not producing good health.⁸ Only 15% to 20% of the healing of an individual or a population comes from health care.⁹ The rest—nearly 80%—comes from other factors rarely addressed in the health care system: behavioral and lifestyle choices that people make in their daily life, including those related to food, movement, sleep, stress, and substance use.¹⁰ Increasingly, it is the economic and social determinants of health that influence this behavior and have a greater impact on health and lifespan than physiology or genes.¹¹ The same social determinants of health also influence patients’ ability to obtain medical care and pursue a meaningful life.¹²

The result of this decline in holism and in the value of health care in general has been a relentless rise in the cost of medical care^13-15 and the need for social services; declining life expectancy^16,17 and quality of life¹⁸; growing patient dissatisfaction; and burnout in providers.^19,20 Health care has become, as investor and business leader Warren Buffet remarked, the “tapeworm” of the economy and a major contributor to growing disparities in health and well-being between the haves and have-nots.²¹ Engel’s prediction that good medicine cannot afford to ignore holism has come to pass.

Family medicine has allowed itself, and patients, to be picked apart by forces of reductionism and a system that profits from the sick and suffering.

3-step solution:Return to whole-person care

Family medicine needs to return to whole-person care, but it can do so only if it attends to, and effectively delivers on, the prevention, treatment, and reversal of chronic disease and the enhancement of health and well-­being. This can happen only if family medicine stops trying to be all things to all people at all times and, instead, focuses on what matters to the patient as a person.

Continue to: This means that the core...

This means that the core interaction in family medicine must be to assess the whole person—mind, body, social, spirit—and help that person make changes that improve his/her/their health and well-being based on his/her/their individualized needs and social context. In other words, family medicine needs to deliver a holistic model of APC that is person centered, relationship based, recovery focused, and paid for comprehensively.

How does one get from “standard” primary care of today (the innermost circle of the FIGURE) to a framework that truly delivers on the promise of healing? I propose 3 steps to return holism to family medicine.

STEP 1: Start with comprehensive, coordinated primary care. We know that this works. Starfield and others demonstrated this 2 decades ago, defining and devising what we know as quality primary care—characterized by first-contact care, comprehensive primary care (CPC), continuous care, and coordinated care.²² This type of primary care improves outcomes, lowers costs, and is satisfying to patients and providers.²³ The physician cares for the patient throughout that person’s entire life cycle and provides all evidence-based services needed to prevent and treat common conditions. Comprehensive primary care is positioned in the first circle outward from the innermost circle of the FIGURE.

As medicine has become increasingly complex and subspecialized, however, the ability to coordinate care is often frayed, adding cost and reducing quality.^24-26 Today, comprehensive primary care needs enhanced coordination. At a minimum, this means coordinating services for:

• chronic disease management (outpatient and inpatient transitions and emergency department use)
• referral (specialists and tests)
• pharmacy services (including delivery and patient education support).

An example of a primary care system that meets these requirements is the Catalyst Health Network in central Texas, which supplies coordination services to more than 1000 comprehensive primary care practices and 1.5 million patients.²⁷ The Catalyst Network makes money for those practices, saves money in the system, enhances patient and provider satisfaction, and improves population health in the community.²⁷ I call this enhanced primary care (EPC), shown in the second circle out from the innermost circle of the FIGURE.

STEP 2: Add integrative medicine and mental health. EPC improves fragmented care but does not necessarily address a patient’s underlying determinants of healing. We know that health behaviors such as smoking cessation, avoidance of alcohol and drug abuse, improved diet, physical activity, sleep, and stress management contribute 40% to 60% of a person’s and a population’s health.¹⁰ In addition, evidence shows that behavioral health services, along with lifestyle change support, can even reverse many chronic diseases seen in primary care, such as obesity, diabetes, hypertension, cardiovascular disease, depression, and substance abuse.^28,29

Continue to: Therefore, we need to add...

Therefore, we need to add routine mental health services and nonpharmacotherapeutic approaches (eg, complementary and alternative medicine) to primary care.³⁰ Doing so requires that behavioral change and self-care become a central feature of the ­doctor–patient dialogue and team skills³¹ and be added to primary care.^30,31 I call this integrative primary care (IPC), shown on the left side in the third circle out from the innermost circle of the FIGURE.
 

Only 15% to 20% of individual and population healing comes from health care; the rest, from behavioral and lifestyle choices rarely addressed in primary care.

An example of IPC is Whole Health, an initiative of the US Veteran’s Health Administration. Whole Health empowers and informs a person-centered approach and integrates it into the delivery of routine care.³² Evaluation of Whole Health implementation, which involved more than 130,000 veterans followed for 2 years, found a net overall reduction in the total cost of care of 20%—saving nearly $650 million or, on average, more than $4500 per veteran.³³

STEP 3: Address social determinants of health. Primary care will not fully be part of the solution for producing health and well-being unless it becomes instrumental in addressing the social determinants of health (SDH), defined as “… conditions in the environments in which people are born, live, learn, work, play, worship, and age that affect a wide range of health, functioning, and quality-of-life outcomes and risks.”³⁴ These determinants include not only basic needs, such as housing, food, safety, and transportation (ie, social needs), but also what are known as structural determinants, such as income, education, language, and racial and ethnic bias. Health care cannot solve all of these social ills,but it is increasingly being called on to be the nexus of coordination for services that address these needs when they affect health outcomes.^35,36

Examples of health systems that provide for social needs include the free “food prescription” program of Pennsylvania’s Geisinger Health System, for patients with diabetes who do not have the resources to pay for food.³⁷ This approach improves blood glucose control by patients and saves money on medications and other interventions. Similarly, Kaiser Permanente has experimented with housing vouchers for homeless patients,and most Federally Qualified Health Centers provide bus or other transportation tickets to patients for their appointments and free or discounted tests and specialty care.³⁸

Implementing whole-person care for all

I propose that we make APC the central focus of family medicine. This model would comprise CPC, plus EPC, IPC, and community coordination to address SDH. This is expressed as:

CPC + EPC + IPC + SDH = APC

Continue to: APC would mean...

APC would mean health for the whole person and for all people. Again, the FIGURE shows how this model, encompassing the entire third circle out from the center circle, could be created from current models of care.

How do we pay for this? We already do—and way too much. The problem is not lack of money in the health care system but how it is organized and distributed. The Centers for Medicare and Medicaid Services and other payers are developing value-based payment models to help cover this type of care,³⁹ but payers cannot pay for something if it is unavailable.

Can family physicians deliver APC? I believe they can, and have given a few examples here to show how this is already happening. To help primary care providers start to deliver APC in their system, my team and I have built the HOPE (Healing Oriented Practices & Environments) Note Toolkit to use in daily practice.⁴⁰ These and other tools are being used by a number of large hospital systems and health care networks around the country. (You can download the HOPE Note Toolkit, at no cost, at https://drwaynejonas.com/­resources/hope-note/.)

At a minimum, comprehensive primary care needs to coordinate services for chronic disease management, referral (to specialists and testing), and pharmacy services.

Whatever we call this new type of primary care, it needs to care for the whole person and to be available to all. It finds expression in these assertions:

• We cannot ignore an essential part of what a human being is and expect them to heal or become whole.
• We cannot ignore essential people in our communities and expect our costs to go down or our compassion to go up.
• We need to stop allowing family medicine to be co-opted by reductionism and its profits.

In sum, we need a new vision of primary care—like Engel’s holistic vision in the 1970s—to motivate us, and we need to return to fundamental concepts of how healing works in medicine.⁴¹

CORRESPONDENCE

Wayne B. Jonas, MD, Samueli Integrative Health Programs, 1800 Diagonal Road, Suite 617, Alexandria, VA 22314; [email protected].

Here is our problem: Family medicine has allowed itself, and its patients, to be picked apart by the forces of reductionism and a system that profits from the sick and suffering. We have lost sight of our purpose and our vision to care for the whole person. We have lost our way as healers.

The result is not only a decline in the specialty of family medicine as a leader in primary care but declining value and worsening outcomes in health care overall. We need to get our mojo back. We can do this by focusing less on trying to be all things to all people at all times, and more on creating better models for preventing, managing, and reversing chronic disease. This means providing health care that is person centered, relationship based, recovery focused, and paid for comprehensively.

I call this model Advanced Primary Care, or APC ­(FIGURE). In this article, I describe exemplars of APC from across the United States. I also provide tools to help you recover its central feature, holism—care of the whole person in mind, body, community, and spirit—in your practice, thus returning us to the core purpose of family medicine.

Holism is central to family medicine

More than 40 years ago, psychiatrist George Engel, MD, published a seminal article in Science that inspired a radical vision of how health care should be practiced.¹ Called the biopsychosocial model, it stated what, in some ways, is obvious: Human beings are complex organisms embedded in complex environments made up of distinct, yet interacting, dimensions. These dimensions included physical, psychological, and social components. Engel’s radical proposition was that these dimensions are definable and measurable and that good medicine cannot afford to ignore any of them.

Engel’s assertion that good medicine requires holism was a clarion call during a time of rapidly expanding knowledge and subspecialization. That call was the inspiration for a new medical specialty called family medicine, which dared to proclaim that the best way to heal was to care for the whole person within the context of that person’s emotional and social environment. Family medicine reinvigorated primary care and grew rapidly, becoming a preeminent primary care specialty in the United States.

Continue to : Reductionism is relentless

Reductionism is relentless

But the forces of medicine were—and still are—driving relentlessly the other way. The science of the small and particular (reductionism), with dazzling technology and exploding subspecialty knowledge, and backed by powerful economic drivers, rewards health care for pulling the patient and the medical profession apart. We pay more to those who treat small parts of a person over a short period than to those who attend to the whole person over the lifetime.

Today, family medicine—for all of its common sense, scientific soundness, connectedness to patients, and demonstrated value—struggles to survive.^2-6 The holistic vision of Engel is declining. The struggle in primary care is that its holistic vision gets co-opted by specialized medical science—and then it desperately attempts to apply those small and specialized tools to the care of patients in their wholeness. Holism is largely dead in health care, and everyone pays the consequences.⁷

Health care is losing its value

The damage from this decline in holism is not just to primary care but to the value of health care in general. Most medical care being delivered today—comprising diagnosis, treatment, and payment (the innermost circle of the FIGURE)—is not producing good health.⁸ Only 15% to 20% of the healing of an individual or a population comes from health care.⁹ The rest—nearly 80%—comes from other factors rarely addressed in the health care system: behavioral and lifestyle choices that people make in their daily life, including those related to food, movement, sleep, stress, and substance use.¹⁰ Increasingly, it is the economic and social determinants of health that influence this behavior and have a greater impact on health and lifespan than physiology or genes.¹¹ The same social determinants of health also influence patients’ ability to obtain medical care and pursue a meaningful life.¹²

The result of this decline in holism and in the value of health care in general has been a relentless rise in the cost of medical care^13-15 and the need for social services; declining life expectancy^16,17 and quality of life¹⁸; growing patient dissatisfaction; and burnout in providers.^19,20 Health care has become, as investor and business leader Warren Buffet remarked, the “tapeworm” of the economy and a major contributor to growing disparities in health and well-being between the haves and have-nots.²¹ Engel’s prediction that good medicine cannot afford to ignore holism has come to pass.

Family medicine has allowed itself, and patients, to be picked apart by forces of reductionism and a system that profits from the sick and suffering.

3-step solution:Return to whole-person care

Family medicine needs to return to whole-person care, but it can do so only if it attends to, and effectively delivers on, the prevention, treatment, and reversal of chronic disease and the enhancement of health and well-­being. This can happen only if family medicine stops trying to be all things to all people at all times and, instead, focuses on what matters to the patient as a person.

Continue to: This means that the core...

This means that the core interaction in family medicine must be to assess the whole person—mind, body, social, spirit—and help that person make changes that improve his/her/their health and well-being based on his/her/their individualized needs and social context. In other words, family medicine needs to deliver a holistic model of APC that is person centered, relationship based, recovery focused, and paid for comprehensively.

How does one get from “standard” primary care of today (the innermost circle of the FIGURE) to a framework that truly delivers on the promise of healing? I propose 3 steps to return holism to family medicine.

STEP 1: Start with comprehensive, coordinated primary care. We know that this works. Starfield and others demonstrated this 2 decades ago, defining and devising what we know as quality primary care—characterized by first-contact care, comprehensive primary care (CPC), continuous care, and coordinated care.²² This type of primary care improves outcomes, lowers costs, and is satisfying to patients and providers.²³ The physician cares for the patient throughout that person’s entire life cycle and provides all evidence-based services needed to prevent and treat common conditions. Comprehensive primary care is positioned in the first circle outward from the innermost circle of the FIGURE.

As medicine has become increasingly complex and subspecialized, however, the ability to coordinate care is often frayed, adding cost and reducing quality.^24-26 Today, comprehensive primary care needs enhanced coordination. At a minimum, this means coordinating services for:

• chronic disease management (outpatient and inpatient transitions and emergency department use)
• referral (specialists and tests)
• pharmacy services (including delivery and patient education support).

An example of a primary care system that meets these requirements is the Catalyst Health Network in central Texas, which supplies coordination services to more than 1000 comprehensive primary care practices and 1.5 million patients.²⁷ The Catalyst Network makes money for those practices, saves money in the system, enhances patient and provider satisfaction, and improves population health in the community.²⁷ I call this enhanced primary care (EPC), shown in the second circle out from the innermost circle of the FIGURE.

STEP 2: Add integrative medicine and mental health. EPC improves fragmented care but does not necessarily address a patient’s underlying determinants of healing. We know that health behaviors such as smoking cessation, avoidance of alcohol and drug abuse, improved diet, physical activity, sleep, and stress management contribute 40% to 60% of a person’s and a population’s health.¹⁰ In addition, evidence shows that behavioral health services, along with lifestyle change support, can even reverse many chronic diseases seen in primary care, such as obesity, diabetes, hypertension, cardiovascular disease, depression, and substance abuse.^28,29

Continue to: Therefore, we need to add...

Therefore, we need to add routine mental health services and nonpharmacotherapeutic approaches (eg, complementary and alternative medicine) to primary care.³⁰ Doing so requires that behavioral change and self-care become a central feature of the ­doctor–patient dialogue and team skills³¹ and be added to primary care.^30,31 I call this integrative primary care (IPC), shown on the left side in the third circle out from the innermost circle of the FIGURE.
 

Only 15% to 20% of individual and population healing comes from health care; the rest, from behavioral and lifestyle choices rarely addressed in primary care.

An example of IPC is Whole Health, an initiative of the US Veteran’s Health Administration. Whole Health empowers and informs a person-centered approach and integrates it into the delivery of routine care.³² Evaluation of Whole Health implementation, which involved more than 130,000 veterans followed for 2 years, found a net overall reduction in the total cost of care of 20%—saving nearly $650 million or, on average, more than $4500 per veteran.³³

STEP 3: Address social determinants of health. Primary care will not fully be part of the solution for producing health and well-being unless it becomes instrumental in addressing the social determinants of health (SDH), defined as “… conditions in the environments in which people are born, live, learn, work, play, worship, and age that affect a wide range of health, functioning, and quality-of-life outcomes and risks.”³⁴ These determinants include not only basic needs, such as housing, food, safety, and transportation (ie, social needs), but also what are known as structural determinants, such as income, education, language, and racial and ethnic bias. Health care cannot solve all of these social ills,but it is increasingly being called on to be the nexus of coordination for services that address these needs when they affect health outcomes.^35,36

Examples of health systems that provide for social needs include the free “food prescription” program of Pennsylvania’s Geisinger Health System, for patients with diabetes who do not have the resources to pay for food.³⁷ This approach improves blood glucose control by patients and saves money on medications and other interventions. Similarly, Kaiser Permanente has experimented with housing vouchers for homeless patients,and most Federally Qualified Health Centers provide bus or other transportation tickets to patients for their appointments and free or discounted tests and specialty care.³⁸

Implementing whole-person care for all

I propose that we make APC the central focus of family medicine. This model would comprise CPC, plus EPC, IPC, and community coordination to address SDH. This is expressed as:

CPC + EPC + IPC + SDH = APC

Continue to: APC would mean...

APC would mean health for the whole person and for all people. Again, the FIGURE shows how this model, encompassing the entire third circle out from the center circle, could be created from current models of care.

How do we pay for this? We already do—and way too much. The problem is not lack of money in the health care system but how it is organized and distributed. The Centers for Medicare and Medicaid Services and other payers are developing value-based payment models to help cover this type of care,³⁹ but payers cannot pay for something if it is unavailable.

Can family physicians deliver APC? I believe they can, and have given a few examples here to show how this is already happening. To help primary care providers start to deliver APC in their system, my team and I have built the HOPE (Healing Oriented Practices & Environments) Note Toolkit to use in daily practice.⁴⁰ These and other tools are being used by a number of large hospital systems and health care networks around the country. (You can download the HOPE Note Toolkit, at no cost, at https://drwaynejonas.com/­resources/hope-note/.)

At a minimum, comprehensive primary care needs to coordinate services for chronic disease management, referral (to specialists and testing), and pharmacy services.

Whatever we call this new type of primary care, it needs to care for the whole person and to be available to all. It finds expression in these assertions:

• We cannot ignore an essential part of what a human being is and expect them to heal or become whole.
• We cannot ignore essential people in our communities and expect our costs to go down or our compassion to go up.
• We need to stop allowing family medicine to be co-opted by reductionism and its profits.

In sum, we need a new vision of primary care—like Engel’s holistic vision in the 1970s—to motivate us, and we need to return to fundamental concepts of how healing works in medicine.⁴¹

CORRESPONDENCE

Wayne B. Jonas, MD, Samueli Integrative Health Programs, 1800 Diagonal Road, Suite 617, Alexandria, VA 22314; [email protected].

Here is our problem: Family medicine has allowed itself, and its patients, to be picked apart by the forces of reductionism and a system that profits from the sick and suffering. We have lost sight of our purpose and our vision to care for the whole person. We have lost our way as healers.

The result is not only a decline in the specialty of family medicine as a leader in primary care but declining value and worsening outcomes in health care overall. We need to get our mojo back. We can do this by focusing less on trying to be all things to all people at all times, and more on creating better models for preventing, managing, and reversing chronic disease. This means providing health care that is person centered, relationship based, recovery focused, and paid for comprehensively.

I call this model Advanced Primary Care, or APC ­(FIGURE). In this article, I describe exemplars of APC from across the United States. I also provide tools to help you recover its central feature, holism—care of the whole person in mind, body, community, and spirit—in your practice, thus returning us to the core purpose of family medicine.

Holism is central to family medicine

More than 40 years ago, psychiatrist George Engel, MD, published a seminal article in Science that inspired a radical vision of how health care should be practiced.¹ Called the biopsychosocial model, it stated what, in some ways, is obvious: Human beings are complex organisms embedded in complex environments made up of distinct, yet interacting, dimensions. These dimensions included physical, psychological, and social components. Engel’s radical proposition was that these dimensions are definable and measurable and that good medicine cannot afford to ignore any of them.

Engel’s assertion that good medicine requires holism was a clarion call during a time of rapidly expanding knowledge and subspecialization. That call was the inspiration for a new medical specialty called family medicine, which dared to proclaim that the best way to heal was to care for the whole person within the context of that person’s emotional and social environment. Family medicine reinvigorated primary care and grew rapidly, becoming a preeminent primary care specialty in the United States.

Continue to : Reductionism is relentless

Reductionism is relentless

But the forces of medicine were—and still are—driving relentlessly the other way. The science of the small and particular (reductionism), with dazzling technology and exploding subspecialty knowledge, and backed by powerful economic drivers, rewards health care for pulling the patient and the medical profession apart. We pay more to those who treat small parts of a person over a short period than to those who attend to the whole person over the lifetime.

Today, family medicine—for all of its common sense, scientific soundness, connectedness to patients, and demonstrated value—struggles to survive.^2-6 The holistic vision of Engel is declining. The struggle in primary care is that its holistic vision gets co-opted by specialized medical science—and then it desperately attempts to apply those small and specialized tools to the care of patients in their wholeness. Holism is largely dead in health care, and everyone pays the consequences.⁷

Health care is losing its value

The damage from this decline in holism is not just to primary care but to the value of health care in general. Most medical care being delivered today—comprising diagnosis, treatment, and payment (the innermost circle of the FIGURE)—is not producing good health.⁸ Only 15% to 20% of the healing of an individual or a population comes from health care.⁹ The rest—nearly 80%—comes from other factors rarely addressed in the health care system: behavioral and lifestyle choices that people make in their daily life, including those related to food, movement, sleep, stress, and substance use.¹⁰ Increasingly, it is the economic and social determinants of health that influence this behavior and have a greater impact on health and lifespan than physiology or genes.¹¹ The same social determinants of health also influence patients’ ability to obtain medical care and pursue a meaningful life.¹²

The result of this decline in holism and in the value of health care in general has been a relentless rise in the cost of medical care^13-15 and the need for social services; declining life expectancy^16,17 and quality of life¹⁸; growing patient dissatisfaction; and burnout in providers.^19,20 Health care has become, as investor and business leader Warren Buffet remarked, the “tapeworm” of the economy and a major contributor to growing disparities in health and well-being between the haves and have-nots.²¹ Engel’s prediction that good medicine cannot afford to ignore holism has come to pass.

Family medicine has allowed itself, and patients, to be picked apart by forces of reductionism and a system that profits from the sick and suffering.

3-step solution:Return to whole-person care

Family medicine needs to return to whole-person care, but it can do so only if it attends to, and effectively delivers on, the prevention, treatment, and reversal of chronic disease and the enhancement of health and well-­being. This can happen only if family medicine stops trying to be all things to all people at all times and, instead, focuses on what matters to the patient as a person.

Continue to: This means that the core...

This means that the core interaction in family medicine must be to assess the whole person—mind, body, social, spirit—and help that person make changes that improve his/her/their health and well-being based on his/her/their individualized needs and social context. In other words, family medicine needs to deliver a holistic model of APC that is person centered, relationship based, recovery focused, and paid for comprehensively.

How does one get from “standard” primary care of today (the innermost circle of the FIGURE) to a framework that truly delivers on the promise of healing? I propose 3 steps to return holism to family medicine.

STEP 1: Start with comprehensive, coordinated primary care. We know that this works. Starfield and others demonstrated this 2 decades ago, defining and devising what we know as quality primary care—characterized by first-contact care, comprehensive primary care (CPC), continuous care, and coordinated care.²² This type of primary care improves outcomes, lowers costs, and is satisfying to patients and providers.²³ The physician cares for the patient throughout that person’s entire life cycle and provides all evidence-based services needed to prevent and treat common conditions. Comprehensive primary care is positioned in the first circle outward from the innermost circle of the FIGURE.

As medicine has become increasingly complex and subspecialized, however, the ability to coordinate care is often frayed, adding cost and reducing quality.^24-26 Today, comprehensive primary care needs enhanced coordination. At a minimum, this means coordinating services for:

• chronic disease management (outpatient and inpatient transitions and emergency department use)
• referral (specialists and tests)
• pharmacy services (including delivery and patient education support).

An example of a primary care system that meets these requirements is the Catalyst Health Network in central Texas, which supplies coordination services to more than 1000 comprehensive primary care practices and 1.5 million patients.²⁷ The Catalyst Network makes money for those practices, saves money in the system, enhances patient and provider satisfaction, and improves population health in the community.²⁷ I call this enhanced primary care (EPC), shown in the second circle out from the innermost circle of the FIGURE.

STEP 2: Add integrative medicine and mental health. EPC improves fragmented care but does not necessarily address a patient’s underlying determinants of healing. We know that health behaviors such as smoking cessation, avoidance of alcohol and drug abuse, improved diet, physical activity, sleep, and stress management contribute 40% to 60% of a person’s and a population’s health.¹⁰ In addition, evidence shows that behavioral health services, along with lifestyle change support, can even reverse many chronic diseases seen in primary care, such as obesity, diabetes, hypertension, cardiovascular disease, depression, and substance abuse.^28,29

Continue to: Therefore, we need to add...

Therefore, we need to add routine mental health services and nonpharmacotherapeutic approaches (eg, complementary and alternative medicine) to primary care.³⁰ Doing so requires that behavioral change and self-care become a central feature of the ­doctor–patient dialogue and team skills³¹ and be added to primary care.^30,31 I call this integrative primary care (IPC), shown on the left side in the third circle out from the innermost circle of the FIGURE.
 

Only 15% to 20% of individual and population healing comes from health care; the rest, from behavioral and lifestyle choices rarely addressed in primary care.

An example of IPC is Whole Health, an initiative of the US Veteran’s Health Administration. Whole Health empowers and informs a person-centered approach and integrates it into the delivery of routine care.³² Evaluation of Whole Health implementation, which involved more than 130,000 veterans followed for 2 years, found a net overall reduction in the total cost of care of 20%—saving nearly $650 million or, on average, more than $4500 per veteran.³³

STEP 3: Address social determinants of health. Primary care will not fully be part of the solution for producing health and well-being unless it becomes instrumental in addressing the social determinants of health (SDH), defined as “… conditions in the environments in which people are born, live, learn, work, play, worship, and age that affect a wide range of health, functioning, and quality-of-life outcomes and risks.”³⁴ These determinants include not only basic needs, such as housing, food, safety, and transportation (ie, social needs), but also what are known as structural determinants, such as income, education, language, and racial and ethnic bias. Health care cannot solve all of these social ills,but it is increasingly being called on to be the nexus of coordination for services that address these needs when they affect health outcomes.^35,36

Examples of health systems that provide for social needs include the free “food prescription” program of Pennsylvania’s Geisinger Health System, for patients with diabetes who do not have the resources to pay for food.³⁷ This approach improves blood glucose control by patients and saves money on medications and other interventions. Similarly, Kaiser Permanente has experimented with housing vouchers for homeless patients,and most Federally Qualified Health Centers provide bus or other transportation tickets to patients for their appointments and free or discounted tests and specialty care.³⁸

Implementing whole-person care for all

I propose that we make APC the central focus of family medicine. This model would comprise CPC, plus EPC, IPC, and community coordination to address SDH. This is expressed as:

CPC + EPC + IPC + SDH = APC

Continue to: APC would mean...

APC would mean health for the whole person and for all people. Again, the FIGURE shows how this model, encompassing the entire third circle out from the center circle, could be created from current models of care.

How do we pay for this? We already do—and way too much. The problem is not lack of money in the health care system but how it is organized and distributed. The Centers for Medicare and Medicaid Services and other payers are developing value-based payment models to help cover this type of care,³⁹ but payers cannot pay for something if it is unavailable.

Can family physicians deliver APC? I believe they can, and have given a few examples here to show how this is already happening. To help primary care providers start to deliver APC in their system, my team and I have built the HOPE (Healing Oriented Practices & Environments) Note Toolkit to use in daily practice.⁴⁰ These and other tools are being used by a number of large hospital systems and health care networks around the country. (You can download the HOPE Note Toolkit, at no cost, at https://drwaynejonas.com/­resources/hope-note/.)

At a minimum, comprehensive primary care needs to coordinate services for chronic disease management, referral (to specialists and testing), and pharmacy services.

Whatever we call this new type of primary care, it needs to care for the whole person and to be available to all. It finds expression in these assertions:

• We cannot ignore an essential part of what a human being is and expect them to heal or become whole.
• We cannot ignore essential people in our communities and expect our costs to go down or our compassion to go up.
• We need to stop allowing family medicine to be co-opted by reductionism and its profits.

In sum, we need a new vision of primary care—like Engel’s holistic vision in the 1970s—to motivate us, and we need to return to fundamental concepts of how healing works in medicine.⁴¹

CORRESPONDENCE

Wayne B. Jonas, MD, Samueli Integrative Health Programs, 1800 Diagonal Road, Suite 617, Alexandria, VA 22314; [email protected].

Peripheral neuropathy is common in U.S. adults and is associated with an increased risk of death, even in the absence of diabetes, researchers reported  in Annals of Internal Medicine.

©mheim3011/thinkstockphotos.com

The findings do not necessarily mean that doctors should implement broader screening for peripheral neuropathy at this time, however, the investigators said.

“Doctors don’t typically screen for peripheral neuropathy in persons without diabetes,” senior author Elizabeth Selvin, PhD, MPH, professor of epidemiology at the Johns Hopkins Bloomberg School of Public Health, Baltimore, said in an interview.

“Our study shows that peripheral neuropathy – as assessed by decreased sensation in the feet – is common, even in people without diabetes,” Dr. Selvin explained. “It is not yet clear whether we should be screening people without diabetes since we don’t have clear treatments, but our study does suggest that this condition is an underrecognized condition that is associated with poor outcomes.”

Patients with diabetes typically undergo annual foot examinations that include screening for peripheral neuropathy, but that’s not the case for most adults in the absence of diabetes.

“I don’t know if we can make the jump that we should be screening people without diabetes,” said first author Caitlin W. Hicks, MD, assistant professor of surgery, division of vascular surgery and endovascular therapy, Johns Hopkins University, Baltimore. “Right now, we do not exactly know what it means in the people without diabetes, and we definitely do not know how to treat it. So, screening for it will tell us that this person has this and is at higher risk of mortality than someone who doesn’t, but we do not know what to do with that information yet.”

Nevertheless, the study raises the question of whether physicians should pay more attention to peripheral neuropathy in people without diabetes, said Dr. Hicks, director of research at the university’s diabetic foot and wound service.
 

Heightened risk

To examine associations between peripheral neuropathy and all-cause and cardiovascular mortality in U.S. adults, Dr. Hicks and colleagues analyzed data from 7,116 adults aged 40 years or older who participated in the National Health and Nutrition Examination Survey (NHANES) between 1999 and 2004.

The study included participants who underwent monofilament testing for peripheral neuropathy. During testing, technicians used a standard 5.07 Semmes-Weinstein nylon monofilament to apply slight pressure to the bottom of each foot at three sites. If participants could not correctly identify where pressure was applied, the test was repeated. After participants gave two incorrect or undeterminable responses for a site, the site was defined as insensate. The researchers defined peripheral neuropathy as at least one insensate site on either foot.

The researchers determined deaths and causes of death using death certificate records from the National Death Index through 2015.

In all, 13.5% of the participants had peripheral neuropathy, including 27% of adults with diabetes and 11.6% of adults without diabetes. Those with peripheral neuropathy were older, were more likely to be male, and had lower levels of education, compared with participants without peripheral neuropathy. They also had higher body mass index, were more often former or current smokers, and had a higher prevalence of hypertension, hypercholesterolemia, and cardiovascular disease.

During a median follow-up of 13 years, 2,128 participants died, including 488 who died of cardiovascular causes.

The incidence rate of all-cause mortality per 1,000 person-years was 57.6 in adults with diabetes and peripheral neuropathy, 34.3 in adults with peripheral neuropathy but no diabetes, 27.1 in adults with diabetes but no peripheral neuropathy, and 13.0 in adults without diabetes or peripheral neuropathy.

Among participants with diabetes, the leading cause of death was cardiovascular disease (31% of deaths), whereas among participants without diabetes, the leading cause of death was malignant neoplasms (27% of deaths).

After adjustment for age, sex, race, or ethnicity, and risk factors such as cardiovascular disease, peripheral neuropathy was significantly associated with all-cause mortality (hazard ratio [HR], 1.49) and cardiovascular mortality (HR, 1.66) in participants with diabetes. In participants without diabetes, peripheral neuropathy was significantly associated with all-cause mortality (HR, 1.31), but its association with cardiovascular mortality was not statistically significant.

The association between peripheral neuropathy and all-cause mortality persisted in a sensitivity analysis that focused on adults with normoglycemia.
 

Related conditions

The study confirms findings from prior studies that examined the prevalence of loss of peripheral sensation in populations of older adults with and without diabetes, said Elsa S. Strotmeyer, PhD, MPH, associate professor of epidemiology at the University of Pittsburgh. “The clinical significance of the loss of peripheral sensation in older adults without diabetes is not fully appreciated,” she said.

A limitation of the study is that peripheral neuropathy was not a clinical diagnosis. “Monofilament testing at the foot is a quick clinical screen for decreased lower-extremity sensation that likely is a result of sensory peripheral nerve decline,” Dr. Strotmeyer said.

Another limitation is that death certificates are less accurate than medical records for determining cause of death.

“Past studies have indicated that peripheral nerve decline is related to common conditions in aging such as the metabolic syndrome and cardiovascular disease, cancer treatment, and physical function loss,” Dr. Strotmeyer said. “Therefore it is not surprising that is related to mortality as these conditions in aging are associated with increased mortality. Loss of peripheral sensation at the foot may also be related to fall injuries, and mortality from fall injuries has increased dramatically in older adults over the past several decades.”

Prior research has suggested that monofilament testing may play a role in screening for fall risk in older adults without diabetes, Dr. Strotmeyer added.

“For older adults both with and without diabetes, past studies have recommended monofilament testing be incorporated in geriatric screening for fall risk. Therefore, this article expands implications of clinical importance to understanding the pathology and consequences of loss of sensation at the foot in older patients,” she said.

The study was funded by the National Institute of Diabetes and Digestive and Kidney Diseases and the National Heart, Lung, and Blood Institute. Dr. Hicks, Dr. Selvin, and a coauthor, Kunihiro Matsushita, MD, PhD, disclosed NIH grants. In addition, Dr. Selvin disclosed personal fees from Novo Nordisk and grants from the Foundation for the National Institutes of Health outside the submitted work, and Dr. Matsushita disclosed grants and personal fees from Fukuda Denshi outside the submitted work. Dr. Strotmeyer receives funding from the National Institute on Aging and the National Institute of Arthritis and Musculoskeletal and Skin Diseases and is chair of the health sciences section of the Gerontological Society of America.

A version of this article originally appeared on Medscape.com.

Peripheral neuropathy is common in U.S. adults and is associated with an increased risk of death, even in the absence of diabetes, researchers reported  in Annals of Internal Medicine.

©mheim3011/thinkstockphotos.com

The findings do not necessarily mean that doctors should implement broader screening for peripheral neuropathy at this time, however, the investigators said.

“Doctors don’t typically screen for peripheral neuropathy in persons without diabetes,” senior author Elizabeth Selvin, PhD, MPH, professor of epidemiology at the Johns Hopkins Bloomberg School of Public Health, Baltimore, said in an interview.

“Our study shows that peripheral neuropathy – as assessed by decreased sensation in the feet – is common, even in people without diabetes,” Dr. Selvin explained. “It is not yet clear whether we should be screening people without diabetes since we don’t have clear treatments, but our study does suggest that this condition is an underrecognized condition that is associated with poor outcomes.”

Patients with diabetes typically undergo annual foot examinations that include screening for peripheral neuropathy, but that’s not the case for most adults in the absence of diabetes.

“I don’t know if we can make the jump that we should be screening people without diabetes,” said first author Caitlin W. Hicks, MD, assistant professor of surgery, division of vascular surgery and endovascular therapy, Johns Hopkins University, Baltimore. “Right now, we do not exactly know what it means in the people without diabetes, and we definitely do not know how to treat it. So, screening for it will tell us that this person has this and is at higher risk of mortality than someone who doesn’t, but we do not know what to do with that information yet.”

Nevertheless, the study raises the question of whether physicians should pay more attention to peripheral neuropathy in people without diabetes, said Dr. Hicks, director of research at the university’s diabetic foot and wound service.
 

Heightened risk

To examine associations between peripheral neuropathy and all-cause and cardiovascular mortality in U.S. adults, Dr. Hicks and colleagues analyzed data from 7,116 adults aged 40 years or older who participated in the National Health and Nutrition Examination Survey (NHANES) between 1999 and 2004.

The study included participants who underwent monofilament testing for peripheral neuropathy. During testing, technicians used a standard 5.07 Semmes-Weinstein nylon monofilament to apply slight pressure to the bottom of each foot at three sites. If participants could not correctly identify where pressure was applied, the test was repeated. After participants gave two incorrect or undeterminable responses for a site, the site was defined as insensate. The researchers defined peripheral neuropathy as at least one insensate site on either foot.

The researchers determined deaths and causes of death using death certificate records from the National Death Index through 2015.

In all, 13.5% of the participants had peripheral neuropathy, including 27% of adults with diabetes and 11.6% of adults without diabetes. Those with peripheral neuropathy were older, were more likely to be male, and had lower levels of education, compared with participants without peripheral neuropathy. They also had higher body mass index, were more often former or current smokers, and had a higher prevalence of hypertension, hypercholesterolemia, and cardiovascular disease.

During a median follow-up of 13 years, 2,128 participants died, including 488 who died of cardiovascular causes.

The incidence rate of all-cause mortality per 1,000 person-years was 57.6 in adults with diabetes and peripheral neuropathy, 34.3 in adults with peripheral neuropathy but no diabetes, 27.1 in adults with diabetes but no peripheral neuropathy, and 13.0 in adults without diabetes or peripheral neuropathy.

Among participants with diabetes, the leading cause of death was cardiovascular disease (31% of deaths), whereas among participants without diabetes, the leading cause of death was malignant neoplasms (27% of deaths).

After adjustment for age, sex, race, or ethnicity, and risk factors such as cardiovascular disease, peripheral neuropathy was significantly associated with all-cause mortality (hazard ratio [HR], 1.49) and cardiovascular mortality (HR, 1.66) in participants with diabetes. In participants without diabetes, peripheral neuropathy was significantly associated with all-cause mortality (HR, 1.31), but its association with cardiovascular mortality was not statistically significant.

The association between peripheral neuropathy and all-cause mortality persisted in a sensitivity analysis that focused on adults with normoglycemia.
 

Related conditions

The study confirms findings from prior studies that examined the prevalence of loss of peripheral sensation in populations of older adults with and without diabetes, said Elsa S. Strotmeyer, PhD, MPH, associate professor of epidemiology at the University of Pittsburgh. “The clinical significance of the loss of peripheral sensation in older adults without diabetes is not fully appreciated,” she said.

A limitation of the study is that peripheral neuropathy was not a clinical diagnosis. “Monofilament testing at the foot is a quick clinical screen for decreased lower-extremity sensation that likely is a result of sensory peripheral nerve decline,” Dr. Strotmeyer said.

Another limitation is that death certificates are less accurate than medical records for determining cause of death.

“Past studies have indicated that peripheral nerve decline is related to common conditions in aging such as the metabolic syndrome and cardiovascular disease, cancer treatment, and physical function loss,” Dr. Strotmeyer said. “Therefore it is not surprising that is related to mortality as these conditions in aging are associated with increased mortality. Loss of peripheral sensation at the foot may also be related to fall injuries, and mortality from fall injuries has increased dramatically in older adults over the past several decades.”

Prior research has suggested that monofilament testing may play a role in screening for fall risk in older adults without diabetes, Dr. Strotmeyer added.

“For older adults both with and without diabetes, past studies have recommended monofilament testing be incorporated in geriatric screening for fall risk. Therefore, this article expands implications of clinical importance to understanding the pathology and consequences of loss of sensation at the foot in older patients,” she said.

The study was funded by the National Institute of Diabetes and Digestive and Kidney Diseases and the National Heart, Lung, and Blood Institute. Dr. Hicks, Dr. Selvin, and a coauthor, Kunihiro Matsushita, MD, PhD, disclosed NIH grants. In addition, Dr. Selvin disclosed personal fees from Novo Nordisk and grants from the Foundation for the National Institutes of Health outside the submitted work, and Dr. Matsushita disclosed grants and personal fees from Fukuda Denshi outside the submitted work. Dr. Strotmeyer receives funding from the National Institute on Aging and the National Institute of Arthritis and Musculoskeletal and Skin Diseases and is chair of the health sciences section of the Gerontological Society of America.

A version of this article originally appeared on Medscape.com.

Peripheral neuropathy is common in U.S. adults and is associated with an increased risk of death, even in the absence of diabetes, researchers reported  in Annals of Internal Medicine.

©mheim3011/thinkstockphotos.com

The findings do not necessarily mean that doctors should implement broader screening for peripheral neuropathy at this time, however, the investigators said.

“Doctors don’t typically screen for peripheral neuropathy in persons without diabetes,” senior author Elizabeth Selvin, PhD, MPH, professor of epidemiology at the Johns Hopkins Bloomberg School of Public Health, Baltimore, said in an interview.

“Our study shows that peripheral neuropathy – as assessed by decreased sensation in the feet – is common, even in people without diabetes,” Dr. Selvin explained. “It is not yet clear whether we should be screening people without diabetes since we don’t have clear treatments, but our study does suggest that this condition is an underrecognized condition that is associated with poor outcomes.”

Patients with diabetes typically undergo annual foot examinations that include screening for peripheral neuropathy, but that’s not the case for most adults in the absence of diabetes.

“I don’t know if we can make the jump that we should be screening people without diabetes,” said first author Caitlin W. Hicks, MD, assistant professor of surgery, division of vascular surgery and endovascular therapy, Johns Hopkins University, Baltimore. “Right now, we do not exactly know what it means in the people without diabetes, and we definitely do not know how to treat it. So, screening for it will tell us that this person has this and is at higher risk of mortality than someone who doesn’t, but we do not know what to do with that information yet.”

Nevertheless, the study raises the question of whether physicians should pay more attention to peripheral neuropathy in people without diabetes, said Dr. Hicks, director of research at the university’s diabetic foot and wound service.
 

Heightened risk

To examine associations between peripheral neuropathy and all-cause and cardiovascular mortality in U.S. adults, Dr. Hicks and colleagues analyzed data from 7,116 adults aged 40 years or older who participated in the National Health and Nutrition Examination Survey (NHANES) between 1999 and 2004.

The study included participants who underwent monofilament testing for peripheral neuropathy. During testing, technicians used a standard 5.07 Semmes-Weinstein nylon monofilament to apply slight pressure to the bottom of each foot at three sites. If participants could not correctly identify where pressure was applied, the test was repeated. After participants gave two incorrect or undeterminable responses for a site, the site was defined as insensate. The researchers defined peripheral neuropathy as at least one insensate site on either foot.

The researchers determined deaths and causes of death using death certificate records from the National Death Index through 2015.

In all, 13.5% of the participants had peripheral neuropathy, including 27% of adults with diabetes and 11.6% of adults without diabetes. Those with peripheral neuropathy were older, were more likely to be male, and had lower levels of education, compared with participants without peripheral neuropathy. They also had higher body mass index, were more often former or current smokers, and had a higher prevalence of hypertension, hypercholesterolemia, and cardiovascular disease.

During a median follow-up of 13 years, 2,128 participants died, including 488 who died of cardiovascular causes.

The incidence rate of all-cause mortality per 1,000 person-years was 57.6 in adults with diabetes and peripheral neuropathy, 34.3 in adults with peripheral neuropathy but no diabetes, 27.1 in adults with diabetes but no peripheral neuropathy, and 13.0 in adults without diabetes or peripheral neuropathy.

Among participants with diabetes, the leading cause of death was cardiovascular disease (31% of deaths), whereas among participants without diabetes, the leading cause of death was malignant neoplasms (27% of deaths).

After adjustment for age, sex, race, or ethnicity, and risk factors such as cardiovascular disease, peripheral neuropathy was significantly associated with all-cause mortality (hazard ratio [HR], 1.49) and cardiovascular mortality (HR, 1.66) in participants with diabetes. In participants without diabetes, peripheral neuropathy was significantly associated with all-cause mortality (HR, 1.31), but its association with cardiovascular mortality was not statistically significant.

The association between peripheral neuropathy and all-cause mortality persisted in a sensitivity analysis that focused on adults with normoglycemia.
 

Related conditions

The study confirms findings from prior studies that examined the prevalence of loss of peripheral sensation in populations of older adults with and without diabetes, said Elsa S. Strotmeyer, PhD, MPH, associate professor of epidemiology at the University of Pittsburgh. “The clinical significance of the loss of peripheral sensation in older adults without diabetes is not fully appreciated,” she said.

A limitation of the study is that peripheral neuropathy was not a clinical diagnosis. “Monofilament testing at the foot is a quick clinical screen for decreased lower-extremity sensation that likely is a result of sensory peripheral nerve decline,” Dr. Strotmeyer said.

Another limitation is that death certificates are less accurate than medical records for determining cause of death.

“Past studies have indicated that peripheral nerve decline is related to common conditions in aging such as the metabolic syndrome and cardiovascular disease, cancer treatment, and physical function loss,” Dr. Strotmeyer said. “Therefore it is not surprising that is related to mortality as these conditions in aging are associated with increased mortality. Loss of peripheral sensation at the foot may also be related to fall injuries, and mortality from fall injuries has increased dramatically in older adults over the past several decades.”

Prior research has suggested that monofilament testing may play a role in screening for fall risk in older adults without diabetes, Dr. Strotmeyer added.

“For older adults both with and without diabetes, past studies have recommended monofilament testing be incorporated in geriatric screening for fall risk. Therefore, this article expands implications of clinical importance to understanding the pathology and consequences of loss of sensation at the foot in older patients,” she said.

The study was funded by the National Institute of Diabetes and Digestive and Kidney Diseases and the National Heart, Lung, and Blood Institute. Dr. Hicks, Dr. Selvin, and a coauthor, Kunihiro Matsushita, MD, PhD, disclosed NIH grants. In addition, Dr. Selvin disclosed personal fees from Novo Nordisk and grants from the Foundation for the National Institutes of Health outside the submitted work, and Dr. Matsushita disclosed grants and personal fees from Fukuda Denshi outside the submitted work. Dr. Strotmeyer receives funding from the National Institute on Aging and the National Institute of Arthritis and Musculoskeletal and Skin Diseases and is chair of the health sciences section of the Gerontological Society of America.

A version of this article originally appeared on Medscape.com.

Osteoarthritis patients report significant pain relief after treatment with cooled radiofrequency ablation, a new technique that “stuns” sensory nerves in shoulder and hip joints to reduce – and sometimes eliminate – pain.

“We send a small current to the sensory nerve to heat up the tissue and disrupt the fibers,” study lead author Felix Gonzalez, MD, of Emory University, Atlanta, said in an interview. “The effect is that the transmission of pain is significantly slowed or halted altogether.

“We damage something to fix something,” Dr. Gonzalez continued. “We target only the problematic nerve and get a very localized effect.”
 

Two-phase treatment

The treatment is performed in two phases. First, patients with shoulder pain are given an anesthetic to block their suprascapular, lateral pectoral, and axillary sensory articular nerves. Patients with hip pain have their obturator and femoral sensory articular nerves blocked.

A week or two later, the same nerves are treated with cooled radiofrequency ablation. Guided by x-ray imaging, a clinician heats up the affected nerve tissue using the tip of a needle, which is pointed at the nerve. “It’s a 22-gauge needle, slightly thicker than an acupuncture needle,” Dr. Gonzalez explained. “We heat up the nerve for about 2 minutes to about 60 degrees Celsius – it stuns the nerve,” he said.

“The result disrupts or slows down pain transmission while leaving the nerve intact.”

To test the efficacy of the technique, researchers treated 12 shoulders in patients with an average age of 61 years, and 11 hips in patients with an average age of 62 years.

Three months after treatment, patients with hip pain reported improvement in Hip Disability and Osteoarthritis Outcome Score (HOOS) from a baseline of 17.0 to 52.9 (P < .0001).

Shoulder pain was also reduced significantly. Using the American Shoulder and Elbow Surgeons (ASES) score, researchers reported an improvement from 17.2 (±6.6) at baseline to 65.7 (±5.9) at 3 months (P < .0001).

“We are targeting a subset of patients for this that don’t qualify for surgery,” Dr. Gonzalez noted. For patients with a body mass index above 35, or a history of hypertension, heart disease, or multiple strokes, opioids are the most common treatment, he said.

These patients “fall through the cracks,” he explained. Those who have mild to moderate pain are managed with physical therapy and injections, and those with severe pain go into surgery. “But what about the ones in the middle ... who are not eligible for surgery? They are at risk for opioid overuse,” he said. “So this treatment is a good option for them.”
 

Treats the symptoms, not the cause

“This study shows the efficacy of this method in taking care of shoulder and hip pain,” Luca Maria Sconfienza, MD, PhD, of Galeazzi Orthopedic Hospital in Milan, said in an interview. Dr. Sconfienza was not involved in Dr. Gonzalez’s study.

However, like corticosteroid injections, “the drawback of radiofrequency ablation is the fact that it only treats the symptoms and not the cause, and efficacy is usually limited over time,” she said.

Dr. Sconfienza said this study leaves her with three pertinent questions. “First, whether pain control extends beyond the 3-month follow-up reported by authors in the abstract; second, [what] is the efficacy of this method compared to other interventions (e.g., physical therapy, injections) or to doing nothing; and last, radiofrequency ablation is usually not a cheap treatment, thus a cost-efficacy analysis would be desirable, especially in comparison to other procedures.”

Dr. Gonzalez and Dr. Sconfienza have nothing relevant to disclose.

A version of this article originally appeared on Medscape.com.

Osteoarthritis patients report significant pain relief after treatment with cooled radiofrequency ablation, a new technique that “stuns” sensory nerves in shoulder and hip joints to reduce – and sometimes eliminate – pain.

“We send a small current to the sensory nerve to heat up the tissue and disrupt the fibers,” study lead author Felix Gonzalez, MD, of Emory University, Atlanta, said in an interview. “The effect is that the transmission of pain is significantly slowed or halted altogether.

“We damage something to fix something,” Dr. Gonzalez continued. “We target only the problematic nerve and get a very localized effect.”
 

Two-phase treatment

The treatment is performed in two phases. First, patients with shoulder pain are given an anesthetic to block their suprascapular, lateral pectoral, and axillary sensory articular nerves. Patients with hip pain have their obturator and femoral sensory articular nerves blocked.

A week or two later, the same nerves are treated with cooled radiofrequency ablation. Guided by x-ray imaging, a clinician heats up the affected nerve tissue using the tip of a needle, which is pointed at the nerve. “It’s a 22-gauge needle, slightly thicker than an acupuncture needle,” Dr. Gonzalez explained. “We heat up the nerve for about 2 minutes to about 60 degrees Celsius – it stuns the nerve,” he said.

“The result disrupts or slows down pain transmission while leaving the nerve intact.”

To test the efficacy of the technique, researchers treated 12 shoulders in patients with an average age of 61 years, and 11 hips in patients with an average age of 62 years.

Three months after treatment, patients with hip pain reported improvement in Hip Disability and Osteoarthritis Outcome Score (HOOS) from a baseline of 17.0 to 52.9 (P < .0001).

Shoulder pain was also reduced significantly. Using the American Shoulder and Elbow Surgeons (ASES) score, researchers reported an improvement from 17.2 (±6.6) at baseline to 65.7 (±5.9) at 3 months (P < .0001).

“We are targeting a subset of patients for this that don’t qualify for surgery,” Dr. Gonzalez noted. For patients with a body mass index above 35, or a history of hypertension, heart disease, or multiple strokes, opioids are the most common treatment, he said.

These patients “fall through the cracks,” he explained. Those who have mild to moderate pain are managed with physical therapy and injections, and those with severe pain go into surgery. “But what about the ones in the middle ... who are not eligible for surgery? They are at risk for opioid overuse,” he said. “So this treatment is a good option for them.”
 

Treats the symptoms, not the cause

“This study shows the efficacy of this method in taking care of shoulder and hip pain,” Luca Maria Sconfienza, MD, PhD, of Galeazzi Orthopedic Hospital in Milan, said in an interview. Dr. Sconfienza was not involved in Dr. Gonzalez’s study.

However, like corticosteroid injections, “the drawback of radiofrequency ablation is the fact that it only treats the symptoms and not the cause, and efficacy is usually limited over time,” she said.

Dr. Sconfienza said this study leaves her with three pertinent questions. “First, whether pain control extends beyond the 3-month follow-up reported by authors in the abstract; second, [what] is the efficacy of this method compared to other interventions (e.g., physical therapy, injections) or to doing nothing; and last, radiofrequency ablation is usually not a cheap treatment, thus a cost-efficacy analysis would be desirable, especially in comparison to other procedures.”

Dr. Gonzalez and Dr. Sconfienza have nothing relevant to disclose.

A version of this article originally appeared on Medscape.com.

Osteoarthritis patients report significant pain relief after treatment with cooled radiofrequency ablation, a new technique that “stuns” sensory nerves in shoulder and hip joints to reduce – and sometimes eliminate – pain.

“We send a small current to the sensory nerve to heat up the tissue and disrupt the fibers,” study lead author Felix Gonzalez, MD, of Emory University, Atlanta, said in an interview. “The effect is that the transmission of pain is significantly slowed or halted altogether.

“We damage something to fix something,” Dr. Gonzalez continued. “We target only the problematic nerve and get a very localized effect.”
 

Two-phase treatment

The treatment is performed in two phases. First, patients with shoulder pain are given an anesthetic to block their suprascapular, lateral pectoral, and axillary sensory articular nerves. Patients with hip pain have their obturator and femoral sensory articular nerves blocked.

A week or two later, the same nerves are treated with cooled radiofrequency ablation. Guided by x-ray imaging, a clinician heats up the affected nerve tissue using the tip of a needle, which is pointed at the nerve. “It’s a 22-gauge needle, slightly thicker than an acupuncture needle,” Dr. Gonzalez explained. “We heat up the nerve for about 2 minutes to about 60 degrees Celsius – it stuns the nerve,” he said.

“The result disrupts or slows down pain transmission while leaving the nerve intact.”

To test the efficacy of the technique, researchers treated 12 shoulders in patients with an average age of 61 years, and 11 hips in patients with an average age of 62 years.

Three months after treatment, patients with hip pain reported improvement in Hip Disability and Osteoarthritis Outcome Score (HOOS) from a baseline of 17.0 to 52.9 (P < .0001).

Shoulder pain was also reduced significantly. Using the American Shoulder and Elbow Surgeons (ASES) score, researchers reported an improvement from 17.2 (±6.6) at baseline to 65.7 (±5.9) at 3 months (P < .0001).

“We are targeting a subset of patients for this that don’t qualify for surgery,” Dr. Gonzalez noted. For patients with a body mass index above 35, or a history of hypertension, heart disease, or multiple strokes, opioids are the most common treatment, he said.

These patients “fall through the cracks,” he explained. Those who have mild to moderate pain are managed with physical therapy and injections, and those with severe pain go into surgery. “But what about the ones in the middle ... who are not eligible for surgery? They are at risk for opioid overuse,” he said. “So this treatment is a good option for them.”
 

Treats the symptoms, not the cause

“This study shows the efficacy of this method in taking care of shoulder and hip pain,” Luca Maria Sconfienza, MD, PhD, of Galeazzi Orthopedic Hospital in Milan, said in an interview. Dr. Sconfienza was not involved in Dr. Gonzalez’s study.

However, like corticosteroid injections, “the drawback of radiofrequency ablation is the fact that it only treats the symptoms and not the cause, and efficacy is usually limited over time,” she said.

Dr. Sconfienza said this study leaves her with three pertinent questions. “First, whether pain control extends beyond the 3-month follow-up reported by authors in the abstract; second, [what] is the efficacy of this method compared to other interventions (e.g., physical therapy, injections) or to doing nothing; and last, radiofrequency ablation is usually not a cheap treatment, thus a cost-efficacy analysis would be desirable, especially in comparison to other procedures.”

Dr. Gonzalez and Dr. Sconfienza have nothing relevant to disclose.

A version of this article originally appeared on Medscape.com.

New clinical practice guidelines on Lyme disease place a strong emphasis on antibody testing to assess for rheumatologic and neurologic syndromes. “Diagnostically, we recommend testing via antibodies, and an index of antibodies in cerebrospinal fluid [CSF] versus serum. Importantly, we recommend against using polymerase chain reaction [PCR] in CSF,” Jeffrey A. Rumbaugh, MD, PhD, a coauthor of the guidelines and a member of the American Academy of Neurology, said in an interview.

CDC/ Dr. Amanda Loftis, Dr. William Nicholson, Dr. Will Reeves, Dr. Chris Paddock

The Infectious Diseases Society of America, AAN, and the American College of Rheumatology convened a multidisciplinary panel to develop the 43 recommendations, seeking input from 12 additional medical specialties, and patients. The panel conducted a systematic review of available evidence on preventing, diagnosing, and treating Lyme disease, using the Grading of Recommendations Assessment, Development and Evaluation model to evaluate clinical evidence and strength of recommendations. The guidelines were simultaneous published in Clinical Infectious Diseases, Neurology, Arthritis & Rheumatology, and Arthritis Care & Research.

This is the first time these organizations have collaborated on joint Lyme disease guidelines, which focus mainly on neurologic, cardiac, and rheumatologic manifestations.

“We are very excited to provide these updated guidelines to assist clinicians working in numerous medical specialties around the country, and even the world, as they care for patients suffering from Lyme disease,” Dr. Rumbaugh said.
 

When to use and not to use PCR

Guideline authors called for specific testing regimens depending on presentation of symptoms. Generally, they advised that individuals with a skin rash suggestive of early disease seek a clinical diagnosis instead of laboratory testing.

Recommendations on Lyme arthritis support previous IDSA guidelines published in 2006, Linda K. Bockenstedt, MD, professor of medicine at Yale University, New Haven, Conn., and a coauthor of the guidelines, said in an interview.

To evaluate for potential Lyme arthritis, clinicians should choose serum antibody testing over PCR or culture of blood or synovial fluid/tissue. However, if a doctor is assessing a seropositive patient for Lyme arthritis diagnosis but needs more information for treatment decisions, the authors recommended PCR applied to synovial fluid or tissue over Borrelia culture.

“Synovial fluid can be analyzed by PCR, but sensitivity is generally lower than serology,” Dr. Bockenstedt explained. Additionally, culture of joint fluid or synovial tissue for Lyme spirochetes has 0% sensitivity in multiple studies. “For these reasons, we recommend serum antibody testing over PCR of joint fluid or other methods for an initial diagnosis.”

Serum antibody testing over PCR or culture is also recommended for identifying Lyme neuroborreliosis in the peripheral nervous system (PNS) or CNS.

Despite the recent popularity of Lyme PCR testing in hospitals and labs, “with Lyme at least, antibodies are better in the CSF,” Dr. Rumbaugh said. Studies have shown that “most patients with even early neurologic Lyme disease are seropositive by conventional antibody testing at time of initial clinical presentation, and that intrathecal antibody production, as demonstrated by an elevated CSF:serum index, is highly specific for CNS involvement.”

If done correctly, antibody testing is both sensitive and specific for neurologic Lyme disease. “On the other hand, sensitivity of Lyme PCR performed on CSF has been only in the 5%-17% range in studies. Incidentally, Lyme PCR on blood is also not sensitive and therefore not recommended,” Dr. Rumbaugh said.

Guideline authors recommended testing in patients with the following conditions: acute neurologic disorders such as meningitis, painful radiculoneuritis, mononeuropathy multiplex; evidence of spinal cord or brain inflammation; and acute myocarditis/pericarditis of unknown cause in an appropriate epidemiologic setting.

They did not recommend testing in patients with typical amyotrophic lateral sclerosis; relapsing remitting multiple sclerosis; Parkinson’s disease, dementia, or cognitive decline; new-onset seizures; other neurologic syndromes or those lacking clinical or epidemiologic history that would support a diagnosis of Lyme disease; and patients with chronic cardiomyopathy of unknown cause.

The authors also called for judicious use of electrocardiogram to screen for Lyme carditis, recommending it only in patients signs or symptoms of this condition. However, patients at risk for or showing signs of severe cardiac complications of Lyme disease should be hospitalized and monitored via ECG.

Timelines for antibiotics

Most patients with Lyme disease should receive oral antibiotics, although duration times vary depending on the disease state. “We recommend that prophylactic antibiotic therapy be given to adults and children only within 72 hours of removal of an identified high-risk tick bite, but not for bites that are equivocal risk or low risk,” according to the guideline authors.

Specific antibiotic treatment regimens by condition are as follows: 10-14 days for early-stage disease, 14 days for Lyme carditis, 14-21 days for neurologic Lyme disease, and 28 days for late Lyme arthritis.

“Despite arthritis occurring late in the course of infection, treatment with a 28-day course of oral antibiotic is effective, although the rates of complete resolution of joint swelling can vary,” Dr. Bockenstedt said. Clinicians may consider a second 28-day course of oral antibiotics or a 2- to 4-week course of ceftriaxone in patients with persistent swelling, after an initial course of oral antibiotics.

Citing knowledge gaps, the authors made no recommendation on secondary antibiotic treatment for unresolved Lyme arthritis. Rheumatologists can play an important role in the care of this small subset of patients, Dr. Bockenstedt noted. “Studies of patients with ‘postantibiotic Lyme arthritis’ show that they can be treated successfully with intra-articular steroids, nonsteroidal anti-inflammatory drugs, disease-modifying antirheumatic drugs, biologic response modifiers, and even synovectomy with successful outcomes.” Some of these therapies also work in cases where first courses of oral and intravenous antibiotics are unsuccessful.

“Antibiotic therapy for longer than 8 weeks is not expected to provide additional benefit to patients with persistent arthritis if that treatment has included one course of IV therapy,” the authors clarified.

For patients with Lyme disease–associated meningitis, cranial neuropathy, radiculoneuropathy, or other PNS manifestations, the authors recommended intravenous ceftriaxone, cefotaxime, penicillin G, or oral doxycycline over other antimicrobials.

“For most neurologic presentations, oral doxycycline is just as effective as appropriate IV antibiotics,” Dr. Rumbaugh said. “The exception is the relatively rare situation where the patient is felt to have parenchymal involvement of brain or spinal cord, in which case the guidelines recommend IV antibiotics over oral antibiotics.” In the studies, there was no statistically significant difference between oral or intravenous regimens in response rate or risk of adverse effects.

Patients with nonspecific symptoms such as fatigue, pain, or cognitive impairment following treatment should not receive additional antibiotic therapy if there’s no evidence of treatment failure or infection. These two markers “would include objective signs of disease activity, such as arthritis, meningitis, or neuropathy,” the guideline authors wrote in comments accompanying the recommendation.

Clinicians caring for patients with symptomatic bradycardia caused by Lyme carditis should consider temporary pacing measures instead of a permanent pacemaker. For patients hospitalized with Lyme carditis, “we suggest initially using IV ceftriaxone over oral antibiotics until there is evidence of clinical improvement, then switching to oral antibiotics to complete treatment,” they advised. Outpatients with this condition should receive oral antibiotics instead of intravenous antibiotics.

Advice on antibodies testing ‘particularly cogent’

For individuals without expertise in these areas, the recommendations are clear and useful, Daniel E. Furst, MD, professor of medicine (emeritus) at the University of California, Los Angeles, adjunct professor at the University of Washington, Seattle, and research professor at the University of Florence (Italy), said in an interview.

“As a rheumatologist, I would have appreciated literature references for some of the recommendations but, nevertheless, find these useful. I applaud the care with which the evidence was gathered and the general formatting, which tried to review multiple possible scenarios surrounding Lyme arthritis,” said Dr. Furst, offering a third-party perspective.

The advice on using antibodies tests to make a diagnosis of Lyme arthritis “is particularly cogent and more useful than trying to culture these fastidious organisms,” he added.

The IDSA, AAN, and ACR provided support for the guideline. Dr. Bockenstedt reported receiving research funding from the National Institutes of Health and the Gordon and the Llura Gund Foundation and remuneration from L2 Diagnostics for investigator-initiated NIH-sponsored research. Dr. Rumbaugh had no conflicts of interest to disclose. Dr. Furst reported no conflicts of interest in commenting on these guidelines.

SOURCE: Rumbaugh JA et al. Clin Infect Dis. 2020 Nov 30. doi: 10.1093/cid/ciaa1215.

New clinical practice guidelines on Lyme disease place a strong emphasis on antibody testing to assess for rheumatologic and neurologic syndromes. “Diagnostically, we recommend testing via antibodies, and an index of antibodies in cerebrospinal fluid [CSF] versus serum. Importantly, we recommend against using polymerase chain reaction [PCR] in CSF,” Jeffrey A. Rumbaugh, MD, PhD, a coauthor of the guidelines and a member of the American Academy of Neurology, said in an interview.

CDC/ Dr. Amanda Loftis, Dr. William Nicholson, Dr. Will Reeves, Dr. Chris Paddock

The Infectious Diseases Society of America, AAN, and the American College of Rheumatology convened a multidisciplinary panel to develop the 43 recommendations, seeking input from 12 additional medical specialties, and patients. The panel conducted a systematic review of available evidence on preventing, diagnosing, and treating Lyme disease, using the Grading of Recommendations Assessment, Development and Evaluation model to evaluate clinical evidence and strength of recommendations. The guidelines were simultaneous published in Clinical Infectious Diseases, Neurology, Arthritis & Rheumatology, and Arthritis Care & Research.

This is the first time these organizations have collaborated on joint Lyme disease guidelines, which focus mainly on neurologic, cardiac, and rheumatologic manifestations.

“We are very excited to provide these updated guidelines to assist clinicians working in numerous medical specialties around the country, and even the world, as they care for patients suffering from Lyme disease,” Dr. Rumbaugh said.
 

When to use and not to use PCR

Guideline authors called for specific testing regimens depending on presentation of symptoms. Generally, they advised that individuals with a skin rash suggestive of early disease seek a clinical diagnosis instead of laboratory testing.

Recommendations on Lyme arthritis support previous IDSA guidelines published in 2006, Linda K. Bockenstedt, MD, professor of medicine at Yale University, New Haven, Conn., and a coauthor of the guidelines, said in an interview.

To evaluate for potential Lyme arthritis, clinicians should choose serum antibody testing over PCR or culture of blood or synovial fluid/tissue. However, if a doctor is assessing a seropositive patient for Lyme arthritis diagnosis but needs more information for treatment decisions, the authors recommended PCR applied to synovial fluid or tissue over Borrelia culture.

“Synovial fluid can be analyzed by PCR, but sensitivity is generally lower than serology,” Dr. Bockenstedt explained. Additionally, culture of joint fluid or synovial tissue for Lyme spirochetes has 0% sensitivity in multiple studies. “For these reasons, we recommend serum antibody testing over PCR of joint fluid or other methods for an initial diagnosis.”

Serum antibody testing over PCR or culture is also recommended for identifying Lyme neuroborreliosis in the peripheral nervous system (PNS) or CNS.

Despite the recent popularity of Lyme PCR testing in hospitals and labs, “with Lyme at least, antibodies are better in the CSF,” Dr. Rumbaugh said. Studies have shown that “most patients with even early neurologic Lyme disease are seropositive by conventional antibody testing at time of initial clinical presentation, and that intrathecal antibody production, as demonstrated by an elevated CSF:serum index, is highly specific for CNS involvement.”

If done correctly, antibody testing is both sensitive and specific for neurologic Lyme disease. “On the other hand, sensitivity of Lyme PCR performed on CSF has been only in the 5%-17% range in studies. Incidentally, Lyme PCR on blood is also not sensitive and therefore not recommended,” Dr. Rumbaugh said.

Guideline authors recommended testing in patients with the following conditions: acute neurologic disorders such as meningitis, painful radiculoneuritis, mononeuropathy multiplex; evidence of spinal cord or brain inflammation; and acute myocarditis/pericarditis of unknown cause in an appropriate epidemiologic setting.

They did not recommend testing in patients with typical amyotrophic lateral sclerosis; relapsing remitting multiple sclerosis; Parkinson’s disease, dementia, or cognitive decline; new-onset seizures; other neurologic syndromes or those lacking clinical or epidemiologic history that would support a diagnosis of Lyme disease; and patients with chronic cardiomyopathy of unknown cause.

The authors also called for judicious use of electrocardiogram to screen for Lyme carditis, recommending it only in patients signs or symptoms of this condition. However, patients at risk for or showing signs of severe cardiac complications of Lyme disease should be hospitalized and monitored via ECG.

Timelines for antibiotics

Most patients with Lyme disease should receive oral antibiotics, although duration times vary depending on the disease state. “We recommend that prophylactic antibiotic therapy be given to adults and children only within 72 hours of removal of an identified high-risk tick bite, but not for bites that are equivocal risk or low risk,” according to the guideline authors.

Specific antibiotic treatment regimens by condition are as follows: 10-14 days for early-stage disease, 14 days for Lyme carditis, 14-21 days for neurologic Lyme disease, and 28 days for late Lyme arthritis.

“Despite arthritis occurring late in the course of infection, treatment with a 28-day course of oral antibiotic is effective, although the rates of complete resolution of joint swelling can vary,” Dr. Bockenstedt said. Clinicians may consider a second 28-day course of oral antibiotics or a 2- to 4-week course of ceftriaxone in patients with persistent swelling, after an initial course of oral antibiotics.

Citing knowledge gaps, the authors made no recommendation on secondary antibiotic treatment for unresolved Lyme arthritis. Rheumatologists can play an important role in the care of this small subset of patients, Dr. Bockenstedt noted. “Studies of patients with ‘postantibiotic Lyme arthritis’ show that they can be treated successfully with intra-articular steroids, nonsteroidal anti-inflammatory drugs, disease-modifying antirheumatic drugs, biologic response modifiers, and even synovectomy with successful outcomes.” Some of these therapies also work in cases where first courses of oral and intravenous antibiotics are unsuccessful.

“Antibiotic therapy for longer than 8 weeks is not expected to provide additional benefit to patients with persistent arthritis if that treatment has included one course of IV therapy,” the authors clarified.

For patients with Lyme disease–associated meningitis, cranial neuropathy, radiculoneuropathy, or other PNS manifestations, the authors recommended intravenous ceftriaxone, cefotaxime, penicillin G, or oral doxycycline over other antimicrobials.

“For most neurologic presentations, oral doxycycline is just as effective as appropriate IV antibiotics,” Dr. Rumbaugh said. “The exception is the relatively rare situation where the patient is felt to have parenchymal involvement of brain or spinal cord, in which case the guidelines recommend IV antibiotics over oral antibiotics.” In the studies, there was no statistically significant difference between oral or intravenous regimens in response rate or risk of adverse effects.

Patients with nonspecific symptoms such as fatigue, pain, or cognitive impairment following treatment should not receive additional antibiotic therapy if there’s no evidence of treatment failure or infection. These two markers “would include objective signs of disease activity, such as arthritis, meningitis, or neuropathy,” the guideline authors wrote in comments accompanying the recommendation.

Clinicians caring for patients with symptomatic bradycardia caused by Lyme carditis should consider temporary pacing measures instead of a permanent pacemaker. For patients hospitalized with Lyme carditis, “we suggest initially using IV ceftriaxone over oral antibiotics until there is evidence of clinical improvement, then switching to oral antibiotics to complete treatment,” they advised. Outpatients with this condition should receive oral antibiotics instead of intravenous antibiotics.

Advice on antibodies testing ‘particularly cogent’

For individuals without expertise in these areas, the recommendations are clear and useful, Daniel E. Furst, MD, professor of medicine (emeritus) at the University of California, Los Angeles, adjunct professor at the University of Washington, Seattle, and research professor at the University of Florence (Italy), said in an interview.

“As a rheumatologist, I would have appreciated literature references for some of the recommendations but, nevertheless, find these useful. I applaud the care with which the evidence was gathered and the general formatting, which tried to review multiple possible scenarios surrounding Lyme arthritis,” said Dr. Furst, offering a third-party perspective.

The advice on using antibodies tests to make a diagnosis of Lyme arthritis “is particularly cogent and more useful than trying to culture these fastidious organisms,” he added.

The IDSA, AAN, and ACR provided support for the guideline. Dr. Bockenstedt reported receiving research funding from the National Institutes of Health and the Gordon and the Llura Gund Foundation and remuneration from L2 Diagnostics for investigator-initiated NIH-sponsored research. Dr. Rumbaugh had no conflicts of interest to disclose. Dr. Furst reported no conflicts of interest in commenting on these guidelines.

SOURCE: Rumbaugh JA et al. Clin Infect Dis. 2020 Nov 30. doi: 10.1093/cid/ciaa1215.

New clinical practice guidelines on Lyme disease place a strong emphasis on antibody testing to assess for rheumatologic and neurologic syndromes. “Diagnostically, we recommend testing via antibodies, and an index of antibodies in cerebrospinal fluid [CSF] versus serum. Importantly, we recommend against using polymerase chain reaction [PCR] in CSF,” Jeffrey A. Rumbaugh, MD, PhD, a coauthor of the guidelines and a member of the American Academy of Neurology, said in an interview.

CDC/ Dr. Amanda Loftis, Dr. William Nicholson, Dr. Will Reeves, Dr. Chris Paddock

The Infectious Diseases Society of America, AAN, and the American College of Rheumatology convened a multidisciplinary panel to develop the 43 recommendations, seeking input from 12 additional medical specialties, and patients. The panel conducted a systematic review of available evidence on preventing, diagnosing, and treating Lyme disease, using the Grading of Recommendations Assessment, Development and Evaluation model to evaluate clinical evidence and strength of recommendations. The guidelines were simultaneous published in Clinical Infectious Diseases, Neurology, Arthritis & Rheumatology, and Arthritis Care & Research.

This is the first time these organizations have collaborated on joint Lyme disease guidelines, which focus mainly on neurologic, cardiac, and rheumatologic manifestations.

“We are very excited to provide these updated guidelines to assist clinicians working in numerous medical specialties around the country, and even the world, as they care for patients suffering from Lyme disease,” Dr. Rumbaugh said.
 

When to use and not to use PCR

Guideline authors called for specific testing regimens depending on presentation of symptoms. Generally, they advised that individuals with a skin rash suggestive of early disease seek a clinical diagnosis instead of laboratory testing.

Recommendations on Lyme arthritis support previous IDSA guidelines published in 2006, Linda K. Bockenstedt, MD, professor of medicine at Yale University, New Haven, Conn., and a coauthor of the guidelines, said in an interview.

To evaluate for potential Lyme arthritis, clinicians should choose serum antibody testing over PCR or culture of blood or synovial fluid/tissue. However, if a doctor is assessing a seropositive patient for Lyme arthritis diagnosis but needs more information for treatment decisions, the authors recommended PCR applied to synovial fluid or tissue over Borrelia culture.

“Synovial fluid can be analyzed by PCR, but sensitivity is generally lower than serology,” Dr. Bockenstedt explained. Additionally, culture of joint fluid or synovial tissue for Lyme spirochetes has 0% sensitivity in multiple studies. “For these reasons, we recommend serum antibody testing over PCR of joint fluid or other methods for an initial diagnosis.”

Serum antibody testing over PCR or culture is also recommended for identifying Lyme neuroborreliosis in the peripheral nervous system (PNS) or CNS.

Despite the recent popularity of Lyme PCR testing in hospitals and labs, “with Lyme at least, antibodies are better in the CSF,” Dr. Rumbaugh said. Studies have shown that “most patients with even early neurologic Lyme disease are seropositive by conventional antibody testing at time of initial clinical presentation, and that intrathecal antibody production, as demonstrated by an elevated CSF:serum index, is highly specific for CNS involvement.”

If done correctly, antibody testing is both sensitive and specific for neurologic Lyme disease. “On the other hand, sensitivity of Lyme PCR performed on CSF has been only in the 5%-17% range in studies. Incidentally, Lyme PCR on blood is also not sensitive and therefore not recommended,” Dr. Rumbaugh said.

Guideline authors recommended testing in patients with the following conditions: acute neurologic disorders such as meningitis, painful radiculoneuritis, mononeuropathy multiplex; evidence of spinal cord or brain inflammation; and acute myocarditis/pericarditis of unknown cause in an appropriate epidemiologic setting.

They did not recommend testing in patients with typical amyotrophic lateral sclerosis; relapsing remitting multiple sclerosis; Parkinson’s disease, dementia, or cognitive decline; new-onset seizures; other neurologic syndromes or those lacking clinical or epidemiologic history that would support a diagnosis of Lyme disease; and patients with chronic cardiomyopathy of unknown cause.

The authors also called for judicious use of electrocardiogram to screen for Lyme carditis, recommending it only in patients signs or symptoms of this condition. However, patients at risk for or showing signs of severe cardiac complications of Lyme disease should be hospitalized and monitored via ECG.

Timelines for antibiotics

Most patients with Lyme disease should receive oral antibiotics, although duration times vary depending on the disease state. “We recommend that prophylactic antibiotic therapy be given to adults and children only within 72 hours of removal of an identified high-risk tick bite, but not for bites that are equivocal risk or low risk,” according to the guideline authors.

Specific antibiotic treatment regimens by condition are as follows: 10-14 days for early-stage disease, 14 days for Lyme carditis, 14-21 days for neurologic Lyme disease, and 28 days for late Lyme arthritis.

“Despite arthritis occurring late in the course of infection, treatment with a 28-day course of oral antibiotic is effective, although the rates of complete resolution of joint swelling can vary,” Dr. Bockenstedt said. Clinicians may consider a second 28-day course of oral antibiotics or a 2- to 4-week course of ceftriaxone in patients with persistent swelling, after an initial course of oral antibiotics.

Citing knowledge gaps, the authors made no recommendation on secondary antibiotic treatment for unresolved Lyme arthritis. Rheumatologists can play an important role in the care of this small subset of patients, Dr. Bockenstedt noted. “Studies of patients with ‘postantibiotic Lyme arthritis’ show that they can be treated successfully with intra-articular steroids, nonsteroidal anti-inflammatory drugs, disease-modifying antirheumatic drugs, biologic response modifiers, and even synovectomy with successful outcomes.” Some of these therapies also work in cases where first courses of oral and intravenous antibiotics are unsuccessful.

“Antibiotic therapy for longer than 8 weeks is not expected to provide additional benefit to patients with persistent arthritis if that treatment has included one course of IV therapy,” the authors clarified.

For patients with Lyme disease–associated meningitis, cranial neuropathy, radiculoneuropathy, or other PNS manifestations, the authors recommended intravenous ceftriaxone, cefotaxime, penicillin G, or oral doxycycline over other antimicrobials.

“For most neurologic presentations, oral doxycycline is just as effective as appropriate IV antibiotics,” Dr. Rumbaugh said. “The exception is the relatively rare situation where the patient is felt to have parenchymal involvement of brain or spinal cord, in which case the guidelines recommend IV antibiotics over oral antibiotics.” In the studies, there was no statistically significant difference between oral or intravenous regimens in response rate or risk of adverse effects.

Patients with nonspecific symptoms such as fatigue, pain, or cognitive impairment following treatment should not receive additional antibiotic therapy if there’s no evidence of treatment failure or infection. These two markers “would include objective signs of disease activity, such as arthritis, meningitis, or neuropathy,” the guideline authors wrote in comments accompanying the recommendation.

Clinicians caring for patients with symptomatic bradycardia caused by Lyme carditis should consider temporary pacing measures instead of a permanent pacemaker. For patients hospitalized with Lyme carditis, “we suggest initially using IV ceftriaxone over oral antibiotics until there is evidence of clinical improvement, then switching to oral antibiotics to complete treatment,” they advised. Outpatients with this condition should receive oral antibiotics instead of intravenous antibiotics.

Advice on antibodies testing ‘particularly cogent’

For individuals without expertise in these areas, the recommendations are clear and useful, Daniel E. Furst, MD, professor of medicine (emeritus) at the University of California, Los Angeles, adjunct professor at the University of Washington, Seattle, and research professor at the University of Florence (Italy), said in an interview.

“As a rheumatologist, I would have appreciated literature references for some of the recommendations but, nevertheless, find these useful. I applaud the care with which the evidence was gathered and the general formatting, which tried to review multiple possible scenarios surrounding Lyme arthritis,” said Dr. Furst, offering a third-party perspective.

The advice on using antibodies tests to make a diagnosis of Lyme arthritis “is particularly cogent and more useful than trying to culture these fastidious organisms,” he added.

The IDSA, AAN, and ACR provided support for the guideline. Dr. Bockenstedt reported receiving research funding from the National Institutes of Health and the Gordon and the Llura Gund Foundation and remuneration from L2 Diagnostics for investigator-initiated NIH-sponsored research. Dr. Rumbaugh had no conflicts of interest to disclose. Dr. Furst reported no conflicts of interest in commenting on these guidelines.

SOURCE: Rumbaugh JA et al. Clin Infect Dis. 2020 Nov 30. doi: 10.1093/cid/ciaa1215.

Electro-acupuncture resulted in significant improvement in pain and function, compared with sham acupuncture, in a randomized trial of more than 400 adults with knee OA.

The socioeconomic burden of knee OA (KOA) remains high, and will likely increase with the aging population and rising rates of obesity, wrote first author Jian-Feng Tu, MD, PhD, of Beijing University of Chinese Medicine and colleagues. “Since no disease-modifying pharmaceutical agents have been approved, current KOA treatments are mainly symptomatic,” and identifying new therapies in addition to pharmacological agents or surgery is a research priority, they added. The research on acupuncture as a treatment for KOA has increased, but remains controversial as researchers attempt to determine the number of sessions needed for effectiveness.

In a study published in Arthritis & Rheumatology, the researchers recruited 480 adults aged 45-75 years with confirmed KOA who reported knee pain for longer than 6 months. Participants were randomized to three groups: electroacupuncture (EA), manual acupuncture (MA), or sham acupuncture (SA). Each group received three treatment sessions per week. In all groups, electrodes were attached to selected acupuncture needles, but the current was turned on only in the EA treatment group.

The primary outcome was the response rate after 8 weeks of treatment, defined as patients who achieved the minimal clinically important improvement (MCII) on both the Numeric Rating Scale and the Western Ontario and McMaster Universities Osteoarthritis Index function subscale.

Overall, response rates at 8 weeks were 60.3%, 58.6%, and 47.3% for the EA, MA, and SA groups, respectively.

Between-group differences were statistically significant for EA versus SA (13%, P = .0234) but not for MA versus SA (11.3%, P = .0507) at 8 weeks; however, both EA and MA groups showed significantly higher response rates, compared with the SA group at 16 and 26 weeks. “Although a clinically meaningful response rate for KOA is not available in the literature, the difference of 11.3%, which indicates the number needed to treat of 9, is acceptable in clinical practices,” the researchers noted.

Adverse events occurred in 11.5% of the EA group, 14.2% of the MA group, and 10.8% of the SA group, and included subcutaneous hematoma, post-needling pain, and pantalgia. All adverse events related to acupuncture resolved within a week and none were serious, the researchers wrote.

The study findings were limited by several factors, including the potential burden on patients of three sessions per week, the limited study population of patients with radiologic grades of II or III only, the use of self-reports, and the lack of blinding for outcome assessors, the researchers noted.

However, the results show persistent effects in reducing pain and improving function with EA or MA, compared with SA, the researchers wrote. The findings were strengthened by “adequate dosage of acupuncture, the use of the primary outcome at an individual level, and the rigorous methodology.” The use of the MCII in the primary outcome “can provide patients and policy makers with more straightforward information to decide whether a treatment should be used.”

Optimal dosing questions remain

Current options for managing KOA are limited by factors that include low efficacy and unwanted side effects, while joint replacements increase the burden on health care systems, wrote David J. Hunter, MBBS, PhD, of the University of Sydney, and Richard E. Harris, PhD, of the University of Michigan, Ann Arbor, in an accompanying editorial. “In this context, development of new treatments or identification of efficacy of existing therapies to address the huge unmet need of pain are strongly desired.” Acupuncture continues to gain popularity in North and South America, but its efficacy for pain and KOA remain controversial.

The question of dose is challenging when assessing acupuncture because the optimal dose and how to classify it remains unknown. “In this study, the authors used three treatments a week, which is more frequent than typical studies done in the West and potentially may not be feasible in some health care settings. A recent systematic review suggests that treatment frequency matters and a dose of three sessions per week may be superior to less frequent treatment,” they emphasized. Acupuncture is generally considered to be safe, but many health systems do not reimburse for it. Patients may have large out-of-pocket expenses because of the number of visits required, which may be a barrier to further implementation in practice.

“Acupuncture is already widely practiced and readily available in many countries and health care systems,” the editorialists said. However, “more research is needed in the areas of dose-response relationships, effects of blinding the acupuncturist, feasibility of three times weekly regimens, and clarifying the mechanism of effect, particularly given the persistence of benefit.”

The study was funded by Beijing Municipal Science & Technology Commission and Beijing Municipal Administration of Hospitals. The researchers had no financial conflicts to disclose. Dr. Hunter disclosed support from a National Health and Medical Research Council Investigator Grant and providing consulting advice for Merck Serono, TLC Bio, Tissuegene, Lilly, and Pfizer.

SOURCE: Tu J-F et al. Arthritis Rheumatol. 2020 Nov 10. doi: 10.1002/art.41584.

Electro-acupuncture resulted in significant improvement in pain and function, compared with sham acupuncture, in a randomized trial of more than 400 adults with knee OA.

The socioeconomic burden of knee OA (KOA) remains high, and will likely increase with the aging population and rising rates of obesity, wrote first author Jian-Feng Tu, MD, PhD, of Beijing University of Chinese Medicine and colleagues. “Since no disease-modifying pharmaceutical agents have been approved, current KOA treatments are mainly symptomatic,” and identifying new therapies in addition to pharmacological agents or surgery is a research priority, they added. The research on acupuncture as a treatment for KOA has increased, but remains controversial as researchers attempt to determine the number of sessions needed for effectiveness.

In a study published in Arthritis & Rheumatology, the researchers recruited 480 adults aged 45-75 years with confirmed KOA who reported knee pain for longer than 6 months. Participants were randomized to three groups: electroacupuncture (EA), manual acupuncture (MA), or sham acupuncture (SA). Each group received three treatment sessions per week. In all groups, electrodes were attached to selected acupuncture needles, but the current was turned on only in the EA treatment group.

The primary outcome was the response rate after 8 weeks of treatment, defined as patients who achieved the minimal clinically important improvement (MCII) on both the Numeric Rating Scale and the Western Ontario and McMaster Universities Osteoarthritis Index function subscale.

Overall, response rates at 8 weeks were 60.3%, 58.6%, and 47.3% for the EA, MA, and SA groups, respectively.

Between-group differences were statistically significant for EA versus SA (13%, P = .0234) but not for MA versus SA (11.3%, P = .0507) at 8 weeks; however, both EA and MA groups showed significantly higher response rates, compared with the SA group at 16 and 26 weeks. “Although a clinically meaningful response rate for KOA is not available in the literature, the difference of 11.3%, which indicates the number needed to treat of 9, is acceptable in clinical practices,” the researchers noted.

Adverse events occurred in 11.5% of the EA group, 14.2% of the MA group, and 10.8% of the SA group, and included subcutaneous hematoma, post-needling pain, and pantalgia. All adverse events related to acupuncture resolved within a week and none were serious, the researchers wrote.

The study findings were limited by several factors, including the potential burden on patients of three sessions per week, the limited study population of patients with radiologic grades of II or III only, the use of self-reports, and the lack of blinding for outcome assessors, the researchers noted.

However, the results show persistent effects in reducing pain and improving function with EA or MA, compared with SA, the researchers wrote. The findings were strengthened by “adequate dosage of acupuncture, the use of the primary outcome at an individual level, and the rigorous methodology.” The use of the MCII in the primary outcome “can provide patients and policy makers with more straightforward information to decide whether a treatment should be used.”

Optimal dosing questions remain

Current options for managing KOA are limited by factors that include low efficacy and unwanted side effects, while joint replacements increase the burden on health care systems, wrote David J. Hunter, MBBS, PhD, of the University of Sydney, and Richard E. Harris, PhD, of the University of Michigan, Ann Arbor, in an accompanying editorial. “In this context, development of new treatments or identification of efficacy of existing therapies to address the huge unmet need of pain are strongly desired.” Acupuncture continues to gain popularity in North and South America, but its efficacy for pain and KOA remain controversial.

The question of dose is challenging when assessing acupuncture because the optimal dose and how to classify it remains unknown. “In this study, the authors used three treatments a week, which is more frequent than typical studies done in the West and potentially may not be feasible in some health care settings. A recent systematic review suggests that treatment frequency matters and a dose of three sessions per week may be superior to less frequent treatment,” they emphasized. Acupuncture is generally considered to be safe, but many health systems do not reimburse for it. Patients may have large out-of-pocket expenses because of the number of visits required, which may be a barrier to further implementation in practice.

“Acupuncture is already widely practiced and readily available in many countries and health care systems,” the editorialists said. However, “more research is needed in the areas of dose-response relationships, effects of blinding the acupuncturist, feasibility of three times weekly regimens, and clarifying the mechanism of effect, particularly given the persistence of benefit.”

The study was funded by Beijing Municipal Science & Technology Commission and Beijing Municipal Administration of Hospitals. The researchers had no financial conflicts to disclose. Dr. Hunter disclosed support from a National Health and Medical Research Council Investigator Grant and providing consulting advice for Merck Serono, TLC Bio, Tissuegene, Lilly, and Pfizer.

SOURCE: Tu J-F et al. Arthritis Rheumatol. 2020 Nov 10. doi: 10.1002/art.41584.

Electro-acupuncture resulted in significant improvement in pain and function, compared with sham acupuncture, in a randomized trial of more than 400 adults with knee OA.

The socioeconomic burden of knee OA (KOA) remains high, and will likely increase with the aging population and rising rates of obesity, wrote first author Jian-Feng Tu, MD, PhD, of Beijing University of Chinese Medicine and colleagues. “Since no disease-modifying pharmaceutical agents have been approved, current KOA treatments are mainly symptomatic,” and identifying new therapies in addition to pharmacological agents or surgery is a research priority, they added. The research on acupuncture as a treatment for KOA has increased, but remains controversial as researchers attempt to determine the number of sessions needed for effectiveness.

In a study published in Arthritis & Rheumatology, the researchers recruited 480 adults aged 45-75 years with confirmed KOA who reported knee pain for longer than 6 months. Participants were randomized to three groups: electroacupuncture (EA), manual acupuncture (MA), or sham acupuncture (SA). Each group received three treatment sessions per week. In all groups, electrodes were attached to selected acupuncture needles, but the current was turned on only in the EA treatment group.

The primary outcome was the response rate after 8 weeks of treatment, defined as patients who achieved the minimal clinically important improvement (MCII) on both the Numeric Rating Scale and the Western Ontario and McMaster Universities Osteoarthritis Index function subscale.

Overall, response rates at 8 weeks were 60.3%, 58.6%, and 47.3% for the EA, MA, and SA groups, respectively.

Between-group differences were statistically significant for EA versus SA (13%, P = .0234) but not for MA versus SA (11.3%, P = .0507) at 8 weeks; however, both EA and MA groups showed significantly higher response rates, compared with the SA group at 16 and 26 weeks. “Although a clinically meaningful response rate for KOA is not available in the literature, the difference of 11.3%, which indicates the number needed to treat of 9, is acceptable in clinical practices,” the researchers noted.

Adverse events occurred in 11.5% of the EA group, 14.2% of the MA group, and 10.8% of the SA group, and included subcutaneous hematoma, post-needling pain, and pantalgia. All adverse events related to acupuncture resolved within a week and none were serious, the researchers wrote.

The study findings were limited by several factors, including the potential burden on patients of three sessions per week, the limited study population of patients with radiologic grades of II or III only, the use of self-reports, and the lack of blinding for outcome assessors, the researchers noted.

However, the results show persistent effects in reducing pain and improving function with EA or MA, compared with SA, the researchers wrote. The findings were strengthened by “adequate dosage of acupuncture, the use of the primary outcome at an individual level, and the rigorous methodology.” The use of the MCII in the primary outcome “can provide patients and policy makers with more straightforward information to decide whether a treatment should be used.”

Optimal dosing questions remain

Current options for managing KOA are limited by factors that include low efficacy and unwanted side effects, while joint replacements increase the burden on health care systems, wrote David J. Hunter, MBBS, PhD, of the University of Sydney, and Richard E. Harris, PhD, of the University of Michigan, Ann Arbor, in an accompanying editorial. “In this context, development of new treatments or identification of efficacy of existing therapies to address the huge unmet need of pain are strongly desired.” Acupuncture continues to gain popularity in North and South America, but its efficacy for pain and KOA remain controversial.

The question of dose is challenging when assessing acupuncture because the optimal dose and how to classify it remains unknown. “In this study, the authors used three treatments a week, which is more frequent than typical studies done in the West and potentially may not be feasible in some health care settings. A recent systematic review suggests that treatment frequency matters and a dose of three sessions per week may be superior to less frequent treatment,” they emphasized. Acupuncture is generally considered to be safe, but many health systems do not reimburse for it. Patients may have large out-of-pocket expenses because of the number of visits required, which may be a barrier to further implementation in practice.

“Acupuncture is already widely practiced and readily available in many countries and health care systems,” the editorialists said. However, “more research is needed in the areas of dose-response relationships, effects of blinding the acupuncturist, feasibility of three times weekly regimens, and clarifying the mechanism of effect, particularly given the persistence of benefit.”

The study was funded by Beijing Municipal Science & Technology Commission and Beijing Municipal Administration of Hospitals. The researchers had no financial conflicts to disclose. Dr. Hunter disclosed support from a National Health and Medical Research Council Investigator Grant and providing consulting advice for Merck Serono, TLC Bio, Tissuegene, Lilly, and Pfizer.

SOURCE: Tu J-F et al. Arthritis Rheumatol. 2020 Nov 10. doi: 10.1002/art.41584.

Study Overview

Objective. To examine whether discontinuation of nonsteroidal anti-inflammatory drug (NSAID) therapy and initiation of telephone-based cognitive behavioral therapy (CBT) is not worse than continuation of NSAIDs in the management of arthritis pain.

Design. Randomized controlled trial with noninferiority design.

Setting and participants. This study was a multicenter trial conducted across 4 Veterans Affairs health care systems in Boston, Providence, Connecticut, and North Florida/South Georgia that started September 2013 and ended September 2018. Eligibility criteria included being age 20 years or older, radiographic evidence of knee osteoarthritis, and use of an NSAID for knee pain on most days of the month for at least the past 3 months. Exclusion criteria included significant hearing impairments that may impede the conduct of the trial, current opioid prescriptions excluding tramadol, contraindications to NSAID use, recent or scheduled intra-articular injections or surgery, comorbid conditions other than knee pain that limited walking, and bilateral knee replacements or pain only in the replaced knee. Concurrent use of tramadol and other non-NSAID analgesics was permitted.

A total of 490 participants took part in the 2-week run-in period where their NSAID regimen was discontinued and they were started on a standardized dose of the NSAID meloxicam 15 mg daily. During the run-in period, 126 participants were excluded for several reasons, including worsening pain and patient withdrawal, yielding 364 participants who were randomized to continue meloxicam treatment or placebo for 4 weeks with blinding.

Intervention. Subsequent to the 4-week phase 1 placebo controlled trial, participants in the placebo group were given CBT via telephone (unblinded) for 10 weeks, and the meloxicam group continued treatment with meloxicam for phase 2. The CBT group received 10 modules over 10 weeks in 30- to 45-minute telephone contacts with a psychologist using a treatment manual modified for knee osteoarthritis. These modules consisted of 1 introductory module, 8 pain coping skills modules (eg, deep breathing and visual imagery, progressive muscle relaxation, physical activity and bodily mechanics, identifying unhealthy thoughts, balancing unhealthy thoughts, managing stress, time-based pacing, and sleep hygiene), and a final module emphasizing skill consolidation and relapse prevention. Outcomes were assessed at the end of the phase 1 and phase 2 periods.

Main outcome measures. Main study outcome measures included pain as measured with the Western Ontario and McMaster Universities Osteoarthritis Index (WOMAC) at 4 weeks. Secondary outcomes included the WOMAC pain score, disability score, and global impression of change after treatment at 14 weeks. The WOMAC pain scale ranges from 0 to 20, and consists of 5 questions regarding severity of pain during walking, stair use, lying in bed at night, sitting, and standing, with 0 indicating no pain; 1, mild pain; 2, moderate pain; 3, severe pain; and 4, very severe pain for each item. The WOMAC disability scale measures self-reported difficulty in performing tasks that reflect lower-extremity physical function, including climbing stairs, rising from a chair, walking, and other activities of daily living. The global impression of change after treatment was measured on a 5-point scale (where 1 indicates much better and 5 indicates much worse). The minimum clinically important difference of the WOMAC pain scale is 2, based on prior literature. With the noninferiority design, the margin was set as a score of 1.

Main results. The placebo group consisted of 180 participants, with an average age of 58.2 years (SD, 11.8 years); 89% of them were male. The meloxicam group consisted of 184 participants, with an average age of 58.6 years (SD, 10 years); 84% of them were male. The average body mass index was 33.9 and 33.4 in each group, respectively. For the primary outcome, the placebo group had a worse pain score than the meloxicam group at 4 weeks (difference of 1.4; 95% confidence interval, 0.8- 2.0). At 14 weeks, the placebo group (with CBT) had a worse pain score than the meloxicam group (difference of 0.8; 95% CI, 0.2-1.4). There was no statistically significant difference in the disability score or global impression of change after treatment score between the 2 groups. The observed difference in pain score did not, however, exceed the minimum clinically important difference.

Conclusion. Placebo treatment and CBT are inferior to NSAIDs in managing pain for patients with knee osteoarthritis. The difference in pain may not be clinically important, and there were no differences in function at 14 weeks.

Commentary

Osteoarthritis is a common chronic condition that causes pain and disability and is often treated with oral analgesics. NSAIDs, despite few high-quality trials demonstrating their efficacy, are among the most commonly used treatment for osteoarthritis pain.¹ NSAID therapy, however, does have potential side effects, such as gastric reflux and renal dysfunction.² This withdrawal trial with placebo control contributes further evidence of the effectiveness of NSAIDs on knee osteoarthritis, demonstrating that indeed NSAIDs improve pain scores to a greater degree than placebo treatment. Augmenting placebo treatment with nonpharmacologic CBT was inferior to NSAIDs in pain management. The authors pointed out that the difference in pain score may not be clinically important, and that lower-extremity function was not different between the groups, concluding that, despite the higher pain score, CBT could be a treatment option, particularly for those who may have difficulty tolerating NSAID treatment.

The study population had a number of chronic conditions in addition to having knee arthritis, and thus likely were taking multiple medications for chronic disease management. Use of multiple medications is associated with an increased risk of rug interactions and adverse effects of medications.³ Thus, this attempt to assess whether a nonpharmacologic alternative treatment is noninferior to a drug treatment is a step toward building the evidence base for deprescribing and enhancing medication safety.⁴ Previous studies have examined other nonpharmacologic treatments for knee arthritis, such as acupuncture,⁵ and it is worthwhile to consider combining nonpharmacological approaches as an alternative to oral analgesic medication use.

Applications for Clinical Practice

This study advances our understanding of the effect of NSAID use on knee osteoarthritis when compared to placebo with CBT. Although this is a negative study that failed to show that placebo combined with CBT is noninferior to NSAIDs, it did quantify the expected treatment effect of NSAIDs and showed that this effect likely is not clinically important and/or does not alter lower-extremity function. Further studies are needed to identify other nonpharmacologic approaches and test whether combinations of approaches are effective in the management of chronic pain from osteoarthritis.

–William W. Hung, MD, MPH

Study Overview

Objective. To examine whether discontinuation of nonsteroidal anti-inflammatory drug (NSAID) therapy and initiation of telephone-based cognitive behavioral therapy (CBT) is not worse than continuation of NSAIDs in the management of arthritis pain.

Design. Randomized controlled trial with noninferiority design.

Setting and participants. This study was a multicenter trial conducted across 4 Veterans Affairs health care systems in Boston, Providence, Connecticut, and North Florida/South Georgia that started September 2013 and ended September 2018. Eligibility criteria included being age 20 years or older, radiographic evidence of knee osteoarthritis, and use of an NSAID for knee pain on most days of the month for at least the past 3 months. Exclusion criteria included significant hearing impairments that may impede the conduct of the trial, current opioid prescriptions excluding tramadol, contraindications to NSAID use, recent or scheduled intra-articular injections or surgery, comorbid conditions other than knee pain that limited walking, and bilateral knee replacements or pain only in the replaced knee. Concurrent use of tramadol and other non-NSAID analgesics was permitted.

A total of 490 participants took part in the 2-week run-in period where their NSAID regimen was discontinued and they were started on a standardized dose of the NSAID meloxicam 15 mg daily. During the run-in period, 126 participants were excluded for several reasons, including worsening pain and patient withdrawal, yielding 364 participants who were randomized to continue meloxicam treatment or placebo for 4 weeks with blinding.

Intervention. Subsequent to the 4-week phase 1 placebo controlled trial, participants in the placebo group were given CBT via telephone (unblinded) for 10 weeks, and the meloxicam group continued treatment with meloxicam for phase 2. The CBT group received 10 modules over 10 weeks in 30- to 45-minute telephone contacts with a psychologist using a treatment manual modified for knee osteoarthritis. These modules consisted of 1 introductory module, 8 pain coping skills modules (eg, deep breathing and visual imagery, progressive muscle relaxation, physical activity and bodily mechanics, identifying unhealthy thoughts, balancing unhealthy thoughts, managing stress, time-based pacing, and sleep hygiene), and a final module emphasizing skill consolidation and relapse prevention. Outcomes were assessed at the end of the phase 1 and phase 2 periods.

Main outcome measures. Main study outcome measures included pain as measured with the Western Ontario and McMaster Universities Osteoarthritis Index (WOMAC) at 4 weeks. Secondary outcomes included the WOMAC pain score, disability score, and global impression of change after treatment at 14 weeks. The WOMAC pain scale ranges from 0 to 20, and consists of 5 questions regarding severity of pain during walking, stair use, lying in bed at night, sitting, and standing, with 0 indicating no pain; 1, mild pain; 2, moderate pain; 3, severe pain; and 4, very severe pain for each item. The WOMAC disability scale measures self-reported difficulty in performing tasks that reflect lower-extremity physical function, including climbing stairs, rising from a chair, walking, and other activities of daily living. The global impression of change after treatment was measured on a 5-point scale (where 1 indicates much better and 5 indicates much worse). The minimum clinically important difference of the WOMAC pain scale is 2, based on prior literature. With the noninferiority design, the margin was set as a score of 1.

Main results. The placebo group consisted of 180 participants, with an average age of 58.2 years (SD, 11.8 years); 89% of them were male. The meloxicam group consisted of 184 participants, with an average age of 58.6 years (SD, 10 years); 84% of them were male. The average body mass index was 33.9 and 33.4 in each group, respectively. For the primary outcome, the placebo group had a worse pain score than the meloxicam group at 4 weeks (difference of 1.4; 95% confidence interval, 0.8- 2.0). At 14 weeks, the placebo group (with CBT) had a worse pain score than the meloxicam group (difference of 0.8; 95% CI, 0.2-1.4). There was no statistically significant difference in the disability score or global impression of change after treatment score between the 2 groups. The observed difference in pain score did not, however, exceed the minimum clinically important difference.

Conclusion. Placebo treatment and CBT are inferior to NSAIDs in managing pain for patients with knee osteoarthritis. The difference in pain may not be clinically important, and there were no differences in function at 14 weeks.

Commentary

Osteoarthritis is a common chronic condition that causes pain and disability and is often treated with oral analgesics. NSAIDs, despite few high-quality trials demonstrating their efficacy, are among the most commonly used treatment for osteoarthritis pain.¹ NSAID therapy, however, does have potential side effects, such as gastric reflux and renal dysfunction.² This withdrawal trial with placebo control contributes further evidence of the effectiveness of NSAIDs on knee osteoarthritis, demonstrating that indeed NSAIDs improve pain scores to a greater degree than placebo treatment. Augmenting placebo treatment with nonpharmacologic CBT was inferior to NSAIDs in pain management. The authors pointed out that the difference in pain score may not be clinically important, and that lower-extremity function was not different between the groups, concluding that, despite the higher pain score, CBT could be a treatment option, particularly for those who may have difficulty tolerating NSAID treatment.

The study population had a number of chronic conditions in addition to having knee arthritis, and thus likely were taking multiple medications for chronic disease management. Use of multiple medications is associated with an increased risk of rug interactions and adverse effects of medications.³ Thus, this attempt to assess whether a nonpharmacologic alternative treatment is noninferior to a drug treatment is a step toward building the evidence base for deprescribing and enhancing medication safety.⁴ Previous studies have examined other nonpharmacologic treatments for knee arthritis, such as acupuncture,⁵ and it is worthwhile to consider combining nonpharmacological approaches as an alternative to oral analgesic medication use.

Applications for Clinical Practice

This study advances our understanding of the effect of NSAID use on knee osteoarthritis when compared to placebo with CBT. Although this is a negative study that failed to show that placebo combined with CBT is noninferior to NSAIDs, it did quantify the expected treatment effect of NSAIDs and showed that this effect likely is not clinically important and/or does not alter lower-extremity function. Further studies are needed to identify other nonpharmacologic approaches and test whether combinations of approaches are effective in the management of chronic pain from osteoarthritis.

–William W. Hung, MD, MPH

Study Overview

Objective. To examine whether discontinuation of nonsteroidal anti-inflammatory drug (NSAID) therapy and initiation of telephone-based cognitive behavioral therapy (CBT) is not worse than continuation of NSAIDs in the management of arthritis pain.

Design. Randomized controlled trial with noninferiority design.

Setting and participants. This study was a multicenter trial conducted across 4 Veterans Affairs health care systems in Boston, Providence, Connecticut, and North Florida/South Georgia that started September 2013 and ended September 2018. Eligibility criteria included being age 20 years or older, radiographic evidence of knee osteoarthritis, and use of an NSAID for knee pain on most days of the month for at least the past 3 months. Exclusion criteria included significant hearing impairments that may impede the conduct of the trial, current opioid prescriptions excluding tramadol, contraindications to NSAID use, recent or scheduled intra-articular injections or surgery, comorbid conditions other than knee pain that limited walking, and bilateral knee replacements or pain only in the replaced knee. Concurrent use of tramadol and other non-NSAID analgesics was permitted.

A total of 490 participants took part in the 2-week run-in period where their NSAID regimen was discontinued and they were started on a standardized dose of the NSAID meloxicam 15 mg daily. During the run-in period, 126 participants were excluded for several reasons, including worsening pain and patient withdrawal, yielding 364 participants who were randomized to continue meloxicam treatment or placebo for 4 weeks with blinding.

Intervention. Subsequent to the 4-week phase 1 placebo controlled trial, participants in the placebo group were given CBT via telephone (unblinded) for 10 weeks, and the meloxicam group continued treatment with meloxicam for phase 2. The CBT group received 10 modules over 10 weeks in 30- to 45-minute telephone contacts with a psychologist using a treatment manual modified for knee osteoarthritis. These modules consisted of 1 introductory module, 8 pain coping skills modules (eg, deep breathing and visual imagery, progressive muscle relaxation, physical activity and bodily mechanics, identifying unhealthy thoughts, balancing unhealthy thoughts, managing stress, time-based pacing, and sleep hygiene), and a final module emphasizing skill consolidation and relapse prevention. Outcomes were assessed at the end of the phase 1 and phase 2 periods.

Main outcome measures. Main study outcome measures included pain as measured with the Western Ontario and McMaster Universities Osteoarthritis Index (WOMAC) at 4 weeks. Secondary outcomes included the WOMAC pain score, disability score, and global impression of change after treatment at 14 weeks. The WOMAC pain scale ranges from 0 to 20, and consists of 5 questions regarding severity of pain during walking, stair use, lying in bed at night, sitting, and standing, with 0 indicating no pain; 1, mild pain; 2, moderate pain; 3, severe pain; and 4, very severe pain for each item. The WOMAC disability scale measures self-reported difficulty in performing tasks that reflect lower-extremity physical function, including climbing stairs, rising from a chair, walking, and other activities of daily living. The global impression of change after treatment was measured on a 5-point scale (where 1 indicates much better and 5 indicates much worse). The minimum clinically important difference of the WOMAC pain scale is 2, based on prior literature. With the noninferiority design, the margin was set as a score of 1.

Main results. The placebo group consisted of 180 participants, with an average age of 58.2 years (SD, 11.8 years); 89% of them were male. The meloxicam group consisted of 184 participants, with an average age of 58.6 years (SD, 10 years); 84% of them were male. The average body mass index was 33.9 and 33.4 in each group, respectively. For the primary outcome, the placebo group had a worse pain score than the meloxicam group at 4 weeks (difference of 1.4; 95% confidence interval, 0.8- 2.0). At 14 weeks, the placebo group (with CBT) had a worse pain score than the meloxicam group (difference of 0.8; 95% CI, 0.2-1.4). There was no statistically significant difference in the disability score or global impression of change after treatment score between the 2 groups. The observed difference in pain score did not, however, exceed the minimum clinically important difference.

Conclusion. Placebo treatment and CBT are inferior to NSAIDs in managing pain for patients with knee osteoarthritis. The difference in pain may not be clinically important, and there were no differences in function at 14 weeks.

Commentary

Osteoarthritis is a common chronic condition that causes pain and disability and is often treated with oral analgesics. NSAIDs, despite few high-quality trials demonstrating their efficacy, are among the most commonly used treatment for osteoarthritis pain.¹ NSAID therapy, however, does have potential side effects, such as gastric reflux and renal dysfunction.² This withdrawal trial with placebo control contributes further evidence of the effectiveness of NSAIDs on knee osteoarthritis, demonstrating that indeed NSAIDs improve pain scores to a greater degree than placebo treatment. Augmenting placebo treatment with nonpharmacologic CBT was inferior to NSAIDs in pain management. The authors pointed out that the difference in pain score may not be clinically important, and that lower-extremity function was not different between the groups, concluding that, despite the higher pain score, CBT could be a treatment option, particularly for those who may have difficulty tolerating NSAID treatment.

The study population had a number of chronic conditions in addition to having knee arthritis, and thus likely were taking multiple medications for chronic disease management. Use of multiple medications is associated with an increased risk of rug interactions and adverse effects of medications.³ Thus, this attempt to assess whether a nonpharmacologic alternative treatment is noninferior to a drug treatment is a step toward building the evidence base for deprescribing and enhancing medication safety.⁴ Previous studies have examined other nonpharmacologic treatments for knee arthritis, such as acupuncture,⁵ and it is worthwhile to consider combining nonpharmacological approaches as an alternative to oral analgesic medication use.

Applications for Clinical Practice

This study advances our understanding of the effect of NSAID use on knee osteoarthritis when compared to placebo with CBT. Although this is a negative study that failed to show that placebo combined with CBT is noninferior to NSAIDs, it did quantify the expected treatment effect of NSAIDs and showed that this effect likely is not clinically important and/or does not alter lower-extremity function. Further studies are needed to identify other nonpharmacologic approaches and test whether combinations of approaches are effective in the management of chronic pain from osteoarthritis.

–William W. Hung, MD, MPH

Case Presentation: A 45-year-old US Coast Guard veteran with a medical history of asthma and chronic back pain was referred to the VA Boston Healthcare System (VABHS) for evaluation of progressive, unexplained dyspnea. Two years prior to presentation, the patient was an avid outdoorsman and highly active. At the time of his initial primary care physician (PCP) evaluation he reported dyspnea on exertion, and symptoms consistent with an upper respiratory tract infection (URTI) and a recent tick bite with an associated rash. He was treated with intranasal fluticasone and a course of antibiotics. His URTI symptoms and rash improved; however the dyspnea persisted and progressed over the ensuing winter and he was referred for pulmonary function testing. Additional history included a 20 pack-year history of smoking (resolved 10 years prior to the first VABHS clinical encounter) and a family history of premature coronary artery disease (CAD) in his father and 2 paternal uncles. He lived in northern New England where he previously worked as a cemetery groundskeeper.

►Kristopher Clark, MD, Chief Medical Resident, VABHS and Boston University/Boston Medical Center: Dr. Goldstein, how do you approach a patient who presents with progressive dyspnea?

►Ronald Goldstein, MD, Chief of Pulmonary and Critical Care VABHS: The evaluation of dyspnea is a common problem for pulmonary physicians. The sensation of dyspnea may originate from a wide variety of etiologies that involve pulmonary and cardiovascular disorders, neuromuscular impairment, deconditioning, or psychological issues. It is important to characterize the temporal pattern, severity, progression, relation to exertion or other triggers, the smoking history, environmental and occupational exposures to pulmonary toxins, associated symptoms, and the history of pulmonary problems.¹

The physical examination may help to identify an airway or parenchymal disorder. Wheezing on chest examination would point to an obstructive defect and crackles to a possible restrictive problem, including pulmonary fibrosis. A cardiac examination should be performed to assess for evidence of heart failure, valvular heart disease, or the presence of loud P2 suggestive of pulmonary hypertension (PH). Laboratory studies, including complete blood counts are indicated.

A more complete pulmonary evaluation usually involves pulmonary function tests (PFTs), oximetry with exertion, and chest imaging. Additional cardiac testing might include electrocardiogram (ECG) and cardiac echocardiogram, followed by an exercise study, if needed. A B-natriuretic peptide determination could be considered if there is concern for congestive heart failure.²

►Dr. Clark: The initial physical examination was normal and laboratory tests were unrevealing. Given his history of asthma, he underwent spirometry testing (Table 1).

Dr. Goldstein, aside from unexplained dyspnea, what are other indications for spirometry and when should we consider ordering a full PFT, including lung volumes and diffusion capacity? Can you interpret this patient’s spirometry results?
 

►Dr. Goldstein: Spirometry is indicated to evaluate for a suspected obstructive defect. The test is usually performed with and without a bronchodilator to assess airway reactivity. A change in > 12% and > 200 mL suggests acute bronchodilator responsiveness. Periodic spirometry determinations are useful to assess the effect of medications or progression of disease. A reduction in forced vital capacity (FVC) may suggest a restrictive component. This possibility requires measure of lung volumes.

A full set of PFTs (ie, spirometry plus assessment of lung volumes and diffusion capacity) is required to evaluate the abnormalities associated with chronic obstructive pulmonary disease (COPD), interstitial diseases, vascular abnormalities (particularly PH), as well as for certain preoperative assessments. The single breath diffusing capacity for carbon monoxide is a measure of the overall capillary alveolar surface area of the lung. It is decreased in emphysema and interstitial disease as well as pulmonary vascular disorders. It would be particularly useful in this case as the spirometry studies were normal.

In this case, the normal FVC renders a significant restrictive disorder unlikely and his normal forced expiratory volume (FEV₁) and FEV₁/FVC make a significant obstructive disorder unlikely. He did not show any bronchodilator response; however, this finding does not exclude the presence of underlying asthma or reactive airway disease as patients often will not show a bronchodilator response at time of testing if they are not experiencing active bronchospasm or constriction. Further provocative testing with a methacholine challenge could be used to assess for reactive airway disease.

►Dr. Clark: The patient continued to have dyspnea when he returned to his PCP. Given his family history of premature CAD, an ECG was obtained that showed normal sinus rhythm at a rate of 70 beats per minute. A cardiology consult was placed, and he was referred for cardiac stress testing.

Dr. Maron, there are many forms of cardiac stress tests. In this case, the patient is referred for a stress test due his dyspnea. Does that symptom help you decide which test to order? How often does dyspnea present as an anginal equivalent in the absence of other cardiovascular symptoms or known cardiovascular disease?

►Bradley Maron, MD, Codirector, Pulmonary Vascular Disease Center, VABHS: In this case, stress testing should include a functional (ie, exercise) assessment if possible. Exercise capacity is a critical determinant of prognosis across the spectrum of cardiovascular disease and in a young person can be particularly informative on global health status. Furthermore, the chief complaint from this patient is dyspnea on exertion, and therefore, exercise testing is likely to be needed to reproduce or provoke the main symptom in this case. Estimates for dyspnea as a presenting symptom for ischemic heart disease vary but may be as high as 25%.³ It should be noted that cardiopulmonary exercise testing is useful for evaluating patients with unexplained dyspnea, as exercise hypoxemia, blunted decrease in V_D/V_T (ventilatory dead space/tidal volume), and evidence of a pulmonary mechanical limit to physical activity can inform the differential diagnosis.

►Dr. Clark: The patient underwent exercise treadmill testing and was able reach the target heart rate (> 85% age-predicted maximal heart rate) and achieve 11 metabolic equivalents. He had no chest pain or diagnostic ECG changes. The report made no mention of whether he experienced dyspnea during the test and was read as negative for exercise-induced ischemia.

He was seen by a cardiologist who noted an increased intensity S2 heart sound on examination without any other cardiopulmonary findings. It was noted that his symptoms occurred when tamping the ground or starting to walk up a hill but resolved with rest. It was also noted that his symptoms did not occur with gradual increased activity such as that performed during an exercise tolerance test. A 2-view chest X-ray was obtained and read as normal. Given the data from this evaluation thus far, the patient was told that his symptoms were most likely a result of his asthma exacerbated by dirt and dust exposure. Continued use of albuterol inhaler therapy was recommended, and no further diagnostic assessment was pursued.

Approximately 11 months later, the patient presented again to his PCP and reported progressive dyspnea. He had delayed seeking further care as he started to “feel like my symptoms were possibly in my head” given his prior negative workup. His symptoms had escalated drastically to the point where he felt short of breath with minimal exertion in addition to feeling sweaty, dizzy, fatigued, and having near-syncope when standing.

He was referred for a transthoracic echocardiogram (TTE) that revealed a left ventricular ejection fraction (LVEF) of 55 to 60% with diastolic relaxation abnormality and a normal-sized left atrium. The TTE also showed (qualitatively) a moderately dilated right ventricle with reduced systolic function, moderately severe tricuspid regurgitation, and severe elevation (> 60 mm Hg) in estimated right ventricular systolic pressure.

Dr. Maron, can you comment on how these findings may explain the patient’s symptoms? What differential diagnoses would you now consider?
 

►Dr. Maron: These echocardiography results exclude left ventricular systolic dysfunction or primary left-sided valvular disease at rest as a cause of the patient’s symptoms. In light of the patient’s prior normal stress test, high grade coronary disease in the absence of LV systolic dysfunction on echocardiography also seems unlikely. Estimated pulmonary artery systolic pressure > 60 mm Hg by echocardiography is highly suggestive of PH, but in and of itself does not diagnose PH nor inform pulmonary artery wedge pressure or pulmonary vascular resistance. Along with a direct measurement of pulmonary artery (PA) pressure, these data are needed to establish, classify, and prognosticate PH clinically.

►Dr. Clark: The patient was referred to a pulmonologist. His examination included bibasilar crackles and an enhanced P2 heart sound. A comprehensive pulmonary history was obtained, which noted his smoking history, possible asbestos exposure while serving in the Coast Guard, nighttime snoring without witnessed apnea events, and no personal or family history of thromboembolism or connective tissue disease.

Dr. Goldstein, is there anything in this patient’s history that could explain his symptoms and echocardiograph findings? Which tests would you order next?
 

►Dr. Goldstein: PH may be secondary to a wide variety of disorders including left heart disease (Group 2), advanced COPD, interstitial fibrosis, obstructive sleep apnea (OSA), or other lung diseases (Group 3), thromboembolic disorders (Group 4), and other systemic diseases such as sarcoidosis (Group 5). Group 1 is pulmonary arterial hypertension. (Table 2).

A right heart catheterization should be done to confirm the PA pressures estimated by echocardiogram. As to a cause, clinically he does not have heart failure. The limited smoking history and spirometry data do not support advanced COPD. He was noted to have crackles on physical examination suggesting an interstitial disorder. To assess the extent of interstitial disease, we would obtain a noncontrast computed tomography (CT) of the chest. The history of snoring suggesting the possibility of OSA indicating the need for overnight oximetry as significant nocturnal hypoxemia is a possible contributing cause to PH. A polysomnogram would be required to fully evaluate a sleep disturbance. The possible asbestos exposure is not likely a contributing factor as asbestosis requires significant exposure. We would obtain a ventilation/perfusion (V/Q) scan to rule out chronic thromboembolic disease. Targeted tests for causes of Group 5 disease should also be done.
 

►Dr. Clark: The impression from his pulmonologist was that the patient has severe PH, though the specific etiology was not yet known. Dr. Maron, can you review for us the pathophysiology behind PH and describe how the disease is classified?

►Dr. Maron: Elevated mean pulmonary artery pressure (> 20 mm Hg) diagnosed by supine right heart catheterization is the sine qua non of PH.⁴ However, this alone does not inform pathophysiology. As Dr. Goldstein noted, elevated PA pressure may be due to left heart disease, primary parenchymal lung disease/sleep-disordered breathing, in situ thrombotic remodeling of pulmonary arterioles following prior luminal pulmonary embolism, or in the setting of various specific predisposing conditions, such as sickle cell disease and sarcoidosis among others.⁵

Alternatively, pulmonary arterial hypertension (PAH) is suspected in patients with no identifiable cause of PH, pulmonary artery wedge pressure 15 mm Hg and pulmonary vascular resistance of 3.0 Wood units.⁶ Importantly, PAH is not synonymous with PH but is a circumspect PH disease subgroup. In turn, PAH may be idiopathic, hereditary, or associated with other select, predisposing disorders, namely systemic sclerosis. In PAH, the interplay between genetic and molecular factors results in effacement of distal pulmonary arterioles due to plexigenic, fibrotic, and/or concentric hypertrophic remodeling. Increased vascular resistance promotes early right ventricular dilation and impaired systolic function. As a result, patients with PAH are at particularly elevated risk for cor pulmonale.
 

►Dr. Clark: Overnight oximetry revealed baseline oxygen saturation of 94%, an oxygen nadir of 84% with a total of 7 minutes with oxygen < 90%. On a 6-minute walk test, the patient had a max heart rate of 116 and oxygen nadir of 93%. Chest CT with and without contrast showed no evidence of pulmonary emboli but noted mild emphysematous changes. A V/Q revealed no evidence of acute or chronic pulmonary thromboembolic disease. Coronary catheterization showed normal coronary anatomy without significant CAD. A right heart catheterization showed findings consistent with severe PH with normal left-sided filling pressures (Table 3).

The patient returned a normal antinuclear antibody, C-reactive protein, HIV, and liver function panel. Based on these findings, a presumptive diagnosis of group 1 PH (idiopathic PAH) was made. Given the severity of his right heart dysfunction, he was transferred to the cardiac care unit and initiated on epoprostenol.

Dr. Maron, can you review the different treatment options for idiopathic PAH and explain why epoprostenol was chosen for this patient?
 

►Dr. Maron: There are 14 US Food and Drug Administration-approved drug therapies for patients with PAH, which all target either nitric oxide signaling, endothelin receptors, or the prostacyclin pathway. In the current era, treatment-naïve patients with PAH are generally initiated on calcium channel antagonist therapy if there is evidence of vasoreactivity during right heart catheterization (following nitric oxide administration), dual therapy most often with an endothelin receptor antagonist and phosphodiesterase inhibitor, or parenteral prostacyclin therapy. Since < 5% of patients will demonstrate vasoreactivity, the decision at point of care in incident patients with PAH often focuses on dual oral therapy or initiation of parenteral prostacyclin therapy. In this case, the patient reported presyncope with minimal physical activity (eg, bending over or walking up stairs) and severely decreased functional status (ie, New York Heart Association Functional [NYHA] Class III – IV), and he had a cardiac index within the range of cardiogenic shock (< 2.0 L/min/m²). Collectively, this clinical profile is considered particularly high risk, therefore, a recommendation for parenteral continuous prostacyclin therapy was made.

► Dr. Clark: The patient tolerated epoprostenol and reported improvement in his symptoms. He had a tunneled line catheter placed for continuous epoprostenol infusion. He was discharged home and scheduled for outpatient follow-up in a PH clinic. At 4 months following discharge, he was reporting steady clinical and functional improvement as well as improvement in his dyspnea. A second therapy (oral phosphodiesterase type-V inhibitor) was initiated and tolerated well. Overall, he reported resolution of presyncope, NYHA Functional Class II symptoms, and the absence of important drug effects.

Case Presentation: A 45-year-old US Coast Guard veteran with a medical history of asthma and chronic back pain was referred to the VA Boston Healthcare System (VABHS) for evaluation of progressive, unexplained dyspnea. Two years prior to presentation, the patient was an avid outdoorsman and highly active. At the time of his initial primary care physician (PCP) evaluation he reported dyspnea on exertion, and symptoms consistent with an upper respiratory tract infection (URTI) and a recent tick bite with an associated rash. He was treated with intranasal fluticasone and a course of antibiotics. His URTI symptoms and rash improved; however the dyspnea persisted and progressed over the ensuing winter and he was referred for pulmonary function testing. Additional history included a 20 pack-year history of smoking (resolved 10 years prior to the first VABHS clinical encounter) and a family history of premature coronary artery disease (CAD) in his father and 2 paternal uncles. He lived in northern New England where he previously worked as a cemetery groundskeeper.

►Kristopher Clark, MD, Chief Medical Resident, VABHS and Boston University/Boston Medical Center: Dr. Goldstein, how do you approach a patient who presents with progressive dyspnea?

►Ronald Goldstein, MD, Chief of Pulmonary and Critical Care VABHS: The evaluation of dyspnea is a common problem for pulmonary physicians. The sensation of dyspnea may originate from a wide variety of etiologies that involve pulmonary and cardiovascular disorders, neuromuscular impairment, deconditioning, or psychological issues. It is important to characterize the temporal pattern, severity, progression, relation to exertion or other triggers, the smoking history, environmental and occupational exposures to pulmonary toxins, associated symptoms, and the history of pulmonary problems.¹

The physical examination may help to identify an airway or parenchymal disorder. Wheezing on chest examination would point to an obstructive defect and crackles to a possible restrictive problem, including pulmonary fibrosis. A cardiac examination should be performed to assess for evidence of heart failure, valvular heart disease, or the presence of loud P2 suggestive of pulmonary hypertension (PH). Laboratory studies, including complete blood counts are indicated.

A more complete pulmonary evaluation usually involves pulmonary function tests (PFTs), oximetry with exertion, and chest imaging. Additional cardiac testing might include electrocardiogram (ECG) and cardiac echocardiogram, followed by an exercise study, if needed. A B-natriuretic peptide determination could be considered if there is concern for congestive heart failure.²

►Dr. Clark: The initial physical examination was normal and laboratory tests were unrevealing. Given his history of asthma, he underwent spirometry testing (Table 1).

Dr. Goldstein, aside from unexplained dyspnea, what are other indications for spirometry and when should we consider ordering a full PFT, including lung volumes and diffusion capacity? Can you interpret this patient’s spirometry results?
 

►Dr. Goldstein: Spirometry is indicated to evaluate for a suspected obstructive defect. The test is usually performed with and without a bronchodilator to assess airway reactivity. A change in > 12% and > 200 mL suggests acute bronchodilator responsiveness. Periodic spirometry determinations are useful to assess the effect of medications or progression of disease. A reduction in forced vital capacity (FVC) may suggest a restrictive component. This possibility requires measure of lung volumes.

A full set of PFTs (ie, spirometry plus assessment of lung volumes and diffusion capacity) is required to evaluate the abnormalities associated with chronic obstructive pulmonary disease (COPD), interstitial diseases, vascular abnormalities (particularly PH), as well as for certain preoperative assessments. The single breath diffusing capacity for carbon monoxide is a measure of the overall capillary alveolar surface area of the lung. It is decreased in emphysema and interstitial disease as well as pulmonary vascular disorders. It would be particularly useful in this case as the spirometry studies were normal.

In this case, the normal FVC renders a significant restrictive disorder unlikely and his normal forced expiratory volume (FEV₁) and FEV₁/FVC make a significant obstructive disorder unlikely. He did not show any bronchodilator response; however, this finding does not exclude the presence of underlying asthma or reactive airway disease as patients often will not show a bronchodilator response at time of testing if they are not experiencing active bronchospasm or constriction. Further provocative testing with a methacholine challenge could be used to assess for reactive airway disease.

►Dr. Clark: The patient continued to have dyspnea when he returned to his PCP. Given his family history of premature CAD, an ECG was obtained that showed normal sinus rhythm at a rate of 70 beats per minute. A cardiology consult was placed, and he was referred for cardiac stress testing.

Dr. Maron, there are many forms of cardiac stress tests. In this case, the patient is referred for a stress test due his dyspnea. Does that symptom help you decide which test to order? How often does dyspnea present as an anginal equivalent in the absence of other cardiovascular symptoms or known cardiovascular disease?

►Bradley Maron, MD, Codirector, Pulmonary Vascular Disease Center, VABHS: In this case, stress testing should include a functional (ie, exercise) assessment if possible. Exercise capacity is a critical determinant of prognosis across the spectrum of cardiovascular disease and in a young person can be particularly informative on global health status. Furthermore, the chief complaint from this patient is dyspnea on exertion, and therefore, exercise testing is likely to be needed to reproduce or provoke the main symptom in this case. Estimates for dyspnea as a presenting symptom for ischemic heart disease vary but may be as high as 25%.³ It should be noted that cardiopulmonary exercise testing is useful for evaluating patients with unexplained dyspnea, as exercise hypoxemia, blunted decrease in V_D/V_T (ventilatory dead space/tidal volume), and evidence of a pulmonary mechanical limit to physical activity can inform the differential diagnosis.

►Dr. Clark: The patient underwent exercise treadmill testing and was able reach the target heart rate (> 85% age-predicted maximal heart rate) and achieve 11 metabolic equivalents. He had no chest pain or diagnostic ECG changes. The report made no mention of whether he experienced dyspnea during the test and was read as negative for exercise-induced ischemia.

He was seen by a cardiologist who noted an increased intensity S2 heart sound on examination without any other cardiopulmonary findings. It was noted that his symptoms occurred when tamping the ground or starting to walk up a hill but resolved with rest. It was also noted that his symptoms did not occur with gradual increased activity such as that performed during an exercise tolerance test. A 2-view chest X-ray was obtained and read as normal. Given the data from this evaluation thus far, the patient was told that his symptoms were most likely a result of his asthma exacerbated by dirt and dust exposure. Continued use of albuterol inhaler therapy was recommended, and no further diagnostic assessment was pursued.

Approximately 11 months later, the patient presented again to his PCP and reported progressive dyspnea. He had delayed seeking further care as he started to “feel like my symptoms were possibly in my head” given his prior negative workup. His symptoms had escalated drastically to the point where he felt short of breath with minimal exertion in addition to feeling sweaty, dizzy, fatigued, and having near-syncope when standing.

He was referred for a transthoracic echocardiogram (TTE) that revealed a left ventricular ejection fraction (LVEF) of 55 to 60% with diastolic relaxation abnormality and a normal-sized left atrium. The TTE also showed (qualitatively) a moderately dilated right ventricle with reduced systolic function, moderately severe tricuspid regurgitation, and severe elevation (> 60 mm Hg) in estimated right ventricular systolic pressure.

Dr. Maron, can you comment on how these findings may explain the patient’s symptoms? What differential diagnoses would you now consider?
 

►Dr. Maron: These echocardiography results exclude left ventricular systolic dysfunction or primary left-sided valvular disease at rest as a cause of the patient’s symptoms. In light of the patient’s prior normal stress test, high grade coronary disease in the absence of LV systolic dysfunction on echocardiography also seems unlikely. Estimated pulmonary artery systolic pressure > 60 mm Hg by echocardiography is highly suggestive of PH, but in and of itself does not diagnose PH nor inform pulmonary artery wedge pressure or pulmonary vascular resistance. Along with a direct measurement of pulmonary artery (PA) pressure, these data are needed to establish, classify, and prognosticate PH clinically.

►Dr. Clark: The patient was referred to a pulmonologist. His examination included bibasilar crackles and an enhanced P2 heart sound. A comprehensive pulmonary history was obtained, which noted his smoking history, possible asbestos exposure while serving in the Coast Guard, nighttime snoring without witnessed apnea events, and no personal or family history of thromboembolism or connective tissue disease.

Dr. Goldstein, is there anything in this patient’s history that could explain his symptoms and echocardiograph findings? Which tests would you order next?
 

►Dr. Goldstein: PH may be secondary to a wide variety of disorders including left heart disease (Group 2), advanced COPD, interstitial fibrosis, obstructive sleep apnea (OSA), or other lung diseases (Group 3), thromboembolic disorders (Group 4), and other systemic diseases such as sarcoidosis (Group 5). Group 1 is pulmonary arterial hypertension. (Table 2).

A right heart catheterization should be done to confirm the PA pressures estimated by echocardiogram. As to a cause, clinically he does not have heart failure. The limited smoking history and spirometry data do not support advanced COPD. He was noted to have crackles on physical examination suggesting an interstitial disorder. To assess the extent of interstitial disease, we would obtain a noncontrast computed tomography (CT) of the chest. The history of snoring suggesting the possibility of OSA indicating the need for overnight oximetry as significant nocturnal hypoxemia is a possible contributing cause to PH. A polysomnogram would be required to fully evaluate a sleep disturbance. The possible asbestos exposure is not likely a contributing factor as asbestosis requires significant exposure. We would obtain a ventilation/perfusion (V/Q) scan to rule out chronic thromboembolic disease. Targeted tests for causes of Group 5 disease should also be done.
 

►Dr. Clark: The impression from his pulmonologist was that the patient has severe PH, though the specific etiology was not yet known. Dr. Maron, can you review for us the pathophysiology behind PH and describe how the disease is classified?

►Dr. Maron: Elevated mean pulmonary artery pressure (> 20 mm Hg) diagnosed by supine right heart catheterization is the sine qua non of PH.⁴ However, this alone does not inform pathophysiology. As Dr. Goldstein noted, elevated PA pressure may be due to left heart disease, primary parenchymal lung disease/sleep-disordered breathing, in situ thrombotic remodeling of pulmonary arterioles following prior luminal pulmonary embolism, or in the setting of various specific predisposing conditions, such as sickle cell disease and sarcoidosis among others.⁵

Alternatively, pulmonary arterial hypertension (PAH) is suspected in patients with no identifiable cause of PH, pulmonary artery wedge pressure 15 mm Hg and pulmonary vascular resistance of 3.0 Wood units.⁶ Importantly, PAH is not synonymous with PH but is a circumspect PH disease subgroup. In turn, PAH may be idiopathic, hereditary, or associated with other select, predisposing disorders, namely systemic sclerosis. In PAH, the interplay between genetic and molecular factors results in effacement of distal pulmonary arterioles due to plexigenic, fibrotic, and/or concentric hypertrophic remodeling. Increased vascular resistance promotes early right ventricular dilation and impaired systolic function. As a result, patients with PAH are at particularly elevated risk for cor pulmonale.
 

►Dr. Clark: Overnight oximetry revealed baseline oxygen saturation of 94%, an oxygen nadir of 84% with a total of 7 minutes with oxygen < 90%. On a 6-minute walk test, the patient had a max heart rate of 116 and oxygen nadir of 93%. Chest CT with and without contrast showed no evidence of pulmonary emboli but noted mild emphysematous changes. A V/Q revealed no evidence of acute or chronic pulmonary thromboembolic disease. Coronary catheterization showed normal coronary anatomy without significant CAD. A right heart catheterization showed findings consistent with severe PH with normal left-sided filling pressures (Table 3).

The patient returned a normal antinuclear antibody, C-reactive protein, HIV, and liver function panel. Based on these findings, a presumptive diagnosis of group 1 PH (idiopathic PAH) was made. Given the severity of his right heart dysfunction, he was transferred to the cardiac care unit and initiated on epoprostenol.

Dr. Maron, can you review the different treatment options for idiopathic PAH and explain why epoprostenol was chosen for this patient?
 

►Dr. Maron: There are 14 US Food and Drug Administration-approved drug therapies for patients with PAH, which all target either nitric oxide signaling, endothelin receptors, or the prostacyclin pathway. In the current era, treatment-naïve patients with PAH are generally initiated on calcium channel antagonist therapy if there is evidence of vasoreactivity during right heart catheterization (following nitric oxide administration), dual therapy most often with an endothelin receptor antagonist and phosphodiesterase inhibitor, or parenteral prostacyclin therapy. Since < 5% of patients will demonstrate vasoreactivity, the decision at point of care in incident patients with PAH often focuses on dual oral therapy or initiation of parenteral prostacyclin therapy. In this case, the patient reported presyncope with minimal physical activity (eg, bending over or walking up stairs) and severely decreased functional status (ie, New York Heart Association Functional [NYHA] Class III – IV), and he had a cardiac index within the range of cardiogenic shock (< 2.0 L/min/m²). Collectively, this clinical profile is considered particularly high risk, therefore, a recommendation for parenteral continuous prostacyclin therapy was made.

► Dr. Clark: The patient tolerated epoprostenol and reported improvement in his symptoms. He had a tunneled line catheter placed for continuous epoprostenol infusion. He was discharged home and scheduled for outpatient follow-up in a PH clinic. At 4 months following discharge, he was reporting steady clinical and functional improvement as well as improvement in his dyspnea. A second therapy (oral phosphodiesterase type-V inhibitor) was initiated and tolerated well. Overall, he reported resolution of presyncope, NYHA Functional Class II symptoms, and the absence of important drug effects.

Case Presentation: A 45-year-old US Coast Guard veteran with a medical history of asthma and chronic back pain was referred to the VA Boston Healthcare System (VABHS) for evaluation of progressive, unexplained dyspnea. Two years prior to presentation, the patient was an avid outdoorsman and highly active. At the time of his initial primary care physician (PCP) evaluation he reported dyspnea on exertion, and symptoms consistent with an upper respiratory tract infection (URTI) and a recent tick bite with an associated rash. He was treated with intranasal fluticasone and a course of antibiotics. His URTI symptoms and rash improved; however the dyspnea persisted and progressed over the ensuing winter and he was referred for pulmonary function testing. Additional history included a 20 pack-year history of smoking (resolved 10 years prior to the first VABHS clinical encounter) and a family history of premature coronary artery disease (CAD) in his father and 2 paternal uncles. He lived in northern New England where he previously worked as a cemetery groundskeeper.

►Kristopher Clark, MD, Chief Medical Resident, VABHS and Boston University/Boston Medical Center: Dr. Goldstein, how do you approach a patient who presents with progressive dyspnea?

►Ronald Goldstein, MD, Chief of Pulmonary and Critical Care VABHS: The evaluation of dyspnea is a common problem for pulmonary physicians. The sensation of dyspnea may originate from a wide variety of etiologies that involve pulmonary and cardiovascular disorders, neuromuscular impairment, deconditioning, or psychological issues. It is important to characterize the temporal pattern, severity, progression, relation to exertion or other triggers, the smoking history, environmental and occupational exposures to pulmonary toxins, associated symptoms, and the history of pulmonary problems.¹

The physical examination may help to identify an airway or parenchymal disorder. Wheezing on chest examination would point to an obstructive defect and crackles to a possible restrictive problem, including pulmonary fibrosis. A cardiac examination should be performed to assess for evidence of heart failure, valvular heart disease, or the presence of loud P2 suggestive of pulmonary hypertension (PH). Laboratory studies, including complete blood counts are indicated.

A more complete pulmonary evaluation usually involves pulmonary function tests (PFTs), oximetry with exertion, and chest imaging. Additional cardiac testing might include electrocardiogram (ECG) and cardiac echocardiogram, followed by an exercise study, if needed. A B-natriuretic peptide determination could be considered if there is concern for congestive heart failure.²

►Dr. Clark: The initial physical examination was normal and laboratory tests were unrevealing. Given his history of asthma, he underwent spirometry testing (Table 1).

Dr. Goldstein, aside from unexplained dyspnea, what are other indications for spirometry and when should we consider ordering a full PFT, including lung volumes and diffusion capacity? Can you interpret this patient’s spirometry results?
 

►Dr. Goldstein: Spirometry is indicated to evaluate for a suspected obstructive defect. The test is usually performed with and without a bronchodilator to assess airway reactivity. A change in > 12% and > 200 mL suggests acute bronchodilator responsiveness. Periodic spirometry determinations are useful to assess the effect of medications or progression of disease. A reduction in forced vital capacity (FVC) may suggest a restrictive component. This possibility requires measure of lung volumes.

A full set of PFTs (ie, spirometry plus assessment of lung volumes and diffusion capacity) is required to evaluate the abnormalities associated with chronic obstructive pulmonary disease (COPD), interstitial diseases, vascular abnormalities (particularly PH), as well as for certain preoperative assessments. The single breath diffusing capacity for carbon monoxide is a measure of the overall capillary alveolar surface area of the lung. It is decreased in emphysema and interstitial disease as well as pulmonary vascular disorders. It would be particularly useful in this case as the spirometry studies were normal.

In this case, the normal FVC renders a significant restrictive disorder unlikely and his normal forced expiratory volume (FEV₁) and FEV₁/FVC make a significant obstructive disorder unlikely. He did not show any bronchodilator response; however, this finding does not exclude the presence of underlying asthma or reactive airway disease as patients often will not show a bronchodilator response at time of testing if they are not experiencing active bronchospasm or constriction. Further provocative testing with a methacholine challenge could be used to assess for reactive airway disease.

►Dr. Clark: The patient continued to have dyspnea when he returned to his PCP. Given his family history of premature CAD, an ECG was obtained that showed normal sinus rhythm at a rate of 70 beats per minute. A cardiology consult was placed, and he was referred for cardiac stress testing.

Dr. Maron, there are many forms of cardiac stress tests. In this case, the patient is referred for a stress test due his dyspnea. Does that symptom help you decide which test to order? How often does dyspnea present as an anginal equivalent in the absence of other cardiovascular symptoms or known cardiovascular disease?

►Bradley Maron, MD, Codirector, Pulmonary Vascular Disease Center, VABHS: In this case, stress testing should include a functional (ie, exercise) assessment if possible. Exercise capacity is a critical determinant of prognosis across the spectrum of cardiovascular disease and in a young person can be particularly informative on global health status. Furthermore, the chief complaint from this patient is dyspnea on exertion, and therefore, exercise testing is likely to be needed to reproduce or provoke the main symptom in this case. Estimates for dyspnea as a presenting symptom for ischemic heart disease vary but may be as high as 25%.³ It should be noted that cardiopulmonary exercise testing is useful for evaluating patients with unexplained dyspnea, as exercise hypoxemia, blunted decrease in V_D/V_T (ventilatory dead space/tidal volume), and evidence of a pulmonary mechanical limit to physical activity can inform the differential diagnosis.

►Dr. Clark: The patient underwent exercise treadmill testing and was able reach the target heart rate (> 85% age-predicted maximal heart rate) and achieve 11 metabolic equivalents. He had no chest pain or diagnostic ECG changes. The report made no mention of whether he experienced dyspnea during the test and was read as negative for exercise-induced ischemia.

He was seen by a cardiologist who noted an increased intensity S2 heart sound on examination without any other cardiopulmonary findings. It was noted that his symptoms occurred when tamping the ground or starting to walk up a hill but resolved with rest. It was also noted that his symptoms did not occur with gradual increased activity such as that performed during an exercise tolerance test. A 2-view chest X-ray was obtained and read as normal. Given the data from this evaluation thus far, the patient was told that his symptoms were most likely a result of his asthma exacerbated by dirt and dust exposure. Continued use of albuterol inhaler therapy was recommended, and no further diagnostic assessment was pursued.

Approximately 11 months later, the patient presented again to his PCP and reported progressive dyspnea. He had delayed seeking further care as he started to “feel like my symptoms were possibly in my head” given his prior negative workup. His symptoms had escalated drastically to the point where he felt short of breath with minimal exertion in addition to feeling sweaty, dizzy, fatigued, and having near-syncope when standing.

He was referred for a transthoracic echocardiogram (TTE) that revealed a left ventricular ejection fraction (LVEF) of 55 to 60% with diastolic relaxation abnormality and a normal-sized left atrium. The TTE also showed (qualitatively) a moderately dilated right ventricle with reduced systolic function, moderately severe tricuspid regurgitation, and severe elevation (> 60 mm Hg) in estimated right ventricular systolic pressure.

Dr. Maron, can you comment on how these findings may explain the patient’s symptoms? What differential diagnoses would you now consider?
 

►Dr. Maron: These echocardiography results exclude left ventricular systolic dysfunction or primary left-sided valvular disease at rest as a cause of the patient’s symptoms. In light of the patient’s prior normal stress test, high grade coronary disease in the absence of LV systolic dysfunction on echocardiography also seems unlikely. Estimated pulmonary artery systolic pressure > 60 mm Hg by echocardiography is highly suggestive of PH, but in and of itself does not diagnose PH nor inform pulmonary artery wedge pressure or pulmonary vascular resistance. Along with a direct measurement of pulmonary artery (PA) pressure, these data are needed to establish, classify, and prognosticate PH clinically.

►Dr. Clark: The patient was referred to a pulmonologist. His examination included bibasilar crackles and an enhanced P2 heart sound. A comprehensive pulmonary history was obtained, which noted his smoking history, possible asbestos exposure while serving in the Coast Guard, nighttime snoring without witnessed apnea events, and no personal or family history of thromboembolism or connective tissue disease.

Dr. Goldstein, is there anything in this patient’s history that could explain his symptoms and echocardiograph findings? Which tests would you order next?
 

►Dr. Goldstein: PH may be secondary to a wide variety of disorders including left heart disease (Group 2), advanced COPD, interstitial fibrosis, obstructive sleep apnea (OSA), or other lung diseases (Group 3), thromboembolic disorders (Group 4), and other systemic diseases such as sarcoidosis (Group 5). Group 1 is pulmonary arterial hypertension. (Table 2).

A right heart catheterization should be done to confirm the PA pressures estimated by echocardiogram. As to a cause, clinically he does not have heart failure. The limited smoking history and spirometry data do not support advanced COPD. He was noted to have crackles on physical examination suggesting an interstitial disorder. To assess the extent of interstitial disease, we would obtain a noncontrast computed tomography (CT) of the chest. The history of snoring suggesting the possibility of OSA indicating the need for overnight oximetry as significant nocturnal hypoxemia is a possible contributing cause to PH. A polysomnogram would be required to fully evaluate a sleep disturbance. The possible asbestos exposure is not likely a contributing factor as asbestosis requires significant exposure. We would obtain a ventilation/perfusion (V/Q) scan to rule out chronic thromboembolic disease. Targeted tests for causes of Group 5 disease should also be done.
 

►Dr. Clark: The impression from his pulmonologist was that the patient has severe PH, though the specific etiology was not yet known. Dr. Maron, can you review for us the pathophysiology behind PH and describe how the disease is classified?

►Dr. Maron: Elevated mean pulmonary artery pressure (> 20 mm Hg) diagnosed by supine right heart catheterization is the sine qua non of PH.⁴ However, this alone does not inform pathophysiology. As Dr. Goldstein noted, elevated PA pressure may be due to left heart disease, primary parenchymal lung disease/sleep-disordered breathing, in situ thrombotic remodeling of pulmonary arterioles following prior luminal pulmonary embolism, or in the setting of various specific predisposing conditions, such as sickle cell disease and sarcoidosis among others.⁵

Alternatively, pulmonary arterial hypertension (PAH) is suspected in patients with no identifiable cause of PH, pulmonary artery wedge pressure 15 mm Hg and pulmonary vascular resistance of 3.0 Wood units.⁶ Importantly, PAH is not synonymous with PH but is a circumspect PH disease subgroup. In turn, PAH may be idiopathic, hereditary, or associated with other select, predisposing disorders, namely systemic sclerosis. In PAH, the interplay between genetic and molecular factors results in effacement of distal pulmonary arterioles due to plexigenic, fibrotic, and/or concentric hypertrophic remodeling. Increased vascular resistance promotes early right ventricular dilation and impaired systolic function. As a result, patients with PAH are at particularly elevated risk for cor pulmonale.
 

►Dr. Clark: Overnight oximetry revealed baseline oxygen saturation of 94%, an oxygen nadir of 84% with a total of 7 minutes with oxygen < 90%. On a 6-minute walk test, the patient had a max heart rate of 116 and oxygen nadir of 93%. Chest CT with and without contrast showed no evidence of pulmonary emboli but noted mild emphysematous changes. A V/Q revealed no evidence of acute or chronic pulmonary thromboembolic disease. Coronary catheterization showed normal coronary anatomy without significant CAD. A right heart catheterization showed findings consistent with severe PH with normal left-sided filling pressures (Table 3).

The patient returned a normal antinuclear antibody, C-reactive protein, HIV, and liver function panel. Based on these findings, a presumptive diagnosis of group 1 PH (idiopathic PAH) was made. Given the severity of his right heart dysfunction, he was transferred to the cardiac care unit and initiated on epoprostenol.

Dr. Maron, can you review the different treatment options for idiopathic PAH and explain why epoprostenol was chosen for this patient?
 

►Dr. Maron: There are 14 US Food and Drug Administration-approved drug therapies for patients with PAH, which all target either nitric oxide signaling, endothelin receptors, or the prostacyclin pathway. In the current era, treatment-naïve patients with PAH are generally initiated on calcium channel antagonist therapy if there is evidence of vasoreactivity during right heart catheterization (following nitric oxide administration), dual therapy most often with an endothelin receptor antagonist and phosphodiesterase inhibitor, or parenteral prostacyclin therapy. Since < 5% of patients will demonstrate vasoreactivity, the decision at point of care in incident patients with PAH often focuses on dual oral therapy or initiation of parenteral prostacyclin therapy. In this case, the patient reported presyncope with minimal physical activity (eg, bending over or walking up stairs) and severely decreased functional status (ie, New York Heart Association Functional [NYHA] Class III – IV), and he had a cardiac index within the range of cardiogenic shock (< 2.0 L/min/m²). Collectively, this clinical profile is considered particularly high risk, therefore, a recommendation for parenteral continuous prostacyclin therapy was made.

► Dr. Clark: The patient tolerated epoprostenol and reported improvement in his symptoms. He had a tunneled line catheter placed for continuous epoprostenol infusion. He was discharged home and scheduled for outpatient follow-up in a PH clinic. At 4 months following discharge, he was reporting steady clinical and functional improvement as well as improvement in his dyspnea. A second therapy (oral phosphodiesterase type-V inhibitor) was initiated and tolerated well. Overall, he reported resolution of presyncope, NYHA Functional Class II symptoms, and the absence of important drug effects.

A 53-year-old woman presents for evaluation of persistent abdominal pain over the past 6 months. She reports the pain is about a 7 out of 10, located in the right upper quadrant. The pain does not worsen with food and not relieved with bowel movements. She has no nausea or vomiting. She reports that the pain worsens when she is sitting or standing and is relieved by lying down. Her past medical history includes having had a cholecystectomy in 2016, having hypertension, and having type 2 diabetes mellitus.

The patient’s medications include metformin, lisinopril, and empagliflozin. Her blood pressure was 130/70, and her pulse was 80. An abdominal exam of her found tenderness to palpation in the right upper quadrant, and no rebound tenderness. Her labs found a white blood cell count of 5.4, a hematocrit of 44%, an erythrocyte sedimentation rate of 13, a C-reactive protein of 1.0, a bilirubin of .8, an alkaline phosphatase of 100, an aspartate aminotransferase of 30, and an alanine transaminase of 22.



What is the most appropriate next step?

A) Right side up oblique ultrasound.

B) Abdominal CT scan.

C) Upper endoscopy.

D) More detailed physical exam.



The correct answer here is D, a more detailed physical exam is needed. Given the positional nature of this patient’s abdominal pain, an evaluation for an abdominal wall cause is appropriate.

Abdominal wall pain as a cause of chronic abdominal pain is rarely considered, but it really should be. Costanza and colleagues looked at 2,709 patients referred to gastroenterologists for chronic abdominal pain.¹ Chronic abdominal wall pain was diagnosed in 137 patients, with the diagnosis unchanged in 97% of these patients after 4 years. Most of the patients were women (four to one), and the diagnosis was almost always unsuspected by the referring physician. Physical exam was helpful in suggesting the diagnosis of abdominal wall pain.

The use of Carnett sign can be helpful. A positive Carnett sign is when abdominal pain increases or remains unchanged with tensing abdomen or when the examiner palpates the tensed abdomen. Thompson and colleagues looked at the outcome of 72 patients with undiagnosed abdominal pain and a positive Carnett sign.² Despite multiple diagnostic tests and surgeries done on these patients, very few of them had serious underlying pathology.

Thompson and Frances published another study looking at 120 patients presenting to an ED with undiagnosed abdominal pain.³ Twenty-four of the patients had positive abdominal wall tenderness on exam, and of those, only 1 had intra-abdominal pathology.

In another study, 158 patients admitted to the hospital with abdominal pain were evaluated for the presence of abdominal wall pain.⁴ Fifty-three patients were diagnosed with appendicitis, and 5 had abdominal wall tenderness on exam. Thirty-eight patients had other intra-abdominal pathology, and none of those had abdominal wall tenderness on exam. Of the 67 patients in the study who had nonspecific abdominal pain, 19 had abdominal wall tenderness on exam.

Most physicians do not include evaluation for abdominal wall tenderness as part of their evaluation of patients with abdominal pain. I think looking for this is helpful and, if positive, may lead to a diagnosis, as well as reduce the likelihood of intra-abdominal diagnoses.
 

What can we do in regard to therapy for patients with an abdominal wall source of pain?

Many patients with abdominal wall pain have anterior cutaneous nerve entrapment syndrome (ACNES). Patient’s with this often have discrete areas of tenderness on exam, often on the lateral edge of the rectus sheath, frequently on the right side of the abdomen. Anesthetic injection at the point of tenderness provides immediate relief for patients with ACNES, and is helpful in confirming the diagnosis.

Boelens and colleagues did injections in 48 patients suspected of having ACNE, randomizing half to receive lidocaine and half to receive saline placebo.5The majority of the patients receiving lidocaine (54%) had a response, compared with 17% of placebo patients (P less than .007).

Greenbaum and colleagues studied 79 patients with chronic abdominal wall pain.⁶ In this study, 72 of 79 patients had greater than 50% pain relief with anesthetic injection and were followed for a mean of almost 14 months. Only four of these patients ended up having a visceral cause of pain.
 

Can using injections help pain from ACNES longer term?

Koop and colleagues looked at all published studies in regards to both immediate and longer-term pain relief with injections.⁷ Both lidocaine injections and injections with lidocaine plus steroids led to long-term pain relief (40%-50% of patients with multiple lidocaine injections and up to 80% with lidocaine plus steroid injections). I think that injections are certainly worth a try in patients with chronic abdominal wall pain.

Pearl

Consider chronic abdominal wall pain in your differential diagnoses for patients with chronic abdominal pain, and use Carnett sign to help with diagnosis.

Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and serves as third-year medical student clerkship director at the University of Washington. He is a member of the editorial advisory board of Internal Medicine News. Dr. Paauw has no conflicts to disclose. Contact him at [email protected].

References

1. Costanza CD et al. Clin Gastroenterol Hepatol. 2004 May;2(5):395-9.

2. Thomson WH et al. Br J Surg. 1991 Feb;78(2):223-5.

3. Thomson H, Francis DM. Lancet. 1977 Nov 19;2(8047):1053-4.

4. Gray DW et al. Ann R Coll Surg Engl. 1988 Jul;70(4):233-4.

5. Boelens OB et al. Br J Surg. 2013 Jan;100(2):217-21.

6. Greenbaum DS et al. Dig Dis Sci. 1994 Sep;39(9):1935-41.

7. Koop H et al. Dtsch Arztebl Int. 2016 Jan 29;113(4):51-7.


 

A 53-year-old woman presents for evaluation of persistent abdominal pain over the past 6 months. She reports the pain is about a 7 out of 10, located in the right upper quadrant. The pain does not worsen with food and not relieved with bowel movements. She has no nausea or vomiting. She reports that the pain worsens when she is sitting or standing and is relieved by lying down. Her past medical history includes having had a cholecystectomy in 2016, having hypertension, and having type 2 diabetes mellitus.

The patient’s medications include metformin, lisinopril, and empagliflozin. Her blood pressure was 130/70, and her pulse was 80. An abdominal exam of her found tenderness to palpation in the right upper quadrant, and no rebound tenderness. Her labs found a white blood cell count of 5.4, a hematocrit of 44%, an erythrocyte sedimentation rate of 13, a C-reactive protein of 1.0, a bilirubin of .8, an alkaline phosphatase of 100, an aspartate aminotransferase of 30, and an alanine transaminase of 22.



What is the most appropriate next step?

A) Right side up oblique ultrasound.

B) Abdominal CT scan.

C) Upper endoscopy.

D) More detailed physical exam.



The correct answer here is D, a more detailed physical exam is needed. Given the positional nature of this patient’s abdominal pain, an evaluation for an abdominal wall cause is appropriate.

Abdominal wall pain as a cause of chronic abdominal pain is rarely considered, but it really should be. Costanza and colleagues looked at 2,709 patients referred to gastroenterologists for chronic abdominal pain.¹ Chronic abdominal wall pain was diagnosed in 137 patients, with the diagnosis unchanged in 97% of these patients after 4 years. Most of the patients were women (four to one), and the diagnosis was almost always unsuspected by the referring physician. Physical exam was helpful in suggesting the diagnosis of abdominal wall pain.

The use of Carnett sign can be helpful. A positive Carnett sign is when abdominal pain increases or remains unchanged with tensing abdomen or when the examiner palpates the tensed abdomen. Thompson and colleagues looked at the outcome of 72 patients with undiagnosed abdominal pain and a positive Carnett sign.² Despite multiple diagnostic tests and surgeries done on these patients, very few of them had serious underlying pathology.

Thompson and Frances published another study looking at 120 patients presenting to an ED with undiagnosed abdominal pain.³ Twenty-four of the patients had positive abdominal wall tenderness on exam, and of those, only 1 had intra-abdominal pathology.

In another study, 158 patients admitted to the hospital with abdominal pain were evaluated for the presence of abdominal wall pain.⁴ Fifty-three patients were diagnosed with appendicitis, and 5 had abdominal wall tenderness on exam. Thirty-eight patients had other intra-abdominal pathology, and none of those had abdominal wall tenderness on exam. Of the 67 patients in the study who had nonspecific abdominal pain, 19 had abdominal wall tenderness on exam.

Most physicians do not include evaluation for abdominal wall tenderness as part of their evaluation of patients with abdominal pain. I think looking for this is helpful and, if positive, may lead to a diagnosis, as well as reduce the likelihood of intra-abdominal diagnoses.
 

What can we do in regard to therapy for patients with an abdominal wall source of pain?

Many patients with abdominal wall pain have anterior cutaneous nerve entrapment syndrome (ACNES). Patient’s with this often have discrete areas of tenderness on exam, often on the lateral edge of the rectus sheath, frequently on the right side of the abdomen. Anesthetic injection at the point of tenderness provides immediate relief for patients with ACNES, and is helpful in confirming the diagnosis.

Boelens and colleagues did injections in 48 patients suspected of having ACNE, randomizing half to receive lidocaine and half to receive saline placebo.5The majority of the patients receiving lidocaine (54%) had a response, compared with 17% of placebo patients (P less than .007).

Greenbaum and colleagues studied 79 patients with chronic abdominal wall pain.⁶ In this study, 72 of 79 patients had greater than 50% pain relief with anesthetic injection and were followed for a mean of almost 14 months. Only four of these patients ended up having a visceral cause of pain.
 

Can using injections help pain from ACNES longer term?

Koop and colleagues looked at all published studies in regards to both immediate and longer-term pain relief with injections.⁷ Both lidocaine injections and injections with lidocaine plus steroids led to long-term pain relief (40%-50% of patients with multiple lidocaine injections and up to 80% with lidocaine plus steroid injections). I think that injections are certainly worth a try in patients with chronic abdominal wall pain.

Pearl

Consider chronic abdominal wall pain in your differential diagnoses for patients with chronic abdominal pain, and use Carnett sign to help with diagnosis.

Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and serves as third-year medical student clerkship director at the University of Washington. He is a member of the editorial advisory board of Internal Medicine News. Dr. Paauw has no conflicts to disclose. Contact him at [email protected].

References

1. Costanza CD et al. Clin Gastroenterol Hepatol. 2004 May;2(5):395-9.

2. Thomson WH et al. Br J Surg. 1991 Feb;78(2):223-5.

3. Thomson H, Francis DM. Lancet. 1977 Nov 19;2(8047):1053-4.

4. Gray DW et al. Ann R Coll Surg Engl. 1988 Jul;70(4):233-4.

5. Boelens OB et al. Br J Surg. 2013 Jan;100(2):217-21.

6. Greenbaum DS et al. Dig Dis Sci. 1994 Sep;39(9):1935-41.

7. Koop H et al. Dtsch Arztebl Int. 2016 Jan 29;113(4):51-7.


 

A 53-year-old woman presents for evaluation of persistent abdominal pain over the past 6 months. She reports the pain is about a 7 out of 10, located in the right upper quadrant. The pain does not worsen with food and not relieved with bowel movements. She has no nausea or vomiting. She reports that the pain worsens when she is sitting or standing and is relieved by lying down. Her past medical history includes having had a cholecystectomy in 2016, having hypertension, and having type 2 diabetes mellitus.

The patient’s medications include metformin, lisinopril, and empagliflozin. Her blood pressure was 130/70, and her pulse was 80. An abdominal exam of her found tenderness to palpation in the right upper quadrant, and no rebound tenderness. Her labs found a white blood cell count of 5.4, a hematocrit of 44%, an erythrocyte sedimentation rate of 13, a C-reactive protein of 1.0, a bilirubin of .8, an alkaline phosphatase of 100, an aspartate aminotransferase of 30, and an alanine transaminase of 22.



What is the most appropriate next step?

A) Right side up oblique ultrasound.

B) Abdominal CT scan.

C) Upper endoscopy.

D) More detailed physical exam.



The correct answer here is D, a more detailed physical exam is needed. Given the positional nature of this patient’s abdominal pain, an evaluation for an abdominal wall cause is appropriate.

Abdominal wall pain as a cause of chronic abdominal pain is rarely considered, but it really should be. Costanza and colleagues looked at 2,709 patients referred to gastroenterologists for chronic abdominal pain.¹ Chronic abdominal wall pain was diagnosed in 137 patients, with the diagnosis unchanged in 97% of these patients after 4 years. Most of the patients were women (four to one), and the diagnosis was almost always unsuspected by the referring physician. Physical exam was helpful in suggesting the diagnosis of abdominal wall pain.

The use of Carnett sign can be helpful. A positive Carnett sign is when abdominal pain increases or remains unchanged with tensing abdomen or when the examiner palpates the tensed abdomen. Thompson and colleagues looked at the outcome of 72 patients with undiagnosed abdominal pain and a positive Carnett sign.² Despite multiple diagnostic tests and surgeries done on these patients, very few of them had serious underlying pathology.

Thompson and Frances published another study looking at 120 patients presenting to an ED with undiagnosed abdominal pain.³ Twenty-four of the patients had positive abdominal wall tenderness on exam, and of those, only 1 had intra-abdominal pathology.

In another study, 158 patients admitted to the hospital with abdominal pain were evaluated for the presence of abdominal wall pain.⁴ Fifty-three patients were diagnosed with appendicitis, and 5 had abdominal wall tenderness on exam. Thirty-eight patients had other intra-abdominal pathology, and none of those had abdominal wall tenderness on exam. Of the 67 patients in the study who had nonspecific abdominal pain, 19 had abdominal wall tenderness on exam.

Most physicians do not include evaluation for abdominal wall tenderness as part of their evaluation of patients with abdominal pain. I think looking for this is helpful and, if positive, may lead to a diagnosis, as well as reduce the likelihood of intra-abdominal diagnoses.
 

What can we do in regard to therapy for patients with an abdominal wall source of pain?

Many patients with abdominal wall pain have anterior cutaneous nerve entrapment syndrome (ACNES). Patient’s with this often have discrete areas of tenderness on exam, often on the lateral edge of the rectus sheath, frequently on the right side of the abdomen. Anesthetic injection at the point of tenderness provides immediate relief for patients with ACNES, and is helpful in confirming the diagnosis.

Boelens and colleagues did injections in 48 patients suspected of having ACNE, randomizing half to receive lidocaine and half to receive saline placebo.5The majority of the patients receiving lidocaine (54%) had a response, compared with 17% of placebo patients (P less than .007).

Greenbaum and colleagues studied 79 patients with chronic abdominal wall pain.⁶ In this study, 72 of 79 patients had greater than 50% pain relief with anesthetic injection and were followed for a mean of almost 14 months. Only four of these patients ended up having a visceral cause of pain.
 

Can using injections help pain from ACNES longer term?

Koop and colleagues looked at all published studies in regards to both immediate and longer-term pain relief with injections.⁷ Both lidocaine injections and injections with lidocaine plus steroids led to long-term pain relief (40%-50% of patients with multiple lidocaine injections and up to 80% with lidocaine plus steroid injections). I think that injections are certainly worth a try in patients with chronic abdominal wall pain.

Pearl

Consider chronic abdominal wall pain in your differential diagnoses for patients with chronic abdominal pain, and use Carnett sign to help with diagnosis.

Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and serves as third-year medical student clerkship director at the University of Washington. He is a member of the editorial advisory board of Internal Medicine News. Dr. Paauw has no conflicts to disclose. Contact him at [email protected].

References

1. Costanza CD et al. Clin Gastroenterol Hepatol. 2004 May;2(5):395-9.

2. Thomson WH et al. Br J Surg. 1991 Feb;78(2):223-5.

3. Thomson H, Francis DM. Lancet. 1977 Nov 19;2(8047):1053-4.

4. Gray DW et al. Ann R Coll Surg Engl. 1988 Jul;70(4):233-4.

5. Boelens OB et al. Br J Surg. 2013 Jan;100(2):217-21.

6. Greenbaum DS et al. Dig Dis Sci. 1994 Sep;39(9):1935-41.

7. Koop H et al. Dtsch Arztebl Int. 2016 Jan 29;113(4):51-7.