The Journal of Family Practice

Echocardiograms were done, but who was reading them?

A 67-YEAR-OLD MAN had been under the care of his primary care physician for aortic stenosis. The physician was aware of this diagnosis and did periodic echocardiograms to monitor the patient’s heart. The patient was sent to a cardiologist for additional care. Over the next year and a half, the decedent’s condition worsened, and he died of heart failure.

PLAINTIFF’S CLAIM The defendants deviated from the standard of care in not reading the echocardiograms. If they had, they could have treated him and extended his life.

THE DEFENSE The cardiologist said it was not up to him to read the echocardiogram. The primary care physician acknowledged that he deviated from the standard of care.

VERDICT $3 million Connecticut verdict.

Don't assume the specialist has taken charge; verify or manage the patient yourself.

COMMENT This is a clear case of failure to take responsibility. I suspect the failure was based on the assumption by both physicians that the other physician was monitoring the patient’s status.

This happened to me with a patient who gradually drifted into acute heart failure while I assumed the nephrologist was managing his diuretics. A phone call and more furosemide would have prevented that hospital admission. (Luckily, my patient recovered uneventfully.)

Don’t assume the specialist has taken charge; verify or manage the patient yourself.

Third call to help line finally leads to office visit, but it’s too late

A 42-YEAR-OLD WOMAN called a phone help line and told a nurse that she had a fever, chills, sore throat, and severe chest pain. The next day she called again and spoke with a nurse who routed her call to a physician. The physician diagnosed the woman with influenza during their 4-minute conversation. She called again the next day and was told to come in for examination. The woman did so and was admitted. One day later, she died of sepsis secondary to pneumonia.

PLAINTIFF’S CLAIM The standard of care required immediate examination by the time of the second call.

THE DEFENSE The plaintiff did not actually report chest pain until the second call, and she contracted an unusually fast-acting strain of pneumonia.

VERDICT $3.5 million California arbitration award.

COMMENT Delayed diagnosis is one of the main reasons family physicians are successfully sued. Management of this patient may have been reasonable the first day. The second call should have prompted a same day visit or instructions to go to the emergency department or at least an urgent care facility. The third call was too late.

Echocardiograms were done, but who was reading them?

A 67-YEAR-OLD MAN had been under the care of his primary care physician for aortic stenosis. The physician was aware of this diagnosis and did periodic echocardiograms to monitor the patient’s heart. The patient was sent to a cardiologist for additional care. Over the next year and a half, the decedent’s condition worsened, and he died of heart failure.

PLAINTIFF’S CLAIM The defendants deviated from the standard of care in not reading the echocardiograms. If they had, they could have treated him and extended his life.

THE DEFENSE The cardiologist said it was not up to him to read the echocardiogram. The primary care physician acknowledged that he deviated from the standard of care.

VERDICT $3 million Connecticut verdict.

Don't assume the specialist has taken charge; verify or manage the patient yourself.

COMMENT This is a clear case of failure to take responsibility. I suspect the failure was based on the assumption by both physicians that the other physician was monitoring the patient’s status.

This happened to me with a patient who gradually drifted into acute heart failure while I assumed the nephrologist was managing his diuretics. A phone call and more furosemide would have prevented that hospital admission. (Luckily, my patient recovered uneventfully.)

Don’t assume the specialist has taken charge; verify or manage the patient yourself.

Third call to help line finally leads to office visit, but it’s too late

A 42-YEAR-OLD WOMAN called a phone help line and told a nurse that she had a fever, chills, sore throat, and severe chest pain. The next day she called again and spoke with a nurse who routed her call to a physician. The physician diagnosed the woman with influenza during their 4-minute conversation. She called again the next day and was told to come in for examination. The woman did so and was admitted. One day later, she died of sepsis secondary to pneumonia.

PLAINTIFF’S CLAIM The standard of care required immediate examination by the time of the second call.

THE DEFENSE The plaintiff did not actually report chest pain until the second call, and she contracted an unusually fast-acting strain of pneumonia.

VERDICT $3.5 million California arbitration award.

COMMENT Delayed diagnosis is one of the main reasons family physicians are successfully sued. Management of this patient may have been reasonable the first day. The second call should have prompted a same day visit or instructions to go to the emergency department or at least an urgent care facility. The third call was too late.

Echocardiograms were done, but who was reading them?

A 67-YEAR-OLD MAN had been under the care of his primary care physician for aortic stenosis. The physician was aware of this diagnosis and did periodic echocardiograms to monitor the patient’s heart. The patient was sent to a cardiologist for additional care. Over the next year and a half, the decedent’s condition worsened, and he died of heart failure.

PLAINTIFF’S CLAIM The defendants deviated from the standard of care in not reading the echocardiograms. If they had, they could have treated him and extended his life.

THE DEFENSE The cardiologist said it was not up to him to read the echocardiogram. The primary care physician acknowledged that he deviated from the standard of care.

VERDICT $3 million Connecticut verdict.

Don't assume the specialist has taken charge; verify or manage the patient yourself.

COMMENT This is a clear case of failure to take responsibility. I suspect the failure was based on the assumption by both physicians that the other physician was monitoring the patient’s status.

This happened to me with a patient who gradually drifted into acute heart failure while I assumed the nephrologist was managing his diuretics. A phone call and more furosemide would have prevented that hospital admission. (Luckily, my patient recovered uneventfully.)

Don’t assume the specialist has taken charge; verify or manage the patient yourself.

Third call to help line finally leads to office visit, but it’s too late

A 42-YEAR-OLD WOMAN called a phone help line and told a nurse that she had a fever, chills, sore throat, and severe chest pain. The next day she called again and spoke with a nurse who routed her call to a physician. The physician diagnosed the woman with influenza during their 4-minute conversation. She called again the next day and was told to come in for examination. The woman did so and was admitted. One day later, she died of sepsis secondary to pneumonia.

PLAINTIFF’S CLAIM The standard of care required immediate examination by the time of the second call.

THE DEFENSE The plaintiff did not actually report chest pain until the second call, and she contracted an unusually fast-acting strain of pneumonia.

VERDICT $3.5 million California arbitration award.

COMMENT Delayed diagnosis is one of the main reasons family physicians are successfully sued. Management of this patient may have been reasonable the first day. The second call should have prompted a same day visit or instructions to go to the emergency department or at least an urgent care facility. The third call was too late.

THE CASE

A 45-year-old airman presented to our medical group with acute onset of sharp, positional left lateral chest wall pain that he’d had for 2 days. The pain began after an extreme core body workout. Treatment with ibuprofen 800 mg and local electrical stimulation one day prior provided no benefit. The patient reported the pain to be a 6 out of 10 when still and a 9 to 10 when sitting for more than a few minutes, turning, or taking a medium to deep breath. The patient felt “dangerously distracted by the pain” while driving in for his appointment.

We noted focal left lower lateral intercostal muscle tenderness without trigger point-like thickness or spasm. The patient also had restricted inspiration, secondary to the severe pain, and decreased left lower field breath sounds. His vital signs were normal, as was his cardiac exam.

THE DIAGNOSIS

While awaiting a chest x-ray, the patient was offered and opted to try acupuncture for pain relief. (We have medical acupuncturists on staff.) Analgesics had already been used, but had provided little relief.

We identified 4 acupuncture sites in the ear: 2 were battlefield acupuncture (BFA) points (more on this in a bit) and 2 points were deemed active by a skin conductance point finder (a handheld device that assesses changes in electrical skin resistance at auricular acupuncture points). The left ear points that were treated included the cingulate gyrus (intertragic notch), Shen Men (triangular fossa), and chest and abdomen regional points (antihelix) (FIGURE 1).

Within 15 minutes, the patient reported significant pain relief and was able to inspire deeply without pain. The patient also underwent a chest x-ray, which revealed atelectasis of the left lower lobe (FIGURE 2A) caused by pain-induced hypoventilation.

Because the patient’s pain was so well controlled, he returned to work immediately after the appointment. At the end of his shift 6 hours later he returned, unscheduled, to report pain at a level of one out of 10 and said he was able to breathe normally. In addition, lung auscultation was normal and a repeat chest x-ray revealed that the atelectasis had almost completely resolved (FIGURE 2B). This occurred without medication or other therapy. The pain did not return.

DISCUSSION

Although acupuncture is over 2000 years old, it has been largely disregarded in the United States due to a lack of mainstream evidence supporting its efficacy. Research is hindered by significant variation in approach between providers, the difficulties inherent to blinding patients and providers to treatment vs placebo, and poor insurance coverage and reimbursement.

Acupuncture research is burgeoning. A 2012 meta-analysis concluded that patients receiving acupuncture had less pain than those receiving sham or no acupuncture for several pain conditions. Specifically, scores for back and neck pain, osteoarthritis, and chronic headache were 0.23, 0.16, and 0.15 standard deviations (SDs), respectively, lower for patients receiving acupuncture than for those who got sham acupuncture. The effect sizes for acupuncture patients compared to no acupuncture controls were 0.55, 0.57, and 0.42 respectively (all P<.001).¹

Several theories explain how auricular acupuncture may work. Paul Nogier, MD, noted that the ear is composed of ectodermal, mesodermal, and endodermal tissues, and mapped the “inverted fetus” homunculus in the ear, which corresponds to specific body points.² Functional magnetic resonance imaging has demonstrated increased brain activity in the cingulate gyrus and thalamic regions in response to a painful stimulus, as well as attenuation of this activity after the placement of needles in corresponding auricular cingulate gyrus and thalamus points.³ In addition, research has confirmed that acupuncture raises serum and cerebrospinal levels of endorphins and enkephalins.⁴

Less than 15 minutes after needle placement, our patient reported significant pain relief and was able to inspire deeply without pain.

Battlefield acupuncture (BFA) was developed by Richard Niemtzow, MD, and has been used for acute injuries in the front lines of battle as well as for many health conditions. BFA treats pain using a sequence of 5 predetermined auricular acupuncture points.⁵ Onset and duration of pain relief vary depending on the location and nature of the pathology. We’ve noted that BFA for chronic pain has a shorter duration of benefit and is more likely to need to be repeated.

One randomized pilot study involving 87 patients presenting to the emergency room blinded emergency health care providers to the inclusion of the first 2 BFA points in their otherwise usual care of acute pain patients. Participants in the acupuncture group experienced a 23% reduction in pain before discharge compared to no change in the standard care group (P<.0005).⁶

Our patient. We inserted semi-permanent needles with a needle length of 2 mm into 4 locations on the ear. (These needles can remain in the ear for several days and fall out on their own or they may be removed by pulling the stud ends.) As noted earlier, our patient reported pain relief within 15 minutes and was pain free by the next day.

THE TAKEAWAY

Research confirms that acupuncture raises serum and cerebrospinal levels of endorphins and enkephalins.

Auricular acupuncture can treat acute and chronic pain. As proof, the BFA technique is widely used by health care providers throughout the US military and Department of Veterans Affairs. In this case, the immediate pain relief and x-ray documentation of atelectasis resolution within 6 hours of treatment provide support that auricular acupuncture was beneficial in reversing the cause of this atelectasis, which was pain-induced hypoventilation.

While the acute pain control observed with this patient is not unusual in our experience, what is unusual is the rare visual confirmation of the striking degree of pain reduction possible with auricular acupuncture.

THE CASE

A 45-year-old airman presented to our medical group with acute onset of sharp, positional left lateral chest wall pain that he’d had for 2 days. The pain began after an extreme core body workout. Treatment with ibuprofen 800 mg and local electrical stimulation one day prior provided no benefit. The patient reported the pain to be a 6 out of 10 when still and a 9 to 10 when sitting for more than a few minutes, turning, or taking a medium to deep breath. The patient felt “dangerously distracted by the pain” while driving in for his appointment.

We noted focal left lower lateral intercostal muscle tenderness without trigger point-like thickness or spasm. The patient also had restricted inspiration, secondary to the severe pain, and decreased left lower field breath sounds. His vital signs were normal, as was his cardiac exam.

THE DIAGNOSIS

While awaiting a chest x-ray, the patient was offered and opted to try acupuncture for pain relief. (We have medical acupuncturists on staff.) Analgesics had already been used, but had provided little relief.

We identified 4 acupuncture sites in the ear: 2 were battlefield acupuncture (BFA) points (more on this in a bit) and 2 points were deemed active by a skin conductance point finder (a handheld device that assesses changes in electrical skin resistance at auricular acupuncture points). The left ear points that were treated included the cingulate gyrus (intertragic notch), Shen Men (triangular fossa), and chest and abdomen regional points (antihelix) (FIGURE 1).

Within 15 minutes, the patient reported significant pain relief and was able to inspire deeply without pain. The patient also underwent a chest x-ray, which revealed atelectasis of the left lower lobe (FIGURE 2A) caused by pain-induced hypoventilation.

Because the patient’s pain was so well controlled, he returned to work immediately after the appointment. At the end of his shift 6 hours later he returned, unscheduled, to report pain at a level of one out of 10 and said he was able to breathe normally. In addition, lung auscultation was normal and a repeat chest x-ray revealed that the atelectasis had almost completely resolved (FIGURE 2B). This occurred without medication or other therapy. The pain did not return.

DISCUSSION

Although acupuncture is over 2000 years old, it has been largely disregarded in the United States due to a lack of mainstream evidence supporting its efficacy. Research is hindered by significant variation in approach between providers, the difficulties inherent to blinding patients and providers to treatment vs placebo, and poor insurance coverage and reimbursement.

Acupuncture research is burgeoning. A 2012 meta-analysis concluded that patients receiving acupuncture had less pain than those receiving sham or no acupuncture for several pain conditions. Specifically, scores for back and neck pain, osteoarthritis, and chronic headache were 0.23, 0.16, and 0.15 standard deviations (SDs), respectively, lower for patients receiving acupuncture than for those who got sham acupuncture. The effect sizes for acupuncture patients compared to no acupuncture controls were 0.55, 0.57, and 0.42 respectively (all P<.001).¹

Several theories explain how auricular acupuncture may work. Paul Nogier, MD, noted that the ear is composed of ectodermal, mesodermal, and endodermal tissues, and mapped the “inverted fetus” homunculus in the ear, which corresponds to specific body points.² Functional magnetic resonance imaging has demonstrated increased brain activity in the cingulate gyrus and thalamic regions in response to a painful stimulus, as well as attenuation of this activity after the placement of needles in corresponding auricular cingulate gyrus and thalamus points.³ In addition, research has confirmed that acupuncture raises serum and cerebrospinal levels of endorphins and enkephalins.⁴

Less than 15 minutes after needle placement, our patient reported significant pain relief and was able to inspire deeply without pain.

Battlefield acupuncture (BFA) was developed by Richard Niemtzow, MD, and has been used for acute injuries in the front lines of battle as well as for many health conditions. BFA treats pain using a sequence of 5 predetermined auricular acupuncture points.⁵ Onset and duration of pain relief vary depending on the location and nature of the pathology. We’ve noted that BFA for chronic pain has a shorter duration of benefit and is more likely to need to be repeated.

One randomized pilot study involving 87 patients presenting to the emergency room blinded emergency health care providers to the inclusion of the first 2 BFA points in their otherwise usual care of acute pain patients. Participants in the acupuncture group experienced a 23% reduction in pain before discharge compared to no change in the standard care group (P<.0005).⁶

Our patient. We inserted semi-permanent needles with a needle length of 2 mm into 4 locations on the ear. (These needles can remain in the ear for several days and fall out on their own or they may be removed by pulling the stud ends.) As noted earlier, our patient reported pain relief within 15 minutes and was pain free by the next day.

THE TAKEAWAY

Research confirms that acupuncture raises serum and cerebrospinal levels of endorphins and enkephalins.

Auricular acupuncture can treat acute and chronic pain. As proof, the BFA technique is widely used by health care providers throughout the US military and Department of Veterans Affairs. In this case, the immediate pain relief and x-ray documentation of atelectasis resolution within 6 hours of treatment provide support that auricular acupuncture was beneficial in reversing the cause of this atelectasis, which was pain-induced hypoventilation.

While the acute pain control observed with this patient is not unusual in our experience, what is unusual is the rare visual confirmation of the striking degree of pain reduction possible with auricular acupuncture.

THE CASE

A 45-year-old airman presented to our medical group with acute onset of sharp, positional left lateral chest wall pain that he’d had for 2 days. The pain began after an extreme core body workout. Treatment with ibuprofen 800 mg and local electrical stimulation one day prior provided no benefit. The patient reported the pain to be a 6 out of 10 when still and a 9 to 10 when sitting for more than a few minutes, turning, or taking a medium to deep breath. The patient felt “dangerously distracted by the pain” while driving in for his appointment.

We noted focal left lower lateral intercostal muscle tenderness without trigger point-like thickness or spasm. The patient also had restricted inspiration, secondary to the severe pain, and decreased left lower field breath sounds. His vital signs were normal, as was his cardiac exam.

THE DIAGNOSIS

While awaiting a chest x-ray, the patient was offered and opted to try acupuncture for pain relief. (We have medical acupuncturists on staff.) Analgesics had already been used, but had provided little relief.

We identified 4 acupuncture sites in the ear: 2 were battlefield acupuncture (BFA) points (more on this in a bit) and 2 points were deemed active by a skin conductance point finder (a handheld device that assesses changes in electrical skin resistance at auricular acupuncture points). The left ear points that were treated included the cingulate gyrus (intertragic notch), Shen Men (triangular fossa), and chest and abdomen regional points (antihelix) (FIGURE 1).

Within 15 minutes, the patient reported significant pain relief and was able to inspire deeply without pain. The patient also underwent a chest x-ray, which revealed atelectasis of the left lower lobe (FIGURE 2A) caused by pain-induced hypoventilation.

Because the patient’s pain was so well controlled, he returned to work immediately after the appointment. At the end of his shift 6 hours later he returned, unscheduled, to report pain at a level of one out of 10 and said he was able to breathe normally. In addition, lung auscultation was normal and a repeat chest x-ray revealed that the atelectasis had almost completely resolved (FIGURE 2B). This occurred without medication or other therapy. The pain did not return.

DISCUSSION

Although acupuncture is over 2000 years old, it has been largely disregarded in the United States due to a lack of mainstream evidence supporting its efficacy. Research is hindered by significant variation in approach between providers, the difficulties inherent to blinding patients and providers to treatment vs placebo, and poor insurance coverage and reimbursement.

Acupuncture research is burgeoning. A 2012 meta-analysis concluded that patients receiving acupuncture had less pain than those receiving sham or no acupuncture for several pain conditions. Specifically, scores for back and neck pain, osteoarthritis, and chronic headache were 0.23, 0.16, and 0.15 standard deviations (SDs), respectively, lower for patients receiving acupuncture than for those who got sham acupuncture. The effect sizes for acupuncture patients compared to no acupuncture controls were 0.55, 0.57, and 0.42 respectively (all P<.001).¹

Several theories explain how auricular acupuncture may work. Paul Nogier, MD, noted that the ear is composed of ectodermal, mesodermal, and endodermal tissues, and mapped the “inverted fetus” homunculus in the ear, which corresponds to specific body points.² Functional magnetic resonance imaging has demonstrated increased brain activity in the cingulate gyrus and thalamic regions in response to a painful stimulus, as well as attenuation of this activity after the placement of needles in corresponding auricular cingulate gyrus and thalamus points.³ In addition, research has confirmed that acupuncture raises serum and cerebrospinal levels of endorphins and enkephalins.⁴

Less than 15 minutes after needle placement, our patient reported significant pain relief and was able to inspire deeply without pain.

Battlefield acupuncture (BFA) was developed by Richard Niemtzow, MD, and has been used for acute injuries in the front lines of battle as well as for many health conditions. BFA treats pain using a sequence of 5 predetermined auricular acupuncture points.⁵ Onset and duration of pain relief vary depending on the location and nature of the pathology. We’ve noted that BFA for chronic pain has a shorter duration of benefit and is more likely to need to be repeated.

One randomized pilot study involving 87 patients presenting to the emergency room blinded emergency health care providers to the inclusion of the first 2 BFA points in their otherwise usual care of acute pain patients. Participants in the acupuncture group experienced a 23% reduction in pain before discharge compared to no change in the standard care group (P<.0005).⁶

Our patient. We inserted semi-permanent needles with a needle length of 2 mm into 4 locations on the ear. (These needles can remain in the ear for several days and fall out on their own or they may be removed by pulling the stud ends.) As noted earlier, our patient reported pain relief within 15 minutes and was pain free by the next day.

THE TAKEAWAY

Research confirms that acupuncture raises serum and cerebrospinal levels of endorphins and enkephalins.

Auricular acupuncture can treat acute and chronic pain. As proof, the BFA technique is widely used by health care providers throughout the US military and Department of Veterans Affairs. In this case, the immediate pain relief and x-ray documentation of atelectasis resolution within 6 hours of treatment provide support that auricular acupuncture was beneficial in reversing the cause of this atelectasis, which was pain-induced hypoventilation.

While the acute pain control observed with this patient is not unusual in our experience, what is unusual is the rare visual confirmation of the striking degree of pain reduction possible with auricular acupuncture.

THE CASE

A 16-year-old boy presented to the emergency room (ER) with pain, redness, and swelling of his right upper arm that had been bothering him for 2 days. He was the quarterback of his high school football team, a sport that he’d been playing since he was 8 years old. He indicated that his football training—which involved repetitive throwing with his right arm—had intensified over the previous 2 months.

Prior to the ER visit, the patient was healthy and active with no significant medical history. He’d had no shoulder trauma and there was no family history of any coagulopathies, venous thrombosis, or pulmonary embolism. He denied chest pain, shortness of breath, palpitations, and fever, and said that he did not smoke cigarettes or drink alcohol.

On physical examination, his blood pressure was 118/70 mm Hg and his heart rate was 74 beats per minute. He had nonpitting edema and erythema of his right upper arm. His radial and brachial pulses were strong and equal in both arms. Assessment of neurologic and vascular integrity produced positive Wright’s and Adson’s tests, but a negative Halstead’s test. (For more on these tests, see: Wright’s test, Adson’s test, and Halstead’s test.) The circumference of the patient’s right upper arm was 2.5 cm greater than the left upper arm. The remainder of the physical exam was normal.

THE DIAGNOSIS

A duplex ultrasound of the right upper arm revealed an acute occlusive thrombus in the axillary vein. We started the patient on intravenous heparin. A venogram confirmed thrombosis of the axillary-subclavian vein (FIGURE 1A). Based on the patient’s clinical presentation and the results of the venogram, we diagnosed Paget-Schroetter syndrome. The venogram was followed by thrombolysis with alteplase (FIGURE 1B) and a balloon angioplasty (FIGURE 1C). One week later, a repeat venogram demonstrated partial removal of the thrombus and an area of compression on the inferior aspect of the subclavian vein due to a cervical band (FIGURE 1D).

DISCUSSION

Paget-Schroetter syndrome (PSS), or effort thrombosis of the upper extremities, is defined as spontaneous thrombus in the axillary and subclavian veins that occurs as a consequence of strenuous upper-extremity activity. It is a rare condition with an incidence of one to 2 cases per 100,000 people per year, and represents 1% to 4% of all cases of deep vein thrombosis (DVT).¹

Spontaneous thrombosis of the upper extremities typically presents in young, otherwise healthy individuals. It has been described in athletes who are involved in ball games, games with rackets or clubs, aquatic sports, combatant sports, and in violin players.² The repetitive movements used in these activities can lead to compression of the axillary and subclavian veins by hypertrophied muscles. Repetitive trauma causes intimal damage and thrombogenesis.³

PSS is characterized by the abrupt, spontaneous swelling of the entire arm, cyanosis, and pain that occurs with use or overhead positioning. Enlarged subcutaneous veins are present in the upper arm, around the shoulder, or in the upper anterior chest wall (Urschel’s sign). The classic presentation is acute onset of upper extremity pain and swelling in the dominant arm following a particularly strenuous activity.⁴ A low-grade fever, superficial thrombophlebitis, or neurologic symptoms may coexist. Certain provocative maneuvers can help reproduce the symptoms (TABLE 1^5,6). Complications of PSS include pulmonary embolism, postthrombotic syndrome (pain, heaviness, and swelling), and recurrent thrombosis.⁷

Contrast venography best shows the extent of thrombosis

Duplex ultrasound, with its high sensitivity and specificity, is the initial, noninvasive test of choice (TABLE 2^4,8-11). However, duplex ultrasound has a false-negative rate of 30% because it is highly technician-dependent and can be complicated by acoustic shadows from the clavicle or sternum.⁸

The most direct and definitive means to confirm the diagnosis of PSS is catheter-directed contrast venography.⁹ This method provides complete anatomic information regarding the site and extent of thrombosis, allows definitive evaluation of the collateral venous pathways, and is a necessary step toward the use of thrombolytic therapy. Contrast load, however, contraindicates the procedure in patients with renal failure and in those who are pregnant.

Contrast-enhanced computed tomography (CT) and magnetic resonance angiography (MRA) are also highly sensitive for detecting focal stenosis at the level of the first rib, the presence or absence of enlarged collateral veins, and the chronicity of any thrombus present. However, the usefulness of CT and magnetic resonance venography in initial screening is unclear, due to a lack of randomized controlled trials.

Treatment involves anticoagulants, thrombolytics, and possibly surgery

Prompt use of anticoagulation is indicated in PSS. Initial anticoagulation with low molecular weight unfractionated heparin or a direct thrombin inhibitor followed by warfarin for a minimum of 3 to 6 months is recommended.¹²

Patients treated with anticoagulation alone have a higher incidence of long-term residual symptoms, disability, and recurrent thrombosis.⁷ As a result, a more aggressive approach with the use of thrombolytic therapy is indicated, especially in young, active patients, to minimize long-term consequences. Alteplase or reteplase are used for this purpose. Thrombolysis is less likely to be beneficial if the thrombus is more than 2 weeks old or if there are inflammatory changes in the vein. The use of catheter-directed thrombolysis minimizes the risk of systemic adverse effects and achieves higher clot resolution rates.¹³

Because PSS is caused by compression of the vein, rather than a disorder of blood clotting, there is still a 50% to 70% risk of recurrent thrombosis despite thrombolysis and anticoagulation.¹⁴ Therefore, the most definitive management approach remains surgical treatment. Patients with recent thrombosis who are within the first several weeks of undergoing successful thrombolytic therapy are excellent candidates for surgery. Operative treatment for PSS includes first rib resection, scalene muscle removal, or subclavius muscle removal, along with removal of constricting scar tissue from around the vein.⁷

THE TAKEAWAY

PSS is characterized by upper-extremity DVT resulting from repetitive trauma to the subclavian-axillary vein. Early diagnosis of PSS with contrast venography and prompt use of anticoagulation can effectively restore venous patency, reduce the risk of rethrombosis, and return the patient to normal function. Primary care physicians should be aware of this condition, because delayed recognition in a high-functioning person can be potentially disabling.

Our patient had a first rib resection, partial division of the scalenus anterior and medius muscles, and lysis of the cervical band. Follow-up venography confirmed resolution of thrombosis without any complications. The patient was continued on anticoagulation with warfarin for 3 months.

THE CASE

A 16-year-old boy presented to the emergency room (ER) with pain, redness, and swelling of his right upper arm that had been bothering him for 2 days. He was the quarterback of his high school football team, a sport that he’d been playing since he was 8 years old. He indicated that his football training—which involved repetitive throwing with his right arm—had intensified over the previous 2 months.

Prior to the ER visit, the patient was healthy and active with no significant medical history. He’d had no shoulder trauma and there was no family history of any coagulopathies, venous thrombosis, or pulmonary embolism. He denied chest pain, shortness of breath, palpitations, and fever, and said that he did not smoke cigarettes or drink alcohol.

On physical examination, his blood pressure was 118/70 mm Hg and his heart rate was 74 beats per minute. He had nonpitting edema and erythema of his right upper arm. His radial and brachial pulses were strong and equal in both arms. Assessment of neurologic and vascular integrity produced positive Wright’s and Adson’s tests, but a negative Halstead’s test. (For more on these tests, see: Wright’s test, Adson’s test, and Halstead’s test.) The circumference of the patient’s right upper arm was 2.5 cm greater than the left upper arm. The remainder of the physical exam was normal.

THE DIAGNOSIS

A duplex ultrasound of the right upper arm revealed an acute occlusive thrombus in the axillary vein. We started the patient on intravenous heparin. A venogram confirmed thrombosis of the axillary-subclavian vein (FIGURE 1A). Based on the patient’s clinical presentation and the results of the venogram, we diagnosed Paget-Schroetter syndrome. The venogram was followed by thrombolysis with alteplase (FIGURE 1B) and a balloon angioplasty (FIGURE 1C). One week later, a repeat venogram demonstrated partial removal of the thrombus and an area of compression on the inferior aspect of the subclavian vein due to a cervical band (FIGURE 1D).

DISCUSSION

Paget-Schroetter syndrome (PSS), or effort thrombosis of the upper extremities, is defined as spontaneous thrombus in the axillary and subclavian veins that occurs as a consequence of strenuous upper-extremity activity. It is a rare condition with an incidence of one to 2 cases per 100,000 people per year, and represents 1% to 4% of all cases of deep vein thrombosis (DVT).¹

Spontaneous thrombosis of the upper extremities typically presents in young, otherwise healthy individuals. It has been described in athletes who are involved in ball games, games with rackets or clubs, aquatic sports, combatant sports, and in violin players.² The repetitive movements used in these activities can lead to compression of the axillary and subclavian veins by hypertrophied muscles. Repetitive trauma causes intimal damage and thrombogenesis.³

PSS is characterized by the abrupt, spontaneous swelling of the entire arm, cyanosis, and pain that occurs with use or overhead positioning. Enlarged subcutaneous veins are present in the upper arm, around the shoulder, or in the upper anterior chest wall (Urschel’s sign). The classic presentation is acute onset of upper extremity pain and swelling in the dominant arm following a particularly strenuous activity.⁴ A low-grade fever, superficial thrombophlebitis, or neurologic symptoms may coexist. Certain provocative maneuvers can help reproduce the symptoms (TABLE 1^5,6). Complications of PSS include pulmonary embolism, postthrombotic syndrome (pain, heaviness, and swelling), and recurrent thrombosis.⁷

Contrast venography best shows the extent of thrombosis

Duplex ultrasound, with its high sensitivity and specificity, is the initial, noninvasive test of choice (TABLE 2^4,8-11). However, duplex ultrasound has a false-negative rate of 30% because it is highly technician-dependent and can be complicated by acoustic shadows from the clavicle or sternum.⁸

The most direct and definitive means to confirm the diagnosis of PSS is catheter-directed contrast venography.⁹ This method provides complete anatomic information regarding the site and extent of thrombosis, allows definitive evaluation of the collateral venous pathways, and is a necessary step toward the use of thrombolytic therapy. Contrast load, however, contraindicates the procedure in patients with renal failure and in those who are pregnant.

Contrast-enhanced computed tomography (CT) and magnetic resonance angiography (MRA) are also highly sensitive for detecting focal stenosis at the level of the first rib, the presence or absence of enlarged collateral veins, and the chronicity of any thrombus present. However, the usefulness of CT and magnetic resonance venography in initial screening is unclear, due to a lack of randomized controlled trials.

Treatment involves anticoagulants, thrombolytics, and possibly surgery

Prompt use of anticoagulation is indicated in PSS. Initial anticoagulation with low molecular weight unfractionated heparin or a direct thrombin inhibitor followed by warfarin for a minimum of 3 to 6 months is recommended.¹²

Patients treated with anticoagulation alone have a higher incidence of long-term residual symptoms, disability, and recurrent thrombosis.⁷ As a result, a more aggressive approach with the use of thrombolytic therapy is indicated, especially in young, active patients, to minimize long-term consequences. Alteplase or reteplase are used for this purpose. Thrombolysis is less likely to be beneficial if the thrombus is more than 2 weeks old or if there are inflammatory changes in the vein. The use of catheter-directed thrombolysis minimizes the risk of systemic adverse effects and achieves higher clot resolution rates.¹³

Because PSS is caused by compression of the vein, rather than a disorder of blood clotting, there is still a 50% to 70% risk of recurrent thrombosis despite thrombolysis and anticoagulation.¹⁴ Therefore, the most definitive management approach remains surgical treatment. Patients with recent thrombosis who are within the first several weeks of undergoing successful thrombolytic therapy are excellent candidates for surgery. Operative treatment for PSS includes first rib resection, scalene muscle removal, or subclavius muscle removal, along with removal of constricting scar tissue from around the vein.⁷

THE TAKEAWAY

PSS is characterized by upper-extremity DVT resulting from repetitive trauma to the subclavian-axillary vein. Early diagnosis of PSS with contrast venography and prompt use of anticoagulation can effectively restore venous patency, reduce the risk of rethrombosis, and return the patient to normal function. Primary care physicians should be aware of this condition, because delayed recognition in a high-functioning person can be potentially disabling.

Our patient had a first rib resection, partial division of the scalenus anterior and medius muscles, and lysis of the cervical band. Follow-up venography confirmed resolution of thrombosis without any complications. The patient was continued on anticoagulation with warfarin for 3 months.

THE CASE

A 16-year-old boy presented to the emergency room (ER) with pain, redness, and swelling of his right upper arm that had been bothering him for 2 days. He was the quarterback of his high school football team, a sport that he’d been playing since he was 8 years old. He indicated that his football training—which involved repetitive throwing with his right arm—had intensified over the previous 2 months.

Prior to the ER visit, the patient was healthy and active with no significant medical history. He’d had no shoulder trauma and there was no family history of any coagulopathies, venous thrombosis, or pulmonary embolism. He denied chest pain, shortness of breath, palpitations, and fever, and said that he did not smoke cigarettes or drink alcohol.

On physical examination, his blood pressure was 118/70 mm Hg and his heart rate was 74 beats per minute. He had nonpitting edema and erythema of his right upper arm. His radial and brachial pulses were strong and equal in both arms. Assessment of neurologic and vascular integrity produced positive Wright’s and Adson’s tests, but a negative Halstead’s test. (For more on these tests, see: Wright’s test, Adson’s test, and Halstead’s test.) The circumference of the patient’s right upper arm was 2.5 cm greater than the left upper arm. The remainder of the physical exam was normal.

THE DIAGNOSIS

A duplex ultrasound of the right upper arm revealed an acute occlusive thrombus in the axillary vein. We started the patient on intravenous heparin. A venogram confirmed thrombosis of the axillary-subclavian vein (FIGURE 1A). Based on the patient’s clinical presentation and the results of the venogram, we diagnosed Paget-Schroetter syndrome. The venogram was followed by thrombolysis with alteplase (FIGURE 1B) and a balloon angioplasty (FIGURE 1C). One week later, a repeat venogram demonstrated partial removal of the thrombus and an area of compression on the inferior aspect of the subclavian vein due to a cervical band (FIGURE 1D).

DISCUSSION

Paget-Schroetter syndrome (PSS), or effort thrombosis of the upper extremities, is defined as spontaneous thrombus in the axillary and subclavian veins that occurs as a consequence of strenuous upper-extremity activity. It is a rare condition with an incidence of one to 2 cases per 100,000 people per year, and represents 1% to 4% of all cases of deep vein thrombosis (DVT).¹

Spontaneous thrombosis of the upper extremities typically presents in young, otherwise healthy individuals. It has been described in athletes who are involved in ball games, games with rackets or clubs, aquatic sports, combatant sports, and in violin players.² The repetitive movements used in these activities can lead to compression of the axillary and subclavian veins by hypertrophied muscles. Repetitive trauma causes intimal damage and thrombogenesis.³

PSS is characterized by the abrupt, spontaneous swelling of the entire arm, cyanosis, and pain that occurs with use or overhead positioning. Enlarged subcutaneous veins are present in the upper arm, around the shoulder, or in the upper anterior chest wall (Urschel’s sign). The classic presentation is acute onset of upper extremity pain and swelling in the dominant arm following a particularly strenuous activity.⁴ A low-grade fever, superficial thrombophlebitis, or neurologic symptoms may coexist. Certain provocative maneuvers can help reproduce the symptoms (TABLE 1^5,6). Complications of PSS include pulmonary embolism, postthrombotic syndrome (pain, heaviness, and swelling), and recurrent thrombosis.⁷

Contrast venography best shows the extent of thrombosis

Duplex ultrasound, with its high sensitivity and specificity, is the initial, noninvasive test of choice (TABLE 2^4,8-11). However, duplex ultrasound has a false-negative rate of 30% because it is highly technician-dependent and can be complicated by acoustic shadows from the clavicle or sternum.⁸

The most direct and definitive means to confirm the diagnosis of PSS is catheter-directed contrast venography.⁹ This method provides complete anatomic information regarding the site and extent of thrombosis, allows definitive evaluation of the collateral venous pathways, and is a necessary step toward the use of thrombolytic therapy. Contrast load, however, contraindicates the procedure in patients with renal failure and in those who are pregnant.

Contrast-enhanced computed tomography (CT) and magnetic resonance angiography (MRA) are also highly sensitive for detecting focal stenosis at the level of the first rib, the presence or absence of enlarged collateral veins, and the chronicity of any thrombus present. However, the usefulness of CT and magnetic resonance venography in initial screening is unclear, due to a lack of randomized controlled trials.

Treatment involves anticoagulants, thrombolytics, and possibly surgery

Prompt use of anticoagulation is indicated in PSS. Initial anticoagulation with low molecular weight unfractionated heparin or a direct thrombin inhibitor followed by warfarin for a minimum of 3 to 6 months is recommended.¹²

Patients treated with anticoagulation alone have a higher incidence of long-term residual symptoms, disability, and recurrent thrombosis.⁷ As a result, a more aggressive approach with the use of thrombolytic therapy is indicated, especially in young, active patients, to minimize long-term consequences. Alteplase or reteplase are used for this purpose. Thrombolysis is less likely to be beneficial if the thrombus is more than 2 weeks old or if there are inflammatory changes in the vein. The use of catheter-directed thrombolysis minimizes the risk of systemic adverse effects and achieves higher clot resolution rates.¹³

Because PSS is caused by compression of the vein, rather than a disorder of blood clotting, there is still a 50% to 70% risk of recurrent thrombosis despite thrombolysis and anticoagulation.¹⁴ Therefore, the most definitive management approach remains surgical treatment. Patients with recent thrombosis who are within the first several weeks of undergoing successful thrombolytic therapy are excellent candidates for surgery. Operative treatment for PSS includes first rib resection, scalene muscle removal, or subclavius muscle removal, along with removal of constricting scar tissue from around the vein.⁷

THE TAKEAWAY

PSS is characterized by upper-extremity DVT resulting from repetitive trauma to the subclavian-axillary vein. Early diagnosis of PSS with contrast venography and prompt use of anticoagulation can effectively restore venous patency, reduce the risk of rethrombosis, and return the patient to normal function. Primary care physicians should be aware of this condition, because delayed recognition in a high-functioning person can be potentially disabling.

Our patient had a first rib resection, partial division of the scalenus anterior and medius muscles, and lysis of the cervical band. Follow-up venography confirmed resolution of thrombosis without any complications. The patient was continued on anticoagulation with warfarin for 3 months.

Shorter hospital stay with oral replacement therapy

A 2006 systematic review compared ORT and IVF in 1811 children 0 to 18 years of age with viral gastroenteritis who were treated for failure to rehydrate in both outpatient and inpatient settings (18 randomized controlled trials [RCTs] of poor to moderate quality).¹ The primary outcome was “continued failure to rehydrate,” which varied by study and included persistent vomiting, persistent dehydration, shock, or seizures.

Overall, the risk of failure to rehydrate was 4.9% for ORT and 1.3% for IVF (risk difference [RD]=4%; 95% confidence interval [CI], 1%-7%; number needed to treat [NNT]=25). The length of stay (24-hour observation unit or inpatient hospitalization) was shorter for ORT than IVF (6 studies, 526 patients; weighted mean difference (WMD)= −1.2 days; 95% CI, −2.38 to −0.02). Investigators found no difference in weight gain, hyponatremia, hypernatremia, duration of diarrhea, or total fluid intake at 24 hours.

ORT can be started more quickly than IVF

An RCT conducted in an urban emergency department evaluated ORT and IVF for 4 hours in 72 children ages 8 weeks to 3 years with moderate dehydration from viral gastroenteritis.² This trial was included in the previously described review but evaluated additional outcomes: time required to initiate either ORT or IVF, improvement in symptoms at 2 hours, hospitalization rate, and preference for ORT in the future.

The authors also used a 10-point dehydration scoring system that included: decreased skin elasticity, capillary refill >2 seconds, general appearance, absence of tears, abnormal respirations, dry mucous membranes, sunken eyes, abnormal radial pulse, tachycardia >150 beats per minute, and decreased urine output. Details on the type of ORT or IVF were not reported.

ORT was initiated faster than IVF (mean difference [MD]=21 minutes; 95% CI, 10-32 minutes). No difference in improvement in dehydration scores was observed at 2 hours (ORT 78% vs IVF 80%; MD=1.2%; 95% CI, −20.5% to 18%). Nor was the hospitalization rate significantly different (IVF 48.7% and ORT 30.6%; MD=−18.1%; 95% CI, −40.1% to 4.1%). Most patients preferred to have the same therapy, whether ORT or IVF, with the next episode of gastroenteritis (61.3% vs 51.4%; MD=9.9%; 95% CI, −14 to 34).

Shorter hospital stay with oral replacement therapy

A 2006 systematic review compared ORT and IVF in 1811 children 0 to 18 years of age with viral gastroenteritis who were treated for failure to rehydrate in both outpatient and inpatient settings (18 randomized controlled trials [RCTs] of poor to moderate quality).¹ The primary outcome was “continued failure to rehydrate,” which varied by study and included persistent vomiting, persistent dehydration, shock, or seizures.

Overall, the risk of failure to rehydrate was 4.9% for ORT and 1.3% for IVF (risk difference [RD]=4%; 95% confidence interval [CI], 1%-7%; number needed to treat [NNT]=25). The length of stay (24-hour observation unit or inpatient hospitalization) was shorter for ORT than IVF (6 studies, 526 patients; weighted mean difference (WMD)= −1.2 days; 95% CI, −2.38 to −0.02). Investigators found no difference in weight gain, hyponatremia, hypernatremia, duration of diarrhea, or total fluid intake at 24 hours.

ORT can be started more quickly than IVF

An RCT conducted in an urban emergency department evaluated ORT and IVF for 4 hours in 72 children ages 8 weeks to 3 years with moderate dehydration from viral gastroenteritis.² This trial was included in the previously described review but evaluated additional outcomes: time required to initiate either ORT or IVF, improvement in symptoms at 2 hours, hospitalization rate, and preference for ORT in the future.

The authors also used a 10-point dehydration scoring system that included: decreased skin elasticity, capillary refill >2 seconds, general appearance, absence of tears, abnormal respirations, dry mucous membranes, sunken eyes, abnormal radial pulse, tachycardia >150 beats per minute, and decreased urine output. Details on the type of ORT or IVF were not reported.

ORT was initiated faster than IVF (mean difference [MD]=21 minutes; 95% CI, 10-32 minutes). No difference in improvement in dehydration scores was observed at 2 hours (ORT 78% vs IVF 80%; MD=1.2%; 95% CI, −20.5% to 18%). Nor was the hospitalization rate significantly different (IVF 48.7% and ORT 30.6%; MD=−18.1%; 95% CI, −40.1% to 4.1%). Most patients preferred to have the same therapy, whether ORT or IVF, with the next episode of gastroenteritis (61.3% vs 51.4%; MD=9.9%; 95% CI, −14 to 34).

Shorter hospital stay with oral replacement therapy

A 2006 systematic review compared ORT and IVF in 1811 children 0 to 18 years of age with viral gastroenteritis who were treated for failure to rehydrate in both outpatient and inpatient settings (18 randomized controlled trials [RCTs] of poor to moderate quality).¹ The primary outcome was “continued failure to rehydrate,” which varied by study and included persistent vomiting, persistent dehydration, shock, or seizures.

Overall, the risk of failure to rehydrate was 4.9% for ORT and 1.3% for IVF (risk difference [RD]=4%; 95% confidence interval [CI], 1%-7%; number needed to treat [NNT]=25). The length of stay (24-hour observation unit or inpatient hospitalization) was shorter for ORT than IVF (6 studies, 526 patients; weighted mean difference (WMD)= −1.2 days; 95% CI, −2.38 to −0.02). Investigators found no difference in weight gain, hyponatremia, hypernatremia, duration of diarrhea, or total fluid intake at 24 hours.

ORT can be started more quickly than IVF

An RCT conducted in an urban emergency department evaluated ORT and IVF for 4 hours in 72 children ages 8 weeks to 3 years with moderate dehydration from viral gastroenteritis.² This trial was included in the previously described review but evaluated additional outcomes: time required to initiate either ORT or IVF, improvement in symptoms at 2 hours, hospitalization rate, and preference for ORT in the future.

The authors also used a 10-point dehydration scoring system that included: decreased skin elasticity, capillary refill >2 seconds, general appearance, absence of tears, abnormal respirations, dry mucous membranes, sunken eyes, abnormal radial pulse, tachycardia >150 beats per minute, and decreased urine output. Details on the type of ORT or IVF were not reported.

ORT was initiated faster than IVF (mean difference [MD]=21 minutes; 95% CI, 10-32 minutes). No difference in improvement in dehydration scores was observed at 2 hours (ORT 78% vs IVF 80%; MD=1.2%; 95% CI, −20.5% to 18%). Nor was the hospitalization rate significantly different (IVF 48.7% and ORT 30.6%; MD=−18.1%; 95% CI, −40.1% to 4.1%). Most patients preferred to have the same therapy, whether ORT or IVF, with the next episode of gastroenteritis (61.3% vs 51.4%; MD=9.9%; 95% CI, −14 to 34).

CASE › A 66-year-old man you have seen many times for issues related to his chronic obstructive pulmonary disease (COPD) comes in to your clinic for a routine visit. He has been taking budesonide/formoterol twice a day for the last 3 years; however, he has not always been compliant with his medications and has been hospitalized within the last 6 months for disease exacerbations. Today, he says he has difficulty falling asleep and often becomes short of breath, even when physically inactive. His wife, who is accompanying him today, tells you he has become increasingly distant over the past few months and is not as engaged at family outings, which he attributes to labored breathing. They’re both concerned about this change and ask for advice.

Despite the increased awareness that generalized anxiety disorder (GAD) and major depressive disorder (MDD) are common comorbidities of COPD, they remain underdiagnosed and undertreated in patients with COPD. The results are increased rates of symptom exacerbation and rehospitalization.¹ Family physicians, who are the primary caregivers for most patients with the disease,² can maximize patients’ quality of life by recognizing comorbid mental illness, motivating and engaging patients in their disease management, and initiating appropriate treatment.

Anxiety and depression in COPD: A 2-way street

Several studies have assessed the prevalence of psychological disorders in patients with COPD. Affective disorders, mainly GAD and MDD, are the ones most commonly associated with poor COPD prognoses.^3,4 GAD is at least 3 times more prevalent in patients with COPD than in the general US population,⁵ reaching upwards of 55%.^1,6 Prevalence of MDD is also high, affecting approximately 40% of patients with the disease.¹

GAD and MDD are more prevalent as comorbidities of COPD than they are with other chronic diseases such as orthopedic conditions, pulmonary tuberculosis, hypertension and heart disease, stroke, diabetes, and cancer.^5,7-9 Patients with COPD, more so than patients with other serious chronic diseases, report heightened edginess, anxiousness, tiredness, distractibility, and irritability,⁵ perhaps owing in part to breathlessness and “air hunger.”¹⁰

The connection between COPD and GAD or MDD is not unidirectional, with progression of lung disease exacerbating its psychological comorbidities. The interaction is reciprocal, as clarified by Atlantis, et al, in a 2013 systematic review and meta-analysis that assessed key variables in the development of COPD and GAD or MDD.¹¹

COPD increases the risk of MDD, which is associated with increased tobacco consumption, poor adherence with COPD medications, and decreased physical activity.¹¹ Compounding the problem of inactivity is the fact that COPD—particularly longstanding disease—can lead to volume reductions in the anterior cingulate cortex of patients, which correlates with a persistent fear of performing physical activity.¹² MDD in the setting of COPD also complicates the already complex interplay between nicotine dependence and attempts at smoking cessation.¹¹

GAD/MDD worsens COPD outcomes

Comorbid GAD and MDD increase demands on our health care system and decrease the quality of life for patients with COPD. Anxious or depressed patients have higher 30-day readmission rates and less frequent outpatient follow-up than COPD patients without these mental comorbidities.⁶ Patients with comorbidities tend to have a higher prevalence of systemic symptoms independent of COPD severity,⁷ exhibit poorer physical and social functioning,¹³ and experience greater impairment of quality of life than patients with lung dysfunction alone.^1,14 Patients with GAD or MDD have a 43% increased risk of any adverse COPD outcome, which can include exacerbations, COPD-related diagnoses (eg, emphysema), new anxiety or depression events, and death.¹¹ Specifically, the risk of a COPD exacerbation rises by 31% in patients with comorbid GAD or MDD, and risk of death in those with comorbid MDD increases by 83%.¹¹

Somatic symptoms of anxiety, such as hyperventilation, shortness of breath, and sweating, may easily be attributed to pulmonary disease, instead of a psychological disorder.

GAD or MDD with COPD increases health care utilization and costs per patient when compared with patients who have COPD alone.⁹ Annual physician visits, emergency-room visits, and hospitalizations for any cause are higher in anxious or depressed COPD patients, and they have a 77% increased chance annually of a COPD-related hospitalization.⁹ Annual COPD-related health care costs for patients with GAD or MDD are significantly higher than the average COPD-related costs for patients without depression or anxiety, leading to significantly increased all-cause health care costs: $28,961 vs $22,512.⁹ Addressing and managing comorbid GAD or MDD in COPD patients could substantially reduce health care costs.

Be vigilant for anxiety, depression—even when COPD is mild

One reason comorbid GAD or MDD may be overlooked and underdiagnosed is that the symptoms can overlap those of COPD. In cases where suspicion of GAD or MDD is warranted, providers must keep separate the diagnostic inquiries for COPD and these comorbidities.⁶

Somatic symptoms of anxiety, such as hyperventilation, shortness of breath, and sweating, may easily be attributed to pulmonary disease instead of a psychological disorder. Differentiating the 2 processes becomes more difficult with patients younger than 60 years, as they are more likely to experience symptoms of GAD or MDD than older patients, regardless of COPD severity.¹⁵ Therefore, when assessing COPD patients, physicians need to be more vigilant for anxiety and depression, even in the mildest cases.¹⁴

Several methods exist for assessing anxiety and depression, including the Generalized Anxiety Disorder Screener 7 (GAD-7) and the Patient Health Questionnaire (PHQ) 2 or 9.¹⁶ All PHQ and GAD-7 screeners and translations are downloadable from www.phqscreeners.com/select-screener and permission is not required to reproduce, translate, display, or distribute them (FIGURE).¹⁶ Other anxiety and depression screening instruments are also available.

No one method has been shown to be most effective for rapid screening, and the physician’s comfort level or familiarity with a particular assessment tool may guide selection. One advantage of short screening instruments is that they can be incorporated into electronic health records for easy use across continuity visits. Although routine screening for these mental comorbidities takes slightly more time—especially in high-volume family practice clinics—it needs to become standard practice to protect patients’ quality of life.

Managing psychiatric conditions in COPD

Treatment for GAD and MDD in COPD is often suboptimal and may diminish a patient’s quality of life. In one study, COPD patients with a mental illness were 46% less likely than those with COPD alone to receive medications such as short- or long-acting bronchodilators and inhaled corticosteroids.¹⁷ Therapy for both the physiologic abnormalities and mental disturbances should be initiated promptly to maintain an acceptable state of health.

Pharmacotherapy. Reluctance to give traditional psychiatric medications to COPD patients contributes to the under-treatment of mental comorbidities. While benzodiazepines are generally not recommended—especially in severe COPD cases due to their sedative effect on respiratory drive—alternatives such as buspirone, tricyclic antidepressants (TCAs), selective serotonin reuptake inhibitors (SSRIs), and selective norepinephrine reuptake inhibitors (SNRIs) have been shown to effectively reduce GAD, MDD, and dyspnea in these patients^5,14(TABLE^18,19).

Non-pharmacotherapy approaches. Having patients apply behavioral-modification principles to their own behavior²⁰ has been proposed as a standard of care in the treatment of COPD.²¹ A recent systematic review found that self-management (behavior change) interventions in patients with COPD improved health-related quality of life, reduced hospital admissions, and helped alleviate dyspnea.²² While that review could not make clear recommendations regarding the most effective form and content of self-management in COPD,²² patient engagement and motivation in creating treatment goals are considered critical ingredients for effective self-management.²¹

Motivational Interviewing (MI) is an evidence-based behavioral approach designed for patients who are ambivalent about or resistant to change.²³ MI works by supporting a patient’s autonomy and by activating his/her own internal motivation for change or adherence to treatment. In MI, the physician’s involvement with the patient relies on collaboration, evocation, and autonomy, rather than confrontation, education, and authority. MI involves exploration more than exhortation, and support rather than persuasion or argument. The overall goal of MI is to increase intrinsic motivation so that change arises from within and serves the patient’s goals and values.²³

The risk of a COPD exacerbation rises by 31% in patients with comorbid anxiety or depression; risk of death in those with comorbid depression increases by 83%.

Benzo, et al, provide a very detailed description of a self-management process that includes MI.²¹ Their protocol proved to be feasible in severe COPD and helped increase patient engagement and commitment to self-management.²¹ This finding and similar evidence of MI’s effectiveness in a variety of other health conditions suggest that pharmacotherapy and cognitive-behavior therapy can be delivered in combination with an MI approach.

Self-management depends on a patient’s readiness to implement behavioral changes. Patients engaged in unhealthy behavior may be reluctant to change at a particular time, so the physician may focus efforts on such behaviors as self-monitoring or examining values that may lead to future behavior change.

For example, a patient may not want to stop smoking, but the physician’s willingness to ask about smoking in subsequent visits may catch the patient at a time when motivation has changed—eg, perhaps there is a new child in the home, prompting a recognition that smoking is now inconsistent with one’s values and can be resolved with smoking cessation. Awareness of an individual’s baseline behavior and readiness to change assists physicians and other health professionals in tailoring interventions for the most favorable outcome.

Several other non-pharmacologic methods to reduce symptoms of GAD and MDD in patients with COPD have been studied and supported by the literature.

• Progressive muscle relaxation, stress management, biofeedback, and guided imagery have been shown to decrease symptoms of anxiety, dyspnea, and airway obstruction.^5,14
• Pulmonary rehabilitation programs including psychotherapy sessions have also relieved symptoms of GAD and MDD for patients with COPD.
• Programs that include physiotherapy, physical exercise (arm and leg exercise, aerobic conditioning, flexibility training), patient education, and psychotherapy sessions have significantly lowered GAD and MDD scores when compared with similar rehabilitation programs not offering psychotherapy.²⁴
• Cognitive-behavioral therapy has been variably effective in treating comorbid GAD and MDD, with studies citing either superiority⁵ or equivalence²⁵ to COPD education alone.

Increasingly, psychologists have been integrated into primary care with implementation of the Patient-Centered Medical Home.²⁶ However, if primary care physicians do not have behavioral specialists available, they can contact the American Psychological Association, their state psychological association, or professional organizations, such as the Society of Behavioral Medicine, for referral to professionals trained in behavioral self-management skills.

Initiation of treatment, whether pharmacological or non-pharmacological, and emphasis on self-management of the disease can greatly improve patients' perceptions of their condition and overall quality of life.

CASE › The patient screens positive for GAD and you give him a prescription for venlafaxine to begin immediately. Using an MI approach, you help the patient clarify that being more engaged with his family is important to him. Acknowledging that your recommendations are consistent with his values, the patient agrees to pursue pulmonary rehabilitation and, with the aid of a behavioral health specialist, learn self-management techniques for medication adherence and social reengagement.

CORRESPONDENCE
Ms. Sydney Marsh, 3009 S 35th Ave., Omaha, NE 68105; sydneymarsh@creighton.edu.

CASE › A 66-year-old man you have seen many times for issues related to his chronic obstructive pulmonary disease (COPD) comes in to your clinic for a routine visit. He has been taking budesonide/formoterol twice a day for the last 3 years; however, he has not always been compliant with his medications and has been hospitalized within the last 6 months for disease exacerbations. Today, he says he has difficulty falling asleep and often becomes short of breath, even when physically inactive. His wife, who is accompanying him today, tells you he has become increasingly distant over the past few months and is not as engaged at family outings, which he attributes to labored breathing. They’re both concerned about this change and ask for advice.

Despite the increased awareness that generalized anxiety disorder (GAD) and major depressive disorder (MDD) are common comorbidities of COPD, they remain underdiagnosed and undertreated in patients with COPD. The results are increased rates of symptom exacerbation and rehospitalization.¹ Family physicians, who are the primary caregivers for most patients with the disease,² can maximize patients’ quality of life by recognizing comorbid mental illness, motivating and engaging patients in their disease management, and initiating appropriate treatment.

Anxiety and depression in COPD: A 2-way street

Several studies have assessed the prevalence of psychological disorders in patients with COPD. Affective disorders, mainly GAD and MDD, are the ones most commonly associated with poor COPD prognoses.^3,4 GAD is at least 3 times more prevalent in patients with COPD than in the general US population,⁵ reaching upwards of 55%.^1,6 Prevalence of MDD is also high, affecting approximately 40% of patients with the disease.¹

GAD and MDD are more prevalent as comorbidities of COPD than they are with other chronic diseases such as orthopedic conditions, pulmonary tuberculosis, hypertension and heart disease, stroke, diabetes, and cancer.^5,7-9 Patients with COPD, more so than patients with other serious chronic diseases, report heightened edginess, anxiousness, tiredness, distractibility, and irritability,⁵ perhaps owing in part to breathlessness and “air hunger.”¹⁰

The connection between COPD and GAD or MDD is not unidirectional, with progression of lung disease exacerbating its psychological comorbidities. The interaction is reciprocal, as clarified by Atlantis, et al, in a 2013 systematic review and meta-analysis that assessed key variables in the development of COPD and GAD or MDD.¹¹

COPD increases the risk of MDD, which is associated with increased tobacco consumption, poor adherence with COPD medications, and decreased physical activity.¹¹ Compounding the problem of inactivity is the fact that COPD—particularly longstanding disease—can lead to volume reductions in the anterior cingulate cortex of patients, which correlates with a persistent fear of performing physical activity.¹² MDD in the setting of COPD also complicates the already complex interplay between nicotine dependence and attempts at smoking cessation.¹¹

GAD/MDD worsens COPD outcomes

Comorbid GAD and MDD increase demands on our health care system and decrease the quality of life for patients with COPD. Anxious or depressed patients have higher 30-day readmission rates and less frequent outpatient follow-up than COPD patients without these mental comorbidities.⁶ Patients with comorbidities tend to have a higher prevalence of systemic symptoms independent of COPD severity,⁷ exhibit poorer physical and social functioning,¹³ and experience greater impairment of quality of life than patients with lung dysfunction alone.^1,14 Patients with GAD or MDD have a 43% increased risk of any adverse COPD outcome, which can include exacerbations, COPD-related diagnoses (eg, emphysema), new anxiety or depression events, and death.¹¹ Specifically, the risk of a COPD exacerbation rises by 31% in patients with comorbid GAD or MDD, and risk of death in those with comorbid MDD increases by 83%.¹¹

Somatic symptoms of anxiety, such as hyperventilation, shortness of breath, and sweating, may easily be attributed to pulmonary disease, instead of a psychological disorder.

GAD or MDD with COPD increases health care utilization and costs per patient when compared with patients who have COPD alone.⁹ Annual physician visits, emergency-room visits, and hospitalizations for any cause are higher in anxious or depressed COPD patients, and they have a 77% increased chance annually of a COPD-related hospitalization.⁹ Annual COPD-related health care costs for patients with GAD or MDD are significantly higher than the average COPD-related costs for patients without depression or anxiety, leading to significantly increased all-cause health care costs: $28,961 vs $22,512.⁹ Addressing and managing comorbid GAD or MDD in COPD patients could substantially reduce health care costs.

Be vigilant for anxiety, depression—even when COPD is mild

One reason comorbid GAD or MDD may be overlooked and underdiagnosed is that the symptoms can overlap those of COPD. In cases where suspicion of GAD or MDD is warranted, providers must keep separate the diagnostic inquiries for COPD and these comorbidities.⁶

Somatic symptoms of anxiety, such as hyperventilation, shortness of breath, and sweating, may easily be attributed to pulmonary disease instead of a psychological disorder. Differentiating the 2 processes becomes more difficult with patients younger than 60 years, as they are more likely to experience symptoms of GAD or MDD than older patients, regardless of COPD severity.¹⁵ Therefore, when assessing COPD patients, physicians need to be more vigilant for anxiety and depression, even in the mildest cases.¹⁴

Several methods exist for assessing anxiety and depression, including the Generalized Anxiety Disorder Screener 7 (GAD-7) and the Patient Health Questionnaire (PHQ) 2 or 9.¹⁶ All PHQ and GAD-7 screeners and translations are downloadable from www.phqscreeners.com/select-screener and permission is not required to reproduce, translate, display, or distribute them (FIGURE).¹⁶ Other anxiety and depression screening instruments are also available.

No one method has been shown to be most effective for rapid screening, and the physician’s comfort level or familiarity with a particular assessment tool may guide selection. One advantage of short screening instruments is that they can be incorporated into electronic health records for easy use across continuity visits. Although routine screening for these mental comorbidities takes slightly more time—especially in high-volume family practice clinics—it needs to become standard practice to protect patients’ quality of life.

Managing psychiatric conditions in COPD

Treatment for GAD and MDD in COPD is often suboptimal and may diminish a patient’s quality of life. In one study, COPD patients with a mental illness were 46% less likely than those with COPD alone to receive medications such as short- or long-acting bronchodilators and inhaled corticosteroids.¹⁷ Therapy for both the physiologic abnormalities and mental disturbances should be initiated promptly to maintain an acceptable state of health.

Pharmacotherapy. Reluctance to give traditional psychiatric medications to COPD patients contributes to the under-treatment of mental comorbidities. While benzodiazepines are generally not recommended—especially in severe COPD cases due to their sedative effect on respiratory drive—alternatives such as buspirone, tricyclic antidepressants (TCAs), selective serotonin reuptake inhibitors (SSRIs), and selective norepinephrine reuptake inhibitors (SNRIs) have been shown to effectively reduce GAD, MDD, and dyspnea in these patients^5,14(TABLE^18,19).

Non-pharmacotherapy approaches. Having patients apply behavioral-modification principles to their own behavior²⁰ has been proposed as a standard of care in the treatment of COPD.²¹ A recent systematic review found that self-management (behavior change) interventions in patients with COPD improved health-related quality of life, reduced hospital admissions, and helped alleviate dyspnea.²² While that review could not make clear recommendations regarding the most effective form and content of self-management in COPD,²² patient engagement and motivation in creating treatment goals are considered critical ingredients for effective self-management.²¹

Motivational Interviewing (MI) is an evidence-based behavioral approach designed for patients who are ambivalent about or resistant to change.²³ MI works by supporting a patient’s autonomy and by activating his/her own internal motivation for change or adherence to treatment. In MI, the physician’s involvement with the patient relies on collaboration, evocation, and autonomy, rather than confrontation, education, and authority. MI involves exploration more than exhortation, and support rather than persuasion or argument. The overall goal of MI is to increase intrinsic motivation so that change arises from within and serves the patient’s goals and values.²³

The risk of a COPD exacerbation rises by 31% in patients with comorbid anxiety or depression; risk of death in those with comorbid depression increases by 83%.

Benzo, et al, provide a very detailed description of a self-management process that includes MI.²¹ Their protocol proved to be feasible in severe COPD and helped increase patient engagement and commitment to self-management.²¹ This finding and similar evidence of MI’s effectiveness in a variety of other health conditions suggest that pharmacotherapy and cognitive-behavior therapy can be delivered in combination with an MI approach.

Self-management depends on a patient’s readiness to implement behavioral changes. Patients engaged in unhealthy behavior may be reluctant to change at a particular time, so the physician may focus efforts on such behaviors as self-monitoring or examining values that may lead to future behavior change.

For example, a patient may not want to stop smoking, but the physician’s willingness to ask about smoking in subsequent visits may catch the patient at a time when motivation has changed—eg, perhaps there is a new child in the home, prompting a recognition that smoking is now inconsistent with one’s values and can be resolved with smoking cessation. Awareness of an individual’s baseline behavior and readiness to change assists physicians and other health professionals in tailoring interventions for the most favorable outcome.

Several other non-pharmacologic methods to reduce symptoms of GAD and MDD in patients with COPD have been studied and supported by the literature.

• Progressive muscle relaxation, stress management, biofeedback, and guided imagery have been shown to decrease symptoms of anxiety, dyspnea, and airway obstruction.^5,14
• Pulmonary rehabilitation programs including psychotherapy sessions have also relieved symptoms of GAD and MDD for patients with COPD.
• Programs that include physiotherapy, physical exercise (arm and leg exercise, aerobic conditioning, flexibility training), patient education, and psychotherapy sessions have significantly lowered GAD and MDD scores when compared with similar rehabilitation programs not offering psychotherapy.²⁴
• Cognitive-behavioral therapy has been variably effective in treating comorbid GAD and MDD, with studies citing either superiority⁵ or equivalence²⁵ to COPD education alone.

Increasingly, psychologists have been integrated into primary care with implementation of the Patient-Centered Medical Home.²⁶ However, if primary care physicians do not have behavioral specialists available, they can contact the American Psychological Association, their state psychological association, or professional organizations, such as the Society of Behavioral Medicine, for referral to professionals trained in behavioral self-management skills.

Initiation of treatment, whether pharmacological or non-pharmacological, and emphasis on self-management of the disease can greatly improve patients' perceptions of their condition and overall quality of life.

CASE › The patient screens positive for GAD and you give him a prescription for venlafaxine to begin immediately. Using an MI approach, you help the patient clarify that being more engaged with his family is important to him. Acknowledging that your recommendations are consistent with his values, the patient agrees to pursue pulmonary rehabilitation and, with the aid of a behavioral health specialist, learn self-management techniques for medication adherence and social reengagement.

CORRESPONDENCE
Ms. Sydney Marsh, 3009 S 35th Ave., Omaha, NE 68105; sydneymarsh@creighton.edu.

CASE › A 66-year-old man you have seen many times for issues related to his chronic obstructive pulmonary disease (COPD) comes in to your clinic for a routine visit. He has been taking budesonide/formoterol twice a day for the last 3 years; however, he has not always been compliant with his medications and has been hospitalized within the last 6 months for disease exacerbations. Today, he says he has difficulty falling asleep and often becomes short of breath, even when physically inactive. His wife, who is accompanying him today, tells you he has become increasingly distant over the past few months and is not as engaged at family outings, which he attributes to labored breathing. They’re both concerned about this change and ask for advice.

Despite the increased awareness that generalized anxiety disorder (GAD) and major depressive disorder (MDD) are common comorbidities of COPD, they remain underdiagnosed and undertreated in patients with COPD. The results are increased rates of symptom exacerbation and rehospitalization.¹ Family physicians, who are the primary caregivers for most patients with the disease,² can maximize patients’ quality of life by recognizing comorbid mental illness, motivating and engaging patients in their disease management, and initiating appropriate treatment.

Anxiety and depression in COPD: A 2-way street

Several studies have assessed the prevalence of psychological disorders in patients with COPD. Affective disorders, mainly GAD and MDD, are the ones most commonly associated with poor COPD prognoses.^3,4 GAD is at least 3 times more prevalent in patients with COPD than in the general US population,⁵ reaching upwards of 55%.^1,6 Prevalence of MDD is also high, affecting approximately 40% of patients with the disease.¹

GAD and MDD are more prevalent as comorbidities of COPD than they are with other chronic diseases such as orthopedic conditions, pulmonary tuberculosis, hypertension and heart disease, stroke, diabetes, and cancer.^5,7-9 Patients with COPD, more so than patients with other serious chronic diseases, report heightened edginess, anxiousness, tiredness, distractibility, and irritability,⁵ perhaps owing in part to breathlessness and “air hunger.”¹⁰

The connection between COPD and GAD or MDD is not unidirectional, with progression of lung disease exacerbating its psychological comorbidities. The interaction is reciprocal, as clarified by Atlantis, et al, in a 2013 systematic review and meta-analysis that assessed key variables in the development of COPD and GAD or MDD.¹¹

COPD increases the risk of MDD, which is associated with increased tobacco consumption, poor adherence with COPD medications, and decreased physical activity.¹¹ Compounding the problem of inactivity is the fact that COPD—particularly longstanding disease—can lead to volume reductions in the anterior cingulate cortex of patients, which correlates with a persistent fear of performing physical activity.¹² MDD in the setting of COPD also complicates the already complex interplay between nicotine dependence and attempts at smoking cessation.¹¹

GAD/MDD worsens COPD outcomes

Comorbid GAD and MDD increase demands on our health care system and decrease the quality of life for patients with COPD. Anxious or depressed patients have higher 30-day readmission rates and less frequent outpatient follow-up than COPD patients without these mental comorbidities.⁶ Patients with comorbidities tend to have a higher prevalence of systemic symptoms independent of COPD severity,⁷ exhibit poorer physical and social functioning,¹³ and experience greater impairment of quality of life than patients with lung dysfunction alone.^1,14 Patients with GAD or MDD have a 43% increased risk of any adverse COPD outcome, which can include exacerbations, COPD-related diagnoses (eg, emphysema), new anxiety or depression events, and death.¹¹ Specifically, the risk of a COPD exacerbation rises by 31% in patients with comorbid GAD or MDD, and risk of death in those with comorbid MDD increases by 83%.¹¹

Somatic symptoms of anxiety, such as hyperventilation, shortness of breath, and sweating, may easily be attributed to pulmonary disease, instead of a psychological disorder.

GAD or MDD with COPD increases health care utilization and costs per patient when compared with patients who have COPD alone.⁹ Annual physician visits, emergency-room visits, and hospitalizations for any cause are higher in anxious or depressed COPD patients, and they have a 77% increased chance annually of a COPD-related hospitalization.⁹ Annual COPD-related health care costs for patients with GAD or MDD are significantly higher than the average COPD-related costs for patients without depression or anxiety, leading to significantly increased all-cause health care costs: $28,961 vs $22,512.⁹ Addressing and managing comorbid GAD or MDD in COPD patients could substantially reduce health care costs.

Be vigilant for anxiety, depression—even when COPD is mild

One reason comorbid GAD or MDD may be overlooked and underdiagnosed is that the symptoms can overlap those of COPD. In cases where suspicion of GAD or MDD is warranted, providers must keep separate the diagnostic inquiries for COPD and these comorbidities.⁶

Somatic symptoms of anxiety, such as hyperventilation, shortness of breath, and sweating, may easily be attributed to pulmonary disease instead of a psychological disorder. Differentiating the 2 processes becomes more difficult with patients younger than 60 years, as they are more likely to experience symptoms of GAD or MDD than older patients, regardless of COPD severity.¹⁵ Therefore, when assessing COPD patients, physicians need to be more vigilant for anxiety and depression, even in the mildest cases.¹⁴

Several methods exist for assessing anxiety and depression, including the Generalized Anxiety Disorder Screener 7 (GAD-7) and the Patient Health Questionnaire (PHQ) 2 or 9.¹⁶ All PHQ and GAD-7 screeners and translations are downloadable from www.phqscreeners.com/select-screener and permission is not required to reproduce, translate, display, or distribute them (FIGURE).¹⁶ Other anxiety and depression screening instruments are also available.

No one method has been shown to be most effective for rapid screening, and the physician’s comfort level or familiarity with a particular assessment tool may guide selection. One advantage of short screening instruments is that they can be incorporated into electronic health records for easy use across continuity visits. Although routine screening for these mental comorbidities takes slightly more time—especially in high-volume family practice clinics—it needs to become standard practice to protect patients’ quality of life.

Managing psychiatric conditions in COPD

Treatment for GAD and MDD in COPD is often suboptimal and may diminish a patient’s quality of life. In one study, COPD patients with a mental illness were 46% less likely than those with COPD alone to receive medications such as short- or long-acting bronchodilators and inhaled corticosteroids.¹⁷ Therapy for both the physiologic abnormalities and mental disturbances should be initiated promptly to maintain an acceptable state of health.

Pharmacotherapy. Reluctance to give traditional psychiatric medications to COPD patients contributes to the under-treatment of mental comorbidities. While benzodiazepines are generally not recommended—especially in severe COPD cases due to their sedative effect on respiratory drive—alternatives such as buspirone, tricyclic antidepressants (TCAs), selective serotonin reuptake inhibitors (SSRIs), and selective norepinephrine reuptake inhibitors (SNRIs) have been shown to effectively reduce GAD, MDD, and dyspnea in these patients^5,14(TABLE^18,19).

Non-pharmacotherapy approaches. Having patients apply behavioral-modification principles to their own behavior²⁰ has been proposed as a standard of care in the treatment of COPD.²¹ A recent systematic review found that self-management (behavior change) interventions in patients with COPD improved health-related quality of life, reduced hospital admissions, and helped alleviate dyspnea.²² While that review could not make clear recommendations regarding the most effective form and content of self-management in COPD,²² patient engagement and motivation in creating treatment goals are considered critical ingredients for effective self-management.²¹

Motivational Interviewing (MI) is an evidence-based behavioral approach designed for patients who are ambivalent about or resistant to change.²³ MI works by supporting a patient’s autonomy and by activating his/her own internal motivation for change or adherence to treatment. In MI, the physician’s involvement with the patient relies on collaboration, evocation, and autonomy, rather than confrontation, education, and authority. MI involves exploration more than exhortation, and support rather than persuasion or argument. The overall goal of MI is to increase intrinsic motivation so that change arises from within and serves the patient’s goals and values.²³

The risk of a COPD exacerbation rises by 31% in patients with comorbid anxiety or depression; risk of death in those with comorbid depression increases by 83%.

Benzo, et al, provide a very detailed description of a self-management process that includes MI.²¹ Their protocol proved to be feasible in severe COPD and helped increase patient engagement and commitment to self-management.²¹ This finding and similar evidence of MI’s effectiveness in a variety of other health conditions suggest that pharmacotherapy and cognitive-behavior therapy can be delivered in combination with an MI approach.

Self-management depends on a patient’s readiness to implement behavioral changes. Patients engaged in unhealthy behavior may be reluctant to change at a particular time, so the physician may focus efforts on such behaviors as self-monitoring or examining values that may lead to future behavior change.

For example, a patient may not want to stop smoking, but the physician’s willingness to ask about smoking in subsequent visits may catch the patient at a time when motivation has changed—eg, perhaps there is a new child in the home, prompting a recognition that smoking is now inconsistent with one’s values and can be resolved with smoking cessation. Awareness of an individual’s baseline behavior and readiness to change assists physicians and other health professionals in tailoring interventions for the most favorable outcome.

Several other non-pharmacologic methods to reduce symptoms of GAD and MDD in patients with COPD have been studied and supported by the literature.

• Progressive muscle relaxation, stress management, biofeedback, and guided imagery have been shown to decrease symptoms of anxiety, dyspnea, and airway obstruction.^5,14
• Pulmonary rehabilitation programs including psychotherapy sessions have also relieved symptoms of GAD and MDD for patients with COPD.
• Programs that include physiotherapy, physical exercise (arm and leg exercise, aerobic conditioning, flexibility training), patient education, and psychotherapy sessions have significantly lowered GAD and MDD scores when compared with similar rehabilitation programs not offering psychotherapy.²⁴
• Cognitive-behavioral therapy has been variably effective in treating comorbid GAD and MDD, with studies citing either superiority⁵ or equivalence²⁵ to COPD education alone.

Increasingly, psychologists have been integrated into primary care with implementation of the Patient-Centered Medical Home.²⁶ However, if primary care physicians do not have behavioral specialists available, they can contact the American Psychological Association, their state psychological association, or professional organizations, such as the Society of Behavioral Medicine, for referral to professionals trained in behavioral self-management skills.

Initiation of treatment, whether pharmacological or non-pharmacological, and emphasis on self-management of the disease can greatly improve patients' perceptions of their condition and overall quality of life.

CASE › The patient screens positive for GAD and you give him a prescription for venlafaxine to begin immediately. Using an MI approach, you help the patient clarify that being more engaged with his family is important to him. Acknowledging that your recommendations are consistent with his values, the patient agrees to pursue pulmonary rehabilitation and, with the aid of a behavioral health specialist, learn self-management techniques for medication adherence and social reengagement.

CORRESPONDENCE
Ms. Sydney Marsh, 3009 S 35th Ave., Omaha, NE 68105; sydneymarsh@creighton.edu.

A 53-year-old African American woman was admitted to our hospital for intractable nausea and vomiting that she’d been experiencing for a month. She also reported dysphagia with solids and occasionally with liquids. She had no chest or abdominal pain, and no fever, bleeding, diarrhea, significant weight loss, or significant travel history. The patient was not taking any medication and her physical exam was normal. The patient’s complete blood count and electrolytes were normal. We ordered a chest x-ray (FIGURE 1).

WHAT IS YOUR DIAGNOSIS?
HOW WOULD YOU TREAT THIS PATIENT?

Diagnosis: Achalasia

The radiologist who examined the x-ray noted a dilated esophagus (FIGURE 1, red arrows) with debris behind the heart shadow, which suggested achalasia. Upon further questioning, the patient reported a history of achalasia that had been treated with a myotomy 6 years ago. We performed an esophagogastroscopy, which showed a dilated esophagus with signs of the myotomy (FIGURE 2A), as well as food particles lodged in the esophagus (FIGURE 2B) that were causing the patient’s intractable vomiting.

Achalasia is a motor disorder of the esophagus smooth muscle in which the lower esophageal sphincter does not relax properly with swallowing, and the normal peristalsis of the esophagus body is replaced by abnormal contractions. Primary idiopathic achalasia is the most common form in the United States, but secondary forms caused by gastric carcinoma, lymphoma, or Chagas disease are also seen.¹ The prevalence of achalasia is 1.6 per 100,000 in some populations.² Symptoms can include dysphagia with solids and liquids, chest pain, and regurgitation.

A chest x-ray will show an absence of gastric air, and occasionally, as in this case, a tubular mass (the dilated esophagus) behind the heart and aorta. On fluoroscopy, the lower two-thirds of the esophagus does not have peristalsis and the terminal part has a bird beak appearance. Manometry will show normal or elevated pressure in the lower esophagus. Administration of cholinergic agonists will cause a marked increase in baseline pressure, as well as pain and regurgitation. Endoscopy can exclude secondary causes.

Narrowing the causes of dysphagia

The differential diagnosis is broad because there are 2 types of dysphagia: mechanical and neuromuscular.

Mechanical dysphagia is caused by a food bolus or foreign body, by intrinsic narrowing of the esophagus (from inflammation, esophageal webs, benign and malignant strictures, and tumors) or by extrinsic compression (from bone or thyroid abscesses or vascular tightening).

Neuromuscular dysphagia is either a swallowing reflex problem, a disorder of the pharyngeal and striated esophagus muscles, or an esophageal smooth muscle disorder.³ Close attention to the patient’s history and physical exam is key to zeroing in on the proper diagnosis.

On the other hand, food impaction in the esophagus almost always indicates certain etiologies. Benign esophageal stenosis caused by Schatzki rings (B rings) or by peptic strictures is the most common cause of food impaction, followed by esophageal webs, extrinsic compression, surgical anastomosis, esophagitis (eg, eosinophilic esophagitis), and motor disorders, such as achalasia.

First-line therapy is surgery; pharmacologic Tx is least effective

Treatment should be individualized by age, gender, and patient preference; however, there is no definitive treatment for this condition. First-line therapy includes graded pneumatic dilation or laparoscopic myotomy with a partial fundoplication.⁴ Botulinum toxin injection in the lower esophageal sphincter is recommended for patients who are not good candidates for surgery or dilation.⁵

Pharmacologic therapy, the least effective treatment option, is recommended for patients who are unwilling or unable to undergo myotomy and/or dilation and do not respond to botulinum toxin.^6,7 Long-acting nitrates such as isosorbide, calcium channel blockers such as nifedipine, and phosphodiesterase-5 (PDE5) inhibitors such as sildenafil reduce lower esophageal sphincter tone and pressure.

A chest x-ray will show an absence of gastric air, and occasionally, as in this case, a tubular mass (the dilated esophagus) behind the heart and aorta.

Both nifedipine and isosorbide should be taken sublingually before meals (30 minutes and 10 minutes, respectively). The effects of nifedipine and isosorbide, however, are partial, and these agents do not provide complete relief from symptoms.⁶ PDE5 use has been limited and results are inconclusive.

Our patient. The food particles in the patient’s esophagus were removed during endoscopy, and she stopped vomiting completely. Based on the findings and clinical picture, the patient most likely suffered from mega-esophagus (an end-stage dilated malfunctioning esophagus). Our patient was discharged to follow-up with her gastroenterologist.

Because there is no definitive treatment for achalasia, the patient was counseled about the need for continuous monitoring and dietary precautions, including modification of food texture or change of fluid viscosity. Food may be chopped, minced, or pureed, and fluids may be thickened.

CORRESPONDENCE
Hossein Akhondi, MD, FACP, Georgetown University, 1010 Mass Ave, NW, Unit 904, Washington, DC 20001; h68akhond@hotmail.com.

A 53-year-old African American woman was admitted to our hospital for intractable nausea and vomiting that she’d been experiencing for a month. She also reported dysphagia with solids and occasionally with liquids. She had no chest or abdominal pain, and no fever, bleeding, diarrhea, significant weight loss, or significant travel history. The patient was not taking any medication and her physical exam was normal. The patient’s complete blood count and electrolytes were normal. We ordered a chest x-ray (FIGURE 1).

WHAT IS YOUR DIAGNOSIS?
HOW WOULD YOU TREAT THIS PATIENT?

Diagnosis: Achalasia

The radiologist who examined the x-ray noted a dilated esophagus (FIGURE 1, red arrows) with debris behind the heart shadow, which suggested achalasia. Upon further questioning, the patient reported a history of achalasia that had been treated with a myotomy 6 years ago. We performed an esophagogastroscopy, which showed a dilated esophagus with signs of the myotomy (FIGURE 2A), as well as food particles lodged in the esophagus (FIGURE 2B) that were causing the patient’s intractable vomiting.

Achalasia is a motor disorder of the esophagus smooth muscle in which the lower esophageal sphincter does not relax properly with swallowing, and the normal peristalsis of the esophagus body is replaced by abnormal contractions. Primary idiopathic achalasia is the most common form in the United States, but secondary forms caused by gastric carcinoma, lymphoma, or Chagas disease are also seen.¹ The prevalence of achalasia is 1.6 per 100,000 in some populations.² Symptoms can include dysphagia with solids and liquids, chest pain, and regurgitation.

A chest x-ray will show an absence of gastric air, and occasionally, as in this case, a tubular mass (the dilated esophagus) behind the heart and aorta. On fluoroscopy, the lower two-thirds of the esophagus does not have peristalsis and the terminal part has a bird beak appearance. Manometry will show normal or elevated pressure in the lower esophagus. Administration of cholinergic agonists will cause a marked increase in baseline pressure, as well as pain and regurgitation. Endoscopy can exclude secondary causes.

Narrowing the causes of dysphagia

The differential diagnosis is broad because there are 2 types of dysphagia: mechanical and neuromuscular.

Mechanical dysphagia is caused by a food bolus or foreign body, by intrinsic narrowing of the esophagus (from inflammation, esophageal webs, benign and malignant strictures, and tumors) or by extrinsic compression (from bone or thyroid abscesses or vascular tightening).

Neuromuscular dysphagia is either a swallowing reflex problem, a disorder of the pharyngeal and striated esophagus muscles, or an esophageal smooth muscle disorder.³ Close attention to the patient’s history and physical exam is key to zeroing in on the proper diagnosis.

On the other hand, food impaction in the esophagus almost always indicates certain etiologies. Benign esophageal stenosis caused by Schatzki rings (B rings) or by peptic strictures is the most common cause of food impaction, followed by esophageal webs, extrinsic compression, surgical anastomosis, esophagitis (eg, eosinophilic esophagitis), and motor disorders, such as achalasia.

First-line therapy is surgery; pharmacologic Tx is least effective

Treatment should be individualized by age, gender, and patient preference; however, there is no definitive treatment for this condition. First-line therapy includes graded pneumatic dilation or laparoscopic myotomy with a partial fundoplication.⁴ Botulinum toxin injection in the lower esophageal sphincter is recommended for patients who are not good candidates for surgery or dilation.⁵

Pharmacologic therapy, the least effective treatment option, is recommended for patients who are unwilling or unable to undergo myotomy and/or dilation and do not respond to botulinum toxin.^6,7 Long-acting nitrates such as isosorbide, calcium channel blockers such as nifedipine, and phosphodiesterase-5 (PDE5) inhibitors such as sildenafil reduce lower esophageal sphincter tone and pressure.

A chest x-ray will show an absence of gastric air, and occasionally, as in this case, a tubular mass (the dilated esophagus) behind the heart and aorta.

Both nifedipine and isosorbide should be taken sublingually before meals (30 minutes and 10 minutes, respectively). The effects of nifedipine and isosorbide, however, are partial, and these agents do not provide complete relief from symptoms.⁶ PDE5 use has been limited and results are inconclusive.

Our patient. The food particles in the patient’s esophagus were removed during endoscopy, and she stopped vomiting completely. Based on the findings and clinical picture, the patient most likely suffered from mega-esophagus (an end-stage dilated malfunctioning esophagus). Our patient was discharged to follow-up with her gastroenterologist.

Because there is no definitive treatment for achalasia, the patient was counseled about the need for continuous monitoring and dietary precautions, including modification of food texture or change of fluid viscosity. Food may be chopped, minced, or pureed, and fluids may be thickened.

CORRESPONDENCE
Hossein Akhondi, MD, FACP, Georgetown University, 1010 Mass Ave, NW, Unit 904, Washington, DC 20001; h68akhond@hotmail.com.

A 53-year-old African American woman was admitted to our hospital for intractable nausea and vomiting that she’d been experiencing for a month. She also reported dysphagia with solids and occasionally with liquids. She had no chest or abdominal pain, and no fever, bleeding, diarrhea, significant weight loss, or significant travel history. The patient was not taking any medication and her physical exam was normal. The patient’s complete blood count and electrolytes were normal. We ordered a chest x-ray (FIGURE 1).

WHAT IS YOUR DIAGNOSIS?
HOW WOULD YOU TREAT THIS PATIENT?

Diagnosis: Achalasia

The radiologist who examined the x-ray noted a dilated esophagus (FIGURE 1, red arrows) with debris behind the heart shadow, which suggested achalasia. Upon further questioning, the patient reported a history of achalasia that had been treated with a myotomy 6 years ago. We performed an esophagogastroscopy, which showed a dilated esophagus with signs of the myotomy (FIGURE 2A), as well as food particles lodged in the esophagus (FIGURE 2B) that were causing the patient’s intractable vomiting.

Achalasia is a motor disorder of the esophagus smooth muscle in which the lower esophageal sphincter does not relax properly with swallowing, and the normal peristalsis of the esophagus body is replaced by abnormal contractions. Primary idiopathic achalasia is the most common form in the United States, but secondary forms caused by gastric carcinoma, lymphoma, or Chagas disease are also seen.¹ The prevalence of achalasia is 1.6 per 100,000 in some populations.² Symptoms can include dysphagia with solids and liquids, chest pain, and regurgitation.

A chest x-ray will show an absence of gastric air, and occasionally, as in this case, a tubular mass (the dilated esophagus) behind the heart and aorta. On fluoroscopy, the lower two-thirds of the esophagus does not have peristalsis and the terminal part has a bird beak appearance. Manometry will show normal or elevated pressure in the lower esophagus. Administration of cholinergic agonists will cause a marked increase in baseline pressure, as well as pain and regurgitation. Endoscopy can exclude secondary causes.

Narrowing the causes of dysphagia

The differential diagnosis is broad because there are 2 types of dysphagia: mechanical and neuromuscular.

Mechanical dysphagia is caused by a food bolus or foreign body, by intrinsic narrowing of the esophagus (from inflammation, esophageal webs, benign and malignant strictures, and tumors) or by extrinsic compression (from bone or thyroid abscesses or vascular tightening).

Neuromuscular dysphagia is either a swallowing reflex problem, a disorder of the pharyngeal and striated esophagus muscles, or an esophageal smooth muscle disorder.³ Close attention to the patient’s history and physical exam is key to zeroing in on the proper diagnosis.

On the other hand, food impaction in the esophagus almost always indicates certain etiologies. Benign esophageal stenosis caused by Schatzki rings (B rings) or by peptic strictures is the most common cause of food impaction, followed by esophageal webs, extrinsic compression, surgical anastomosis, esophagitis (eg, eosinophilic esophagitis), and motor disorders, such as achalasia.

First-line therapy is surgery; pharmacologic Tx is least effective

Treatment should be individualized by age, gender, and patient preference; however, there is no definitive treatment for this condition. First-line therapy includes graded pneumatic dilation or laparoscopic myotomy with a partial fundoplication.⁴ Botulinum toxin injection in the lower esophageal sphincter is recommended for patients who are not good candidates for surgery or dilation.⁵

Pharmacologic therapy, the least effective treatment option, is recommended for patients who are unwilling or unable to undergo myotomy and/or dilation and do not respond to botulinum toxin.^6,7 Long-acting nitrates such as isosorbide, calcium channel blockers such as nifedipine, and phosphodiesterase-5 (PDE5) inhibitors such as sildenafil reduce lower esophageal sphincter tone and pressure.

A chest x-ray will show an absence of gastric air, and occasionally, as in this case, a tubular mass (the dilated esophagus) behind the heart and aorta.

Both nifedipine and isosorbide should be taken sublingually before meals (30 minutes and 10 minutes, respectively). The effects of nifedipine and isosorbide, however, are partial, and these agents do not provide complete relief from symptoms.⁶ PDE5 use has been limited and results are inconclusive.

Our patient. The food particles in the patient’s esophagus were removed during endoscopy, and she stopped vomiting completely. Based on the findings and clinical picture, the patient most likely suffered from mega-esophagus (an end-stage dilated malfunctioning esophagus). Our patient was discharged to follow-up with her gastroenterologist.

Because there is no definitive treatment for achalasia, the patient was counseled about the need for continuous monitoring and dietary precautions, including modification of food texture or change of fluid viscosity. Food may be chopped, minced, or pureed, and fluids may be thickened.

CORRESPONDENCE
Hossein Akhondi, MD, FACP, Georgetown University, 1010 Mass Ave, NW, Unit 904, Washington, DC 20001; h68akhond@hotmail.com.

The Systolic Blood Pressure Intervention Trial (SPRINT),¹ a study of more than 9000 patients published late last year, was stopped prematurely when it became clear that those receiving intensive treatment (systolic target 120 mm Hg) had significantly lower rates of myocardial infarction (MI), stroke, cardiovascular death, and other severe heart disease than those getting standard treatment (systolic target 140 mm Hg). Participants had an elevated cardiovascular risk at baseline (age ≥75 years, history of cardiovascular disease [CVD], chronic kidney disease [CKD], or elevated 10-year Framingham CVD risk score ≥15%); those with diabetes, history of stroke, or polycystic kidney disease were excluded.