SAN FRANCISCO – When your first or second attempts to help a skin wound heal haven’t worked, ask yourself three questions, Dr. Theodora Mauro suggested:

• Have you diagnosed the wound correctly?

• What systemic conditions are keeping the wound from healing?

• Have you tailored your treatment to the wound correctly?

Most dermatologists are pretty good at diagnosing ulcers that are caused by single etiologies. What Dr. Mauro sees more commonly in her busy referral practice, however, are wounds that won’t heal because of a combination of causes – often venous insufficiency plus something else, she said at the annual meeting of the Pacific Dermatologic Association.

"That can make the diagnosis a little more confusing," said Dr. Mauro, professor of dermatology at the University of California, San Francisco and chief of the dermatology service at the San Francisco Veterans Affairs Medical Center.

Ulcer types

The most common skin ulcer in the United States is due to venous insufficiency. These patients tend to be spread among dermatologists, vascular surgeons, and podiatrists and "are not well served by being scattered among different disciplines," she said.

Arterial ulcers make up 6%-10% of skin ulcers in the medical literature, and the incidence of diabetic ulcers is increasing, she added. Pressure ulcers are becoming more common as the population ages.

Morphology and the location of ulcers usually can distinguish the different types, but don’t forget to check the patient’s pulses and sensations, Dr. Mauro said. If you can feel pedal pulses, the patient is very likely to have a normal ankle brachial index (greater than 0.8). "It’s an easy thing to do and very helpful," she said. Also, break a Q-tip cotton swab in half and poke the patient with the sharp end. "You’d be surprised at the number of people who have altered sensation" that’s contributing to the ulceration.

A common "combination" that gets missed is a nonmelanoma skin cancer and an ulcer at that site from venous insufficiency. Consider taking biopsies of nonhealing ulcers to look for skin cancer, she said. Long-standing ulcers can develop squamous cell carcinoma within them. A basal cell carcinoma can look like a healing ulcer, but not heal.

Bullous diseases also can be hidden in ulcers, particularly in the elderly. "There seems to be a two-hit thing with venous insufficiency where you have a little bit of blistering disease and you have a lot of hydrostatic pressure, and people will get their bullae on their legs long before they get it anyplace else," Dr. Mauro said. "You put compression on and they come back next week and now they have intact bullae. Think about that as another cause."

Less common ulcerative problems that can be confusing include pyoderma gangrenosum (which may be half as common as people think, studies suggest), an underlying vasculitis, or mycobacterial infections. If you see a nonhealing hyperkeratotic lesion, consider an atypical mycobacterial infection. In Dr. Mauro’s region, these usually are in patients who went mountain biking and inoculated themselves through an ankle scratch or in patients exposed to the organism through infected water during a pedicure.

Systemic conditions

Wound healing can be inhibited by things that doctors do, and by things that patients do.

Taking antimetabolite medications (such as hydroxyurea or methotrexate), prednisone, or nonsteroidal anti-inflammatory drugs can impair wound healing, as does smoking. Radiation to the site also inhibits healing. Think twice before irradiating a basal cell carcinoma on the leg of a patient with venous insufficiency. "It’s much better to either try some topical medication or just bite the bullet, do surgery, and put the Unna boot on after the surgery, because if you irradiate [the basal cell carcinoma] and it ulcerates, then it’s really hard to heal," she said.

Coexisting cancer or arterial disease can inhibit wound healing. If you check pulses and can’t feel them, send the patient for an ankle brachial index to determine if there’s arterial disease, in which case the patient should see a vascular surgeon, she said.

When you’re taking patients’ histories, ask what they’re eating so you can assess whether they’re getting enough protein, zinc, and vitamin C. "You’d be surprised at the number of nutritional deficiencies that we see" in patients with nonhealing wounds. Her clinic picks up a zinc deficiency three to four times per year and a protein deficiency approximately twice a year. "All of these are things that you need to make collagen and granulation tissue," she explained. Supplementation with Ensure can provide these nutrients, but a less-expensive option is Carnation Breakfast Essentials, at about one-fifth the cost, she added.

Tailor therapy appropriately

Dressings can make wounds worse. Most commonly, putting a hydrocolloid dressing (such as DuoDERM) on an ulcer that has a lot of drainage will macerate and enlarge the wound. Putting stiff foams or self-adherent wraps such as Coban on wounds with a lot of edema can create secondary ulcers. And avoid compression on the legs of people with arterial insufficiency, Dr. Mauro said.

Artifactual ulcers from patients scratching or picking at wounds are increasing, she said. These patients usually will not report that they’re messing with the wound, but your level of suspicion should increase if the ulcer is above the knee. Hydrocolloid dressings work pretty well for this problem. Consider sending some of these patients to an expert in the growing field of medication therapy for dysesthesia.

Ask patients about home remedies, because they will put all kinds of things on wounds to try and help them heal. Neomycin can cause contact dermatitis. Patients may apply full-strength hydrogen peroxide, thinking that they need a disinfectant, which tends to damage the epithelium and can impair wound healing. If they insist on using hydrogen peroxide, recommend a half-strength solution.

For patients with venous insufficiency, the hydrostatic pressure from sitting can be nearly as bad as from standing. Ask patients with nonhealing wounds what they do at home and at work. If they’re sitting much of that time, recommend products to alleviate the pressure. Dr. Mauro said she has virtually become a saleswoman for La-Z-Boy furniture during her medical career because La-Z-Boy products allow patients to eat, work at computers, and function in positions with less hydrostatic pressure.

When to refer

Consider referring patients with chronic wounds that have not lost at least 50% of their width and height within 6 weeks. When a wound has been present long enough, the physiology shifts from acute to chronic. "It’s as if the body decides that it’s tired of trying to heal it and its new equilibrium is just going to be, ‘I have a wound,’ " she said.

If you want to try treating chronic wounds, applying Promogran Prisma matrix wound dressing in those without good granulation tissue may stimulate granulation tissue, she said.

Debriding an ulcer is "kind of a poor man’s way of getting platelet-derived growth factor," she added. Dr. Mauro applies a compounded 30% lidocaine ("but you can use any topical lidocaine"), leaves it on for 20-25 minutes, and debrides using a curette, which is much more precise than a scalpel. "What you’re trying to do is ‘reboot the computer’ and trick the ulcer into thinking it’s an acute ulcer rather than a chronic one," she said.

Dr. Mauro said she refers patients with arterial insufficiency to vascular surgeons. She sends patients with diabetes to podiatrists, preferably before they develop ulcers. The podiatrist can regularly trim nails for patients with poor sight and loss of sensation who may cut themselves, and can design footwear to avoid pressure that could cause an ulcer. "That will keep you out of trouble" with diabetic patients, she said.

Dr. Mauro has been a consultant for Unilever, but not in a wound-healing capacity.

[email protected]

On Twitter @sherryboschert

SAN FRANCISCO – When your first or second attempts to help a skin wound heal haven’t worked, ask yourself three questions, Dr. Theodora Mauro suggested:

• Have you diagnosed the wound correctly?

• What systemic conditions are keeping the wound from healing?

• Have you tailored your treatment to the wound correctly?

Most dermatologists are pretty good at diagnosing ulcers that are caused by single etiologies. What Dr. Mauro sees more commonly in her busy referral practice, however, are wounds that won’t heal because of a combination of causes – often venous insufficiency plus something else, she said at the annual meeting of the Pacific Dermatologic Association.

"That can make the diagnosis a little more confusing," said Dr. Mauro, professor of dermatology at the University of California, San Francisco and chief of the dermatology service at the San Francisco Veterans Affairs Medical Center.

Ulcer types

The most common skin ulcer in the United States is due to venous insufficiency. These patients tend to be spread among dermatologists, vascular surgeons, and podiatrists and "are not well served by being scattered among different disciplines," she said.

Arterial ulcers make up 6%-10% of skin ulcers in the medical literature, and the incidence of diabetic ulcers is increasing, she added. Pressure ulcers are becoming more common as the population ages.

Morphology and the location of ulcers usually can distinguish the different types, but don’t forget to check the patient’s pulses and sensations, Dr. Mauro said. If you can feel pedal pulses, the patient is very likely to have a normal ankle brachial index (greater than 0.8). "It’s an easy thing to do and very helpful," she said. Also, break a Q-tip cotton swab in half and poke the patient with the sharp end. "You’d be surprised at the number of people who have altered sensation" that’s contributing to the ulceration.

A common "combination" that gets missed is a nonmelanoma skin cancer and an ulcer at that site from venous insufficiency. Consider taking biopsies of nonhealing ulcers to look for skin cancer, she said. Long-standing ulcers can develop squamous cell carcinoma within them. A basal cell carcinoma can look like a healing ulcer, but not heal.

Bullous diseases also can be hidden in ulcers, particularly in the elderly. "There seems to be a two-hit thing with venous insufficiency where you have a little bit of blistering disease and you have a lot of hydrostatic pressure, and people will get their bullae on their legs long before they get it anyplace else," Dr. Mauro said. "You put compression on and they come back next week and now they have intact bullae. Think about that as another cause."

Less common ulcerative problems that can be confusing include pyoderma gangrenosum (which may be half as common as people think, studies suggest), an underlying vasculitis, or mycobacterial infections. If you see a nonhealing hyperkeratotic lesion, consider an atypical mycobacterial infection. In Dr. Mauro’s region, these usually are in patients who went mountain biking and inoculated themselves through an ankle scratch or in patients exposed to the organism through infected water during a pedicure.

Systemic conditions

Wound healing can be inhibited by things that doctors do, and by things that patients do.

Taking antimetabolite medications (such as hydroxyurea or methotrexate), prednisone, or nonsteroidal anti-inflammatory drugs can impair wound healing, as does smoking. Radiation to the site also inhibits healing. Think twice before irradiating a basal cell carcinoma on the leg of a patient with venous insufficiency. "It’s much better to either try some topical medication or just bite the bullet, do surgery, and put the Unna boot on after the surgery, because if you irradiate [the basal cell carcinoma] and it ulcerates, then it’s really hard to heal," she said.

Coexisting cancer or arterial disease can inhibit wound healing. If you check pulses and can’t feel them, send the patient for an ankle brachial index to determine if there’s arterial disease, in which case the patient should see a vascular surgeon, she said.

When you’re taking patients’ histories, ask what they’re eating so you can assess whether they’re getting enough protein, zinc, and vitamin C. "You’d be surprised at the number of nutritional deficiencies that we see" in patients with nonhealing wounds. Her clinic picks up a zinc deficiency three to four times per year and a protein deficiency approximately twice a year. "All of these are things that you need to make collagen and granulation tissue," she explained. Supplementation with Ensure can provide these nutrients, but a less-expensive option is Carnation Breakfast Essentials, at about one-fifth the cost, she added.

Tailor therapy appropriately

Dressings can make wounds worse. Most commonly, putting a hydrocolloid dressing (such as DuoDERM) on an ulcer that has a lot of drainage will macerate and enlarge the wound. Putting stiff foams or self-adherent wraps such as Coban on wounds with a lot of edema can create secondary ulcers. And avoid compression on the legs of people with arterial insufficiency, Dr. Mauro said.

Artifactual ulcers from patients scratching or picking at wounds are increasing, she said. These patients usually will not report that they’re messing with the wound, but your level of suspicion should increase if the ulcer is above the knee. Hydrocolloid dressings work pretty well for this problem. Consider sending some of these patients to an expert in the growing field of medication therapy for dysesthesia.

Ask patients about home remedies, because they will put all kinds of things on wounds to try and help them heal. Neomycin can cause contact dermatitis. Patients may apply full-strength hydrogen peroxide, thinking that they need a disinfectant, which tends to damage the epithelium and can impair wound healing. If they insist on using hydrogen peroxide, recommend a half-strength solution.

For patients with venous insufficiency, the hydrostatic pressure from sitting can be nearly as bad as from standing. Ask patients with nonhealing wounds what they do at home and at work. If they’re sitting much of that time, recommend products to alleviate the pressure. Dr. Mauro said she has virtually become a saleswoman for La-Z-Boy furniture during her medical career because La-Z-Boy products allow patients to eat, work at computers, and function in positions with less hydrostatic pressure.

When to refer

Consider referring patients with chronic wounds that have not lost at least 50% of their width and height within 6 weeks. When a wound has been present long enough, the physiology shifts from acute to chronic. "It’s as if the body decides that it’s tired of trying to heal it and its new equilibrium is just going to be, ‘I have a wound,’ " she said.

If you want to try treating chronic wounds, applying Promogran Prisma matrix wound dressing in those without good granulation tissue may stimulate granulation tissue, she said.

Debriding an ulcer is "kind of a poor man’s way of getting platelet-derived growth factor," she added. Dr. Mauro applies a compounded 30% lidocaine ("but you can use any topical lidocaine"), leaves it on for 20-25 minutes, and debrides using a curette, which is much more precise than a scalpel. "What you’re trying to do is ‘reboot the computer’ and trick the ulcer into thinking it’s an acute ulcer rather than a chronic one," she said.

Dr. Mauro said she refers patients with arterial insufficiency to vascular surgeons. She sends patients with diabetes to podiatrists, preferably before they develop ulcers. The podiatrist can regularly trim nails for patients with poor sight and loss of sensation who may cut themselves, and can design footwear to avoid pressure that could cause an ulcer. "That will keep you out of trouble" with diabetic patients, she said.

Dr. Mauro has been a consultant for Unilever, but not in a wound-healing capacity.

[email protected]

On Twitter @sherryboschert

SAN FRANCISCO – When your first or second attempts to help a skin wound heal haven’t worked, ask yourself three questions, Dr. Theodora Mauro suggested:

• Have you diagnosed the wound correctly?

• What systemic conditions are keeping the wound from healing?

• Have you tailored your treatment to the wound correctly?

Most dermatologists are pretty good at diagnosing ulcers that are caused by single etiologies. What Dr. Mauro sees more commonly in her busy referral practice, however, are wounds that won’t heal because of a combination of causes – often venous insufficiency plus something else, she said at the annual meeting of the Pacific Dermatologic Association.

"That can make the diagnosis a little more confusing," said Dr. Mauro, professor of dermatology at the University of California, San Francisco and chief of the dermatology service at the San Francisco Veterans Affairs Medical Center.

Ulcer types

The most common skin ulcer in the United States is due to venous insufficiency. These patients tend to be spread among dermatologists, vascular surgeons, and podiatrists and "are not well served by being scattered among different disciplines," she said.

Arterial ulcers make up 6%-10% of skin ulcers in the medical literature, and the incidence of diabetic ulcers is increasing, she added. Pressure ulcers are becoming more common as the population ages.

Morphology and the location of ulcers usually can distinguish the different types, but don’t forget to check the patient’s pulses and sensations, Dr. Mauro said. If you can feel pedal pulses, the patient is very likely to have a normal ankle brachial index (greater than 0.8). "It’s an easy thing to do and very helpful," she said. Also, break a Q-tip cotton swab in half and poke the patient with the sharp end. "You’d be surprised at the number of people who have altered sensation" that’s contributing to the ulceration.

A common "combination" that gets missed is a nonmelanoma skin cancer and an ulcer at that site from venous insufficiency. Consider taking biopsies of nonhealing ulcers to look for skin cancer, she said. Long-standing ulcers can develop squamous cell carcinoma within them. A basal cell carcinoma can look like a healing ulcer, but not heal.

Bullous diseases also can be hidden in ulcers, particularly in the elderly. "There seems to be a two-hit thing with venous insufficiency where you have a little bit of blistering disease and you have a lot of hydrostatic pressure, and people will get their bullae on their legs long before they get it anyplace else," Dr. Mauro said. "You put compression on and they come back next week and now they have intact bullae. Think about that as another cause."

Less common ulcerative problems that can be confusing include pyoderma gangrenosum (which may be half as common as people think, studies suggest), an underlying vasculitis, or mycobacterial infections. If you see a nonhealing hyperkeratotic lesion, consider an atypical mycobacterial infection. In Dr. Mauro’s region, these usually are in patients who went mountain biking and inoculated themselves through an ankle scratch or in patients exposed to the organism through infected water during a pedicure.

Systemic conditions

Wound healing can be inhibited by things that doctors do, and by things that patients do.

Taking antimetabolite medications (such as hydroxyurea or methotrexate), prednisone, or nonsteroidal anti-inflammatory drugs can impair wound healing, as does smoking. Radiation to the site also inhibits healing. Think twice before irradiating a basal cell carcinoma on the leg of a patient with venous insufficiency. "It’s much better to either try some topical medication or just bite the bullet, do surgery, and put the Unna boot on after the surgery, because if you irradiate [the basal cell carcinoma] and it ulcerates, then it’s really hard to heal," she said.

Coexisting cancer or arterial disease can inhibit wound healing. If you check pulses and can’t feel them, send the patient for an ankle brachial index to determine if there’s arterial disease, in which case the patient should see a vascular surgeon, she said.

When you’re taking patients’ histories, ask what they’re eating so you can assess whether they’re getting enough protein, zinc, and vitamin C. "You’d be surprised at the number of nutritional deficiencies that we see" in patients with nonhealing wounds. Her clinic picks up a zinc deficiency three to four times per year and a protein deficiency approximately twice a year. "All of these are things that you need to make collagen and granulation tissue," she explained. Supplementation with Ensure can provide these nutrients, but a less-expensive option is Carnation Breakfast Essentials, at about one-fifth the cost, she added.

Tailor therapy appropriately

Dressings can make wounds worse. Most commonly, putting a hydrocolloid dressing (such as DuoDERM) on an ulcer that has a lot of drainage will macerate and enlarge the wound. Putting stiff foams or self-adherent wraps such as Coban on wounds with a lot of edema can create secondary ulcers. And avoid compression on the legs of people with arterial insufficiency, Dr. Mauro said.

Artifactual ulcers from patients scratching or picking at wounds are increasing, she said. These patients usually will not report that they’re messing with the wound, but your level of suspicion should increase if the ulcer is above the knee. Hydrocolloid dressings work pretty well for this problem. Consider sending some of these patients to an expert in the growing field of medication therapy for dysesthesia.

Ask patients about home remedies, because they will put all kinds of things on wounds to try and help them heal. Neomycin can cause contact dermatitis. Patients may apply full-strength hydrogen peroxide, thinking that they need a disinfectant, which tends to damage the epithelium and can impair wound healing. If they insist on using hydrogen peroxide, recommend a half-strength solution.

For patients with venous insufficiency, the hydrostatic pressure from sitting can be nearly as bad as from standing. Ask patients with nonhealing wounds what they do at home and at work. If they’re sitting much of that time, recommend products to alleviate the pressure. Dr. Mauro said she has virtually become a saleswoman for La-Z-Boy furniture during her medical career because La-Z-Boy products allow patients to eat, work at computers, and function in positions with less hydrostatic pressure.

When to refer

Consider referring patients with chronic wounds that have not lost at least 50% of their width and height within 6 weeks. When a wound has been present long enough, the physiology shifts from acute to chronic. "It’s as if the body decides that it’s tired of trying to heal it and its new equilibrium is just going to be, ‘I have a wound,’ " she said.

If you want to try treating chronic wounds, applying Promogran Prisma matrix wound dressing in those without good granulation tissue may stimulate granulation tissue, she said.

Debriding an ulcer is "kind of a poor man’s way of getting platelet-derived growth factor," she added. Dr. Mauro applies a compounded 30% lidocaine ("but you can use any topical lidocaine"), leaves it on for 20-25 minutes, and debrides using a curette, which is much more precise than a scalpel. "What you’re trying to do is ‘reboot the computer’ and trick the ulcer into thinking it’s an acute ulcer rather than a chronic one," she said.

Dr. Mauro said she refers patients with arterial insufficiency to vascular surgeons. She sends patients with diabetes to podiatrists, preferably before they develop ulcers. The podiatrist can regularly trim nails for patients with poor sight and loss of sensation who may cut themselves, and can design footwear to avoid pressure that could cause an ulcer. "That will keep you out of trouble" with diabetic patients, she said.

Dr. Mauro has been a consultant for Unilever, but not in a wound-healing capacity.

[email protected]

On Twitter @sherryboschert

When it comes to health, wellness, and fitness apps, we physicians tend to think of our patients. As in, how can this app help my patient lose weight, exercise more, monitor his diabetes, or help her stay compliant with her medications?

But what about physicians and other health care workers? Can apps help us? Absolutely. According to Dr. Craig Burkhart, a dermatologist and apps expert at the University of North Carolina at Chapel Hill, many physicians aren’t taking advantage of apps that can improve efficiency. "Most physicians I encounter have $1,000-$2,000 smartphones and tablets (when you include the service plans) and only make phone calls, check e-mails, text, and listen to music on them – all things they could do with much less expensive devices."

Dr. Burkhart says that many apps "can turn your devices into tools that help organize your e-mails, organize your schedule, bring clinical information to your fingertips, aid patient-doctor communication, secure important information, speed up and improve note taking, and more."

Apps for physicians are available in categories including patient education, drug reference, medical literature, and general reference.

Check out these handy apps and see what works for you:

• Read by QxMD. Staying up to date on medical journals is a challenge. This app lets you access, organize, and share articles from your favorite medical journals. Its magazinelike interface is popular with users, and makes reading medical journals "as fun as it can be," says Dr. Burkhart.

• PDFpen. Dr. Burkhart says this app is "essential to a paperless workflow." It allows users to sign and send documents without printing actual sheets of paper, making for a greener and more efficient office.

• Visual DX. A reference tool for physicians, this app is a digital medical image library with more than 25,000 images. It allows you to visually confirm a diagnosis and to quickly search on a disease, including symptoms and patient care management. A key feature is its ability to let you create a visual differential of medication-induced diseases for more than 700 different drugs.

• 1Password. We’ve all forgotten passwords from time to time. This app allows you to make and store highly secure and complex passwords. For Dr. Burkhart, it has "replaced memory and random sheets of paper as his password repository."

• Draw MD. We know that visuals often help us to explain complex issues to patients more effectively. This app enables you to draw and modify medical images and surgical procedures in a way that is clear and understandable to patients.

• 3D4Medical. This app can enhance patient education by using 3D technology to allow navigation around the body. You can zoom, rotate, and cut images to create different perspectives.

Dr. Jeffrey Benabio is a partner physician in the department of dermatology of the Southern California Permanente Group in San Diego and a volunteer clinical assistant professor at the University of California, San Diego. He has published numerous scientific articles and is a member and fellow of the American Academy of Dermatology, and a member of the Telemedicine Association and the American Medical Association, among others. He is board certified in dermatology as well as medicine and surgery in the state of California. Dr. Benabio has a special interest in the uses of social media for education and building a dermatology practice. He is the founder of The Derm Blog, an educational website which has had over 2 million unique visitors. Dr. Benabio is also a founding member and the skin care expert for Livestrong.com, a health and wellness website of Lance Armstrong’s the Livestrong Foundation. Dr. Benabio is @Dermdoc on Twitter.

When it comes to health, wellness, and fitness apps, we physicians tend to think of our patients. As in, how can this app help my patient lose weight, exercise more, monitor his diabetes, or help her stay compliant with her medications?

But what about physicians and other health care workers? Can apps help us? Absolutely. According to Dr. Craig Burkhart, a dermatologist and apps expert at the University of North Carolina at Chapel Hill, many physicians aren’t taking advantage of apps that can improve efficiency. "Most physicians I encounter have $1,000-$2,000 smartphones and tablets (when you include the service plans) and only make phone calls, check e-mails, text, and listen to music on them – all things they could do with much less expensive devices."

Dr. Burkhart says that many apps "can turn your devices into tools that help organize your e-mails, organize your schedule, bring clinical information to your fingertips, aid patient-doctor communication, secure important information, speed up and improve note taking, and more."

Apps for physicians are available in categories including patient education, drug reference, medical literature, and general reference.

Check out these handy apps and see what works for you:

• Read by QxMD. Staying up to date on medical journals is a challenge. This app lets you access, organize, and share articles from your favorite medical journals. Its magazinelike interface is popular with users, and makes reading medical journals "as fun as it can be," says Dr. Burkhart.

• PDFpen. Dr. Burkhart says this app is "essential to a paperless workflow." It allows users to sign and send documents without printing actual sheets of paper, making for a greener and more efficient office.

• Visual DX. A reference tool for physicians, this app is a digital medical image library with more than 25,000 images. It allows you to visually confirm a diagnosis and to quickly search on a disease, including symptoms and patient care management. A key feature is its ability to let you create a visual differential of medication-induced diseases for more than 700 different drugs.

• 1Password. We’ve all forgotten passwords from time to time. This app allows you to make and store highly secure and complex passwords. For Dr. Burkhart, it has "replaced memory and random sheets of paper as his password repository."

• Draw MD. We know that visuals often help us to explain complex issues to patients more effectively. This app enables you to draw and modify medical images and surgical procedures in a way that is clear and understandable to patients.

• 3D4Medical. This app can enhance patient education by using 3D technology to allow navigation around the body. You can zoom, rotate, and cut images to create different perspectives.

Dr. Jeffrey Benabio is a partner physician in the department of dermatology of the Southern California Permanente Group in San Diego and a volunteer clinical assistant professor at the University of California, San Diego. He has published numerous scientific articles and is a member and fellow of the American Academy of Dermatology, and a member of the Telemedicine Association and the American Medical Association, among others. He is board certified in dermatology as well as medicine and surgery in the state of California. Dr. Benabio has a special interest in the uses of social media for education and building a dermatology practice. He is the founder of The Derm Blog, an educational website which has had over 2 million unique visitors. Dr. Benabio is also a founding member and the skin care expert for Livestrong.com, a health and wellness website of Lance Armstrong’s the Livestrong Foundation. Dr. Benabio is @Dermdoc on Twitter.

When it comes to health, wellness, and fitness apps, we physicians tend to think of our patients. As in, how can this app help my patient lose weight, exercise more, monitor his diabetes, or help her stay compliant with her medications?

But what about physicians and other health care workers? Can apps help us? Absolutely. According to Dr. Craig Burkhart, a dermatologist and apps expert at the University of North Carolina at Chapel Hill, many physicians aren’t taking advantage of apps that can improve efficiency. "Most physicians I encounter have $1,000-$2,000 smartphones and tablets (when you include the service plans) and only make phone calls, check e-mails, text, and listen to music on them – all things they could do with much less expensive devices."

Dr. Burkhart says that many apps "can turn your devices into tools that help organize your e-mails, organize your schedule, bring clinical information to your fingertips, aid patient-doctor communication, secure important information, speed up and improve note taking, and more."

Apps for physicians are available in categories including patient education, drug reference, medical literature, and general reference.

Check out these handy apps and see what works for you:

• Read by QxMD. Staying up to date on medical journals is a challenge. This app lets you access, organize, and share articles from your favorite medical journals. Its magazinelike interface is popular with users, and makes reading medical journals "as fun as it can be," says Dr. Burkhart.

• PDFpen. Dr. Burkhart says this app is "essential to a paperless workflow." It allows users to sign and send documents without printing actual sheets of paper, making for a greener and more efficient office.

• Visual DX. A reference tool for physicians, this app is a digital medical image library with more than 25,000 images. It allows you to visually confirm a diagnosis and to quickly search on a disease, including symptoms and patient care management. A key feature is its ability to let you create a visual differential of medication-induced diseases for more than 700 different drugs.

• 1Password. We’ve all forgotten passwords from time to time. This app allows you to make and store highly secure and complex passwords. For Dr. Burkhart, it has "replaced memory and random sheets of paper as his password repository."

• Draw MD. We know that visuals often help us to explain complex issues to patients more effectively. This app enables you to draw and modify medical images and surgical procedures in a way that is clear and understandable to patients.

• 3D4Medical. This app can enhance patient education by using 3D technology to allow navigation around the body. You can zoom, rotate, and cut images to create different perspectives.

Dr. Jeffrey Benabio is a partner physician in the department of dermatology of the Southern California Permanente Group in San Diego and a volunteer clinical assistant professor at the University of California, San Diego. He has published numerous scientific articles and is a member and fellow of the American Academy of Dermatology, and a member of the Telemedicine Association and the American Medical Association, among others. He is board certified in dermatology as well as medicine and surgery in the state of California. Dr. Benabio has a special interest in the uses of social media for education and building a dermatology practice. He is the founder of The Derm Blog, an educational website which has had over 2 million unique visitors. Dr. Benabio is also a founding member and the skin care expert for Livestrong.com, a health and wellness website of Lance Armstrong’s the Livestrong Foundation. Dr. Benabio is @Dermdoc on Twitter.

A plasma protein involved in tumor oxidation and reduction reactions was useful for detecting and excluding lung cancer in more than three quarters of clinical samples evaluated in a large prospective study.

Isocitrate dehydrogenase 1 (IDH1) measurement was associated with a sensitivity of 77.1% and specificity of 76.2% in a training set of samples (n = 712), and 82.9% sensitivity and 76.6% specificity in a second validation or test set (n = 710).

Sensitivity and specificity were generally improved when the protein’s detection was considered in addition to other known or proposed non–small-cell lung cancer (NSCLC) biomarkers, with sensitivities of 75.8% and 86.3% in the training and test sets, respectively, and specificities of 89.6% and 70.7%.

"Some existing NSCLC biomarkers, such as CEA [carcinoembryonic antigen] and Cyfra21-1 [cytokeratin fragment 21-1], have been used in clinical practice, whereas others, such as CA125 [cancer antigen 125], have been recommended for further validation," Dr. Nan Sun and associates reported in the latest issue of Clinical Cancer Research.

"These biomarkers have low sensitivity, ranging from 50% to 60%, with specificities of approximately 90%," said the researchers, of the department of thoracic surgical oncology at the Cancer Institute and Hospital, Peking Union Medical College and Chinese Academy of Medical Sciences in Beijing.

Previous research by the team had shown IDH1 levels were elevated in tumor samples taken from patients with NSCLC (Mol. Cell. Proteomics 2012;11:M111). Their present investigation (Clin. Cancer. Res. 2013; 19: 5136-45) therefore aimed to see if the protein’s measurement could aid in the diagnosis of lung cancer, differentiating between those who did and those who did not have malignant disease.

For their investigation, the team obtained 1,422 blood samples from 943 patients with previously untreated NSCLC and 479 healthy individuals who were seen for routine examinations between 2007 and 2011 at their institution.

The blood samples from the lung cancer patients were taken 3 days prior to their undergoing surgery and IDH1 levels were immediately determined by enzyme-linked immunosorbent assay, while CEA, Cyfra21-1, and CA125 levels were measured with an Elecys immunoassay analyzer.

Median levels of IDH1 were 2.39 U/L higher than those of healthy controls for squamous cell carcinoma cases (n = 489) cases and 1.96 U/L higher for adenocarcinoma cases (n = 454). Additionally, median plasma levels of IDH1 were higher in patients with adenocarcinomas than in those with squamous cell carcinomas (P = .012)

"We have identified IDH1 as an effective plasma biomarker with high sensitivity and specificity in the diagnosis of NSCLC, especially lung adenocarcinoma," senior study investigator Dr. Jie He said in a press release issued by the American Association for Cancer Research. "Based on the present data, IDH1 can be used to detect stage 1 lung cancer,"

The protein might also detect precancerous lesions, but further studies are required to test that hypothesis, said Dr. He. IDH1 might be a good target for NSCLC treatment as it "may be involved in the development of lung cancer."

A multicenter clinical trial is planned to further validate the diagnostic utility of IDH1.

Research funding was provided by the National High Technology Research and Development Program of China, the International Science and Technology Corporation and Exchange Project, the National Natural Science Foundation of China, the Doctoral Fund of Ministry of Education of China, and the Government Health Care Research Foundation for Senior Officials. The authors had no conflicts of interest to disclose.

A plasma protein involved in tumor oxidation and reduction reactions was useful for detecting and excluding lung cancer in more than three quarters of clinical samples evaluated in a large prospective study.

Isocitrate dehydrogenase 1 (IDH1) measurement was associated with a sensitivity of 77.1% and specificity of 76.2% in a training set of samples (n = 712), and 82.9% sensitivity and 76.6% specificity in a second validation or test set (n = 710).

Sensitivity and specificity were generally improved when the protein’s detection was considered in addition to other known or proposed non–small-cell lung cancer (NSCLC) biomarkers, with sensitivities of 75.8% and 86.3% in the training and test sets, respectively, and specificities of 89.6% and 70.7%.

"Some existing NSCLC biomarkers, such as CEA [carcinoembryonic antigen] and Cyfra21-1 [cytokeratin fragment 21-1], have been used in clinical practice, whereas others, such as CA125 [cancer antigen 125], have been recommended for further validation," Dr. Nan Sun and associates reported in the latest issue of Clinical Cancer Research.

"These biomarkers have low sensitivity, ranging from 50% to 60%, with specificities of approximately 90%," said the researchers, of the department of thoracic surgical oncology at the Cancer Institute and Hospital, Peking Union Medical College and Chinese Academy of Medical Sciences in Beijing.

Previous research by the team had shown IDH1 levels were elevated in tumor samples taken from patients with NSCLC (Mol. Cell. Proteomics 2012;11:M111). Their present investigation (Clin. Cancer. Res. 2013; 19: 5136-45) therefore aimed to see if the protein’s measurement could aid in the diagnosis of lung cancer, differentiating between those who did and those who did not have malignant disease.

For their investigation, the team obtained 1,422 blood samples from 943 patients with previously untreated NSCLC and 479 healthy individuals who were seen for routine examinations between 2007 and 2011 at their institution.

The blood samples from the lung cancer patients were taken 3 days prior to their undergoing surgery and IDH1 levels were immediately determined by enzyme-linked immunosorbent assay, while CEA, Cyfra21-1, and CA125 levels were measured with an Elecys immunoassay analyzer.

Median levels of IDH1 were 2.39 U/L higher than those of healthy controls for squamous cell carcinoma cases (n = 489) cases and 1.96 U/L higher for adenocarcinoma cases (n = 454). Additionally, median plasma levels of IDH1 were higher in patients with adenocarcinomas than in those with squamous cell carcinomas (P = .012)

"We have identified IDH1 as an effective plasma biomarker with high sensitivity and specificity in the diagnosis of NSCLC, especially lung adenocarcinoma," senior study investigator Dr. Jie He said in a press release issued by the American Association for Cancer Research. "Based on the present data, IDH1 can be used to detect stage 1 lung cancer,"

The protein might also detect precancerous lesions, but further studies are required to test that hypothesis, said Dr. He. IDH1 might be a good target for NSCLC treatment as it "may be involved in the development of lung cancer."

A multicenter clinical trial is planned to further validate the diagnostic utility of IDH1.

Research funding was provided by the National High Technology Research and Development Program of China, the International Science and Technology Corporation and Exchange Project, the National Natural Science Foundation of China, the Doctoral Fund of Ministry of Education of China, and the Government Health Care Research Foundation for Senior Officials. The authors had no conflicts of interest to disclose.

A plasma protein involved in tumor oxidation and reduction reactions was useful for detecting and excluding lung cancer in more than three quarters of clinical samples evaluated in a large prospective study.

Isocitrate dehydrogenase 1 (IDH1) measurement was associated with a sensitivity of 77.1% and specificity of 76.2% in a training set of samples (n = 712), and 82.9% sensitivity and 76.6% specificity in a second validation or test set (n = 710).

Sensitivity and specificity were generally improved when the protein’s detection was considered in addition to other known or proposed non–small-cell lung cancer (NSCLC) biomarkers, with sensitivities of 75.8% and 86.3% in the training and test sets, respectively, and specificities of 89.6% and 70.7%.

"Some existing NSCLC biomarkers, such as CEA [carcinoembryonic antigen] and Cyfra21-1 [cytokeratin fragment 21-1], have been used in clinical practice, whereas others, such as CA125 [cancer antigen 125], have been recommended for further validation," Dr. Nan Sun and associates reported in the latest issue of Clinical Cancer Research.

"These biomarkers have low sensitivity, ranging from 50% to 60%, with specificities of approximately 90%," said the researchers, of the department of thoracic surgical oncology at the Cancer Institute and Hospital, Peking Union Medical College and Chinese Academy of Medical Sciences in Beijing.

Previous research by the team had shown IDH1 levels were elevated in tumor samples taken from patients with NSCLC (Mol. Cell. Proteomics 2012;11:M111). Their present investigation (Clin. Cancer. Res. 2013; 19: 5136-45) therefore aimed to see if the protein’s measurement could aid in the diagnosis of lung cancer, differentiating between those who did and those who did not have malignant disease.

For their investigation, the team obtained 1,422 blood samples from 943 patients with previously untreated NSCLC and 479 healthy individuals who were seen for routine examinations between 2007 and 2011 at their institution.

The blood samples from the lung cancer patients were taken 3 days prior to their undergoing surgery and IDH1 levels were immediately determined by enzyme-linked immunosorbent assay, while CEA, Cyfra21-1, and CA125 levels were measured with an Elecys immunoassay analyzer.

Median levels of IDH1 were 2.39 U/L higher than those of healthy controls for squamous cell carcinoma cases (n = 489) cases and 1.96 U/L higher for adenocarcinoma cases (n = 454). Additionally, median plasma levels of IDH1 were higher in patients with adenocarcinomas than in those with squamous cell carcinomas (P = .012)

"We have identified IDH1 as an effective plasma biomarker with high sensitivity and specificity in the diagnosis of NSCLC, especially lung adenocarcinoma," senior study investigator Dr. Jie He said in a press release issued by the American Association for Cancer Research. "Based on the present data, IDH1 can be used to detect stage 1 lung cancer,"

The protein might also detect precancerous lesions, but further studies are required to test that hypothesis, said Dr. He. IDH1 might be a good target for NSCLC treatment as it "may be involved in the development of lung cancer."

A multicenter clinical trial is planned to further validate the diagnostic utility of IDH1.

Research funding was provided by the National High Technology Research and Development Program of China, the International Science and Technology Corporation and Exchange Project, the National Natural Science Foundation of China, the Doctoral Fund of Ministry of Education of China, and the Government Health Care Research Foundation for Senior Officials. The authors had no conflicts of interest to disclose.

CASE Sudden weakness

Ms. G, age 59, presents to a local critical access (rural) hospital after an episode of sudden-onset left-sided weakness followed by unconsciousness. She regained consciousness quickly and is awake when she arrives at the hospital. This event was not witnessed, although family members were nearby to call emergency personnel.

EXAMINATION Unremarkable

In the emergency department, Ms. G demonstrates left facial droop, left-sided weakness of her arm and leg, and aphasia. She says she has a severe headache that began after she regained consciousness. She is unable to see out of her left eye.

Ms. G’s NIH Stroke Scale score is 13, indicating a moderate stroke; an emergent head CT does not demonstrate any acute hemorrhagic process. Tissue plasminogen activator (tPA) is administered for a suspected stroke approximately 2 hours after her symptoms began. She is transferred to a larger, tertiary care hospital for further workup and observation.

Upon admission to the ICU, Ms. G’s laboratory values are: sodium, 137 mEq/L; potassium, 5.1 mEq/L; creatinine, 1.26 mg/dL; lipase, 126 U/L; and lactic acid, 9 mg/dL. The glucose level is within normal limits and her urinalysis is unremarkable.

Vital signs are stable and Ms. G is not in acute distress. A physical exam demonstrates 4/5 strength in the left-upper and -lower extremities. Additionally, there are 2+ deep tendon reflexes bilaterally in the biceps, triceps, and brachioradialis. She has left-sided facial droop while in the ICU, and continues to demonstrate some aphasia—although she is alert and oriented to person, time, and place.

The medical history is significant for depression, restless leg syndrome, tonic-clonic seizures, and previous stroke-like events. Medications include amitriptyline, 25 mg/d; citalopram, 20 mg/d; valproate, 1,200 mg/d; and ropinirole, 0.5 mg/d. Her mother has a history of stroke-like events, but her family history and social history are otherwise unremarkable.

The authors' observations

Conversion disorder requires the exclusion of medical causes that could explain the patient’s neurologic symptoms. It is prudent to rule out the most serious of the potential contributors to Ms. G’s condition—namely, an acute cerebrovascular accident. A CT scan did not find any significant pathology, however. In the ICU, an MRI showed no evidence of acute infarction based on diffusion-weighted imaging. A head and neck MRA demonstrated no hemodynamically significant stenosis of the internal carotid arteries. An EEG revealed generalized, polymorphic slow activity without evidence of seizures or epilepsy. An electrocardiogram showed normal ventricular size with an appropriate ejection fraction.

The ICU staff consulted psychiatry to evaluate a psychiatric cause of Ms. G’s symptoms.

An exhaustive and comprehensive workup was performed; there were no significant findings. Although laboratory tests were performed, it was the physical exam that suggested the diagnosis of conversion disorder. In that sense, the diagnostic tests were more of a supportive adjunct to the findings of the physical examination, which consistently failed to indicate a neurologic insult.

Hoover’s sign is a well-established test of functional weakness, in which the patient extends his (her) hip when the contralateral hip is flexed. However, there are other tests of functional weakness that can be useful when considering a conversion disorder diagnosis, including co-contraction, the so-called arm-drop sign, and the sternocleidomastoid test. Diukova and colleagues reported that 80% of patients with functional weakness demonstrated ipsilateral sternocleidomastoid weakness, compared with 11% with vascular hemiparesis.¹

Ms. G appeared to have suffered an acute ischemic event that caused her neurologic symptoms; her rather extensive psychiatric history was overlooked before the psychiatric service was consulted. When Ms. G was admitted to the ICU, the working differential was postictal seizure state rather than cerebrovascular accident. Ms. G had a poorly defined seizure history, and her history of stroke-like events was murky, at best. She had not been treated previously with tPA, and in all past instances her symptoms resolved spontaneously.

Ms. G’s case illustrates why conversion disorder is difficult to diagnose and why, perhaps, it is even a dangerous diagnostic consideration. Booij and colleagues described two patients with neurologic sequelae thought to be the result of conversion disorder; subsequent imaging demonstrated a posterior stroke.² Over a 6-year period in an emergency department, Glick and coworkers identified six patients with neurologic pathology who were misdiagnosed with conversion disorder.³ In a study of 4,220 patients presenting to a psychiatric emergency service, three patients complained of extremity paralysis or pain, which was attributed to conversion disorder but later attributed to an organic disease.⁴

These studies emphasize the precarious nature of diagnosing conversion disorder. For that reason, an extensive medical workup is necessary prior to considering a diagnosis of conversion disorder. In Ms. G’s case, a reasonably thorough workup failed to reveal any obvious pathology. Only then was conversion disorder included as a diagnostic possibility.

EVALUATION Childhood abuse

When performing a mental status exam, Ms. G has poor eye contact, but is cooperative with our interview. She is disheveled and overweight, and denies suicidal or homicidal ideation. She displays constricted affect.

During the interview, we note a left facial droop, although Ms. G is able to smile fully. As the interview progresses, her facial droop seems to become more apparent as we discuss her past, including a history of childhood physical and sexual abuse. She has a history of depression and has been seeing an outpatient psychiatrist for the past year. Ms. G describes being hospitalized in a psychiatric unit, but she is unable to provide any details about when and where this occurred.

Ms. G admits to occasional auditory and visual hallucinations, mostly relating to the abuse she experienced as a child by her parents. She exhibits no other signs or symptoms of psychosis; the hallucinations she describes are consistent with flashbacks and vivid memories relating to the abuse. Ms. G also recently lost her job and is experiencing numerous financial stressors.

The authors' observations

There are many examples in the literature of patients with conversion disorder (Table 1),⁴ ranging from pseudoseizures, which are relatively common, to intriguing cases, such as cochlear implant failure.⁵

Some studies estimate that the prevalence of conversion disorder symptoms ranges from 16.1% to 21.9% in the general population.⁶ Somatoform disorders, including conversion disorder, often are comorbid with anxiety and depression. In one study, 26% of somatoform disorder patients also had depression or anxiety, or both.⁷ Patients with conversion disorder often report a history of childhood physical or sexual abuse.⁶ In many patients with conversion disorder, there also appears to be a significant association between the disorder and a recent and distant history of psychosocial stressors.⁸

Ms. G had an extensive history of abuse by her parents. Conversion disorder presenting as a stroke with realistic and convincing physical manifestations is an unusual presentation. There are case reports that detail this presentation, particularly in the emergency department setting.⁶

Clinical considerations

The relative uncertainty that accompanies a diagnosis of conversion disorder can be discomforting for clinicians. As demonstrated by Ms. G, as well as other case reports of conversion disorder, it takes time for the patient to find a clinician who will consider a diagnosis of conversion disorder.⁹ Largely, this is because DSM-5 requires that other medical causes be ruled out (Table 2).¹⁰ This often proves to be problematic because feigning, or the lack thereof, is difficult to prove.⁹

Further complicating the diagnosis is the lack of a diagnostic test. Neurologists can use video EEG or physical exam maneuvers such as the Hoover’s sign to help make a diagnosis of conversion disorder.¹¹ In this sense, the physical exam maneuvers form the basis of making a diagnosis, while imaging and lab work support the diagnosis. Hoover’s sign, for example, has not been well studied in a controlled manner, but is recognized as a test that may aid a conversion disorder diagnosis. Clinicians should not solely rely upon these physical exam maneuvers; interpreting them in the context of the patient’s overall presentation is critical. This demonstrates the importance of using the physical exam as a way to guide the diagnosis in association with other tests.¹²

Despite the lack of pathology, studies demonstrate that patients with conversion disorder may have abnormal brain activity that causes them to perceive motor symptoms as involuntary.¹¹ Therefore, there is a clear need for an increased understanding of psychiatric and neurologic components of diagnosing conversion disorder.⁸

With Ms. G, it was prudent to make a conversion disorder diagnosis to prevent harm to the patient should future stroke-like events occur. Without considering a conversion disorder diagnosis, a patient may continue to receive unnecessary interventions. Basic physical exam maneuvers, such as Hoover’s sign, can be performed quickly in the ED setting before proceeding with other potentially harmful interventions, such as administering tPA.

Treatment. There are few therapies for conversion disorder. This is, in part, because of lack of understanding about the disorder’s neurologic and biologic etiologies. Although there are some studies that support the use of cognitive-behavioral therapy (CBT), there is little evidence advocating the use of a single mechanism to treat conversion disorder.¹³ There is evidence that CBT is an effective treatment for several somatoform disorders, including conversion disorder. Research suggests that patients with somatoform disorder have better outcomes when CBT is added to a traditional follow-up.^14,15

In Ms. G’s case, we provided information about the diagnosis and scheduled visits to continue her outpatient therapy.

Bottom Line

Conversion disorder is difficult to diagnose, and can mimic potentially life- threatening medical conditions. Conduct a thorough medical workup of these patients, even when it is tempting to jump to a diagnosis of conversion disorder. The use of physical exam maneuvers such as Hoover’s sign may help guide the diagnosis when used in conjunction with other testing.

Related Resources

• Conversion disorder. www.nlm.nih.gov/medlineplus/ency/ article/000954.htm.
• Couprie W, Wijdicks EF, Rooijmans HG, et al. Outcome in conver- sion disorder: a follow up study. J Neurol Neurosurg Psychiatry. 1995;58(6):750-752.

Drug Brand Names

Amitriptyline • Elavil       Citalopram • Celexa

Ropinirole • Requip         Valproate • Depakote

Disclosure

The authors report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.

CASE Sudden weakness

Ms. G, age 59, presents to a local critical access (rural) hospital after an episode of sudden-onset left-sided weakness followed by unconsciousness. She regained consciousness quickly and is awake when she arrives at the hospital. This event was not witnessed, although family members were nearby to call emergency personnel.

EXAMINATION Unremarkable

In the emergency department, Ms. G demonstrates left facial droop, left-sided weakness of her arm and leg, and aphasia. She says she has a severe headache that began after she regained consciousness. She is unable to see out of her left eye.

Ms. G’s NIH Stroke Scale score is 13, indicating a moderate stroke; an emergent head CT does not demonstrate any acute hemorrhagic process. Tissue plasminogen activator (tPA) is administered for a suspected stroke approximately 2 hours after her symptoms began. She is transferred to a larger, tertiary care hospital for further workup and observation.

Upon admission to the ICU, Ms. G’s laboratory values are: sodium, 137 mEq/L; potassium, 5.1 mEq/L; creatinine, 1.26 mg/dL; lipase, 126 U/L; and lactic acid, 9 mg/dL. The glucose level is within normal limits and her urinalysis is unremarkable.

Vital signs are stable and Ms. G is not in acute distress. A physical exam demonstrates 4/5 strength in the left-upper and -lower extremities. Additionally, there are 2+ deep tendon reflexes bilaterally in the biceps, triceps, and brachioradialis. She has left-sided facial droop while in the ICU, and continues to demonstrate some aphasia—although she is alert and oriented to person, time, and place.

The medical history is significant for depression, restless leg syndrome, tonic-clonic seizures, and previous stroke-like events. Medications include amitriptyline, 25 mg/d; citalopram, 20 mg/d; valproate, 1,200 mg/d; and ropinirole, 0.5 mg/d. Her mother has a history of stroke-like events, but her family history and social history are otherwise unremarkable.

The authors' observations

Conversion disorder requires the exclusion of medical causes that could explain the patient’s neurologic symptoms. It is prudent to rule out the most serious of the potential contributors to Ms. G’s condition—namely, an acute cerebrovascular accident. A CT scan did not find any significant pathology, however. In the ICU, an MRI showed no evidence of acute infarction based on diffusion-weighted imaging. A head and neck MRA demonstrated no hemodynamically significant stenosis of the internal carotid arteries. An EEG revealed generalized, polymorphic slow activity without evidence of seizures or epilepsy. An electrocardiogram showed normal ventricular size with an appropriate ejection fraction.

The ICU staff consulted psychiatry to evaluate a psychiatric cause of Ms. G’s symptoms.

An exhaustive and comprehensive workup was performed; there were no significant findings. Although laboratory tests were performed, it was the physical exam that suggested the diagnosis of conversion disorder. In that sense, the diagnostic tests were more of a supportive adjunct to the findings of the physical examination, which consistently failed to indicate a neurologic insult.

Hoover’s sign is a well-established test of functional weakness, in which the patient extends his (her) hip when the contralateral hip is flexed. However, there are other tests of functional weakness that can be useful when considering a conversion disorder diagnosis, including co-contraction, the so-called arm-drop sign, and the sternocleidomastoid test. Diukova and colleagues reported that 80% of patients with functional weakness demonstrated ipsilateral sternocleidomastoid weakness, compared with 11% with vascular hemiparesis.¹

Ms. G appeared to have suffered an acute ischemic event that caused her neurologic symptoms; her rather extensive psychiatric history was overlooked before the psychiatric service was consulted. When Ms. G was admitted to the ICU, the working differential was postictal seizure state rather than cerebrovascular accident. Ms. G had a poorly defined seizure history, and her history of stroke-like events was murky, at best. She had not been treated previously with tPA, and in all past instances her symptoms resolved spontaneously.

Ms. G’s case illustrates why conversion disorder is difficult to diagnose and why, perhaps, it is even a dangerous diagnostic consideration. Booij and colleagues described two patients with neurologic sequelae thought to be the result of conversion disorder; subsequent imaging demonstrated a posterior stroke.² Over a 6-year period in an emergency department, Glick and coworkers identified six patients with neurologic pathology who were misdiagnosed with conversion disorder.³ In a study of 4,220 patients presenting to a psychiatric emergency service, three patients complained of extremity paralysis or pain, which was attributed to conversion disorder but later attributed to an organic disease.⁴

These studies emphasize the precarious nature of diagnosing conversion disorder. For that reason, an extensive medical workup is necessary prior to considering a diagnosis of conversion disorder. In Ms. G’s case, a reasonably thorough workup failed to reveal any obvious pathology. Only then was conversion disorder included as a diagnostic possibility.

EVALUATION Childhood abuse

When performing a mental status exam, Ms. G has poor eye contact, but is cooperative with our interview. She is disheveled and overweight, and denies suicidal or homicidal ideation. She displays constricted affect.

During the interview, we note a left facial droop, although Ms. G is able to smile fully. As the interview progresses, her facial droop seems to become more apparent as we discuss her past, including a history of childhood physical and sexual abuse. She has a history of depression and has been seeing an outpatient psychiatrist for the past year. Ms. G describes being hospitalized in a psychiatric unit, but she is unable to provide any details about when and where this occurred.

Ms. G admits to occasional auditory and visual hallucinations, mostly relating to the abuse she experienced as a child by her parents. She exhibits no other signs or symptoms of psychosis; the hallucinations she describes are consistent with flashbacks and vivid memories relating to the abuse. Ms. G also recently lost her job and is experiencing numerous financial stressors.

The authors' observations

There are many examples in the literature of patients with conversion disorder (Table 1),⁴ ranging from pseudoseizures, which are relatively common, to intriguing cases, such as cochlear implant failure.⁵

Some studies estimate that the prevalence of conversion disorder symptoms ranges from 16.1% to 21.9% in the general population.⁶ Somatoform disorders, including conversion disorder, often are comorbid with anxiety and depression. In one study, 26% of somatoform disorder patients also had depression or anxiety, or both.⁷ Patients with conversion disorder often report a history of childhood physical or sexual abuse.⁶ In many patients with conversion disorder, there also appears to be a significant association between the disorder and a recent and distant history of psychosocial stressors.⁸

Ms. G had an extensive history of abuse by her parents. Conversion disorder presenting as a stroke with realistic and convincing physical manifestations is an unusual presentation. There are case reports that detail this presentation, particularly in the emergency department setting.⁶

Clinical considerations

The relative uncertainty that accompanies a diagnosis of conversion disorder can be discomforting for clinicians. As demonstrated by Ms. G, as well as other case reports of conversion disorder, it takes time for the patient to find a clinician who will consider a diagnosis of conversion disorder.⁹ Largely, this is because DSM-5 requires that other medical causes be ruled out (Table 2).¹⁰ This often proves to be problematic because feigning, or the lack thereof, is difficult to prove.⁹

Further complicating the diagnosis is the lack of a diagnostic test. Neurologists can use video EEG or physical exam maneuvers such as the Hoover’s sign to help make a diagnosis of conversion disorder.¹¹ In this sense, the physical exam maneuvers form the basis of making a diagnosis, while imaging and lab work support the diagnosis. Hoover’s sign, for example, has not been well studied in a controlled manner, but is recognized as a test that may aid a conversion disorder diagnosis. Clinicians should not solely rely upon these physical exam maneuvers; interpreting them in the context of the patient’s overall presentation is critical. This demonstrates the importance of using the physical exam as a way to guide the diagnosis in association with other tests.¹²

Despite the lack of pathology, studies demonstrate that patients with conversion disorder may have abnormal brain activity that causes them to perceive motor symptoms as involuntary.¹¹ Therefore, there is a clear need for an increased understanding of psychiatric and neurologic components of diagnosing conversion disorder.⁸

With Ms. G, it was prudent to make a conversion disorder diagnosis to prevent harm to the patient should future stroke-like events occur. Without considering a conversion disorder diagnosis, a patient may continue to receive unnecessary interventions. Basic physical exam maneuvers, such as Hoover’s sign, can be performed quickly in the ED setting before proceeding with other potentially harmful interventions, such as administering tPA.

Treatment. There are few therapies for conversion disorder. This is, in part, because of lack of understanding about the disorder’s neurologic and biologic etiologies. Although there are some studies that support the use of cognitive-behavioral therapy (CBT), there is little evidence advocating the use of a single mechanism to treat conversion disorder.¹³ There is evidence that CBT is an effective treatment for several somatoform disorders, including conversion disorder. Research suggests that patients with somatoform disorder have better outcomes when CBT is added to a traditional follow-up.^14,15

In Ms. G’s case, we provided information about the diagnosis and scheduled visits to continue her outpatient therapy.

Bottom Line

Conversion disorder is difficult to diagnose, and can mimic potentially life- threatening medical conditions. Conduct a thorough medical workup of these patients, even when it is tempting to jump to a diagnosis of conversion disorder. The use of physical exam maneuvers such as Hoover’s sign may help guide the diagnosis when used in conjunction with other testing.

Related Resources

• Conversion disorder. www.nlm.nih.gov/medlineplus/ency/ article/000954.htm.
• Couprie W, Wijdicks EF, Rooijmans HG, et al. Outcome in conver- sion disorder: a follow up study. J Neurol Neurosurg Psychiatry. 1995;58(6):750-752.

Drug Brand Names

Amitriptyline • Elavil       Citalopram • Celexa

Ropinirole • Requip         Valproate • Depakote

Disclosure

The authors report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.

CASE Sudden weakness

Ms. G, age 59, presents to a local critical access (rural) hospital after an episode of sudden-onset left-sided weakness followed by unconsciousness. She regained consciousness quickly and is awake when she arrives at the hospital. This event was not witnessed, although family members were nearby to call emergency personnel.

EXAMINATION Unremarkable

In the emergency department, Ms. G demonstrates left facial droop, left-sided weakness of her arm and leg, and aphasia. She says she has a severe headache that began after she regained consciousness. She is unable to see out of her left eye.

Ms. G’s NIH Stroke Scale score is 13, indicating a moderate stroke; an emergent head CT does not demonstrate any acute hemorrhagic process. Tissue plasminogen activator (tPA) is administered for a suspected stroke approximately 2 hours after her symptoms began. She is transferred to a larger, tertiary care hospital for further workup and observation.

Upon admission to the ICU, Ms. G’s laboratory values are: sodium, 137 mEq/L; potassium, 5.1 mEq/L; creatinine, 1.26 mg/dL; lipase, 126 U/L; and lactic acid, 9 mg/dL. The glucose level is within normal limits and her urinalysis is unremarkable.

Vital signs are stable and Ms. G is not in acute distress. A physical exam demonstrates 4/5 strength in the left-upper and -lower extremities. Additionally, there are 2+ deep tendon reflexes bilaterally in the biceps, triceps, and brachioradialis. She has left-sided facial droop while in the ICU, and continues to demonstrate some aphasia—although she is alert and oriented to person, time, and place.

The medical history is significant for depression, restless leg syndrome, tonic-clonic seizures, and previous stroke-like events. Medications include amitriptyline, 25 mg/d; citalopram, 20 mg/d; valproate, 1,200 mg/d; and ropinirole, 0.5 mg/d. Her mother has a history of stroke-like events, but her family history and social history are otherwise unremarkable.

The authors' observations

Conversion disorder requires the exclusion of medical causes that could explain the patient’s neurologic symptoms. It is prudent to rule out the most serious of the potential contributors to Ms. G’s condition—namely, an acute cerebrovascular accident. A CT scan did not find any significant pathology, however. In the ICU, an MRI showed no evidence of acute infarction based on diffusion-weighted imaging. A head and neck MRA demonstrated no hemodynamically significant stenosis of the internal carotid arteries. An EEG revealed generalized, polymorphic slow activity without evidence of seizures or epilepsy. An electrocardiogram showed normal ventricular size with an appropriate ejection fraction.

The ICU staff consulted psychiatry to evaluate a psychiatric cause of Ms. G’s symptoms.

An exhaustive and comprehensive workup was performed; there were no significant findings. Although laboratory tests were performed, it was the physical exam that suggested the diagnosis of conversion disorder. In that sense, the diagnostic tests were more of a supportive adjunct to the findings of the physical examination, which consistently failed to indicate a neurologic insult.

Hoover’s sign is a well-established test of functional weakness, in which the patient extends his (her) hip when the contralateral hip is flexed. However, there are other tests of functional weakness that can be useful when considering a conversion disorder diagnosis, including co-contraction, the so-called arm-drop sign, and the sternocleidomastoid test. Diukova and colleagues reported that 80% of patients with functional weakness demonstrated ipsilateral sternocleidomastoid weakness, compared with 11% with vascular hemiparesis.¹

Ms. G appeared to have suffered an acute ischemic event that caused her neurologic symptoms; her rather extensive psychiatric history was overlooked before the psychiatric service was consulted. When Ms. G was admitted to the ICU, the working differential was postictal seizure state rather than cerebrovascular accident. Ms. G had a poorly defined seizure history, and her history of stroke-like events was murky, at best. She had not been treated previously with tPA, and in all past instances her symptoms resolved spontaneously.

Ms. G’s case illustrates why conversion disorder is difficult to diagnose and why, perhaps, it is even a dangerous diagnostic consideration. Booij and colleagues described two patients with neurologic sequelae thought to be the result of conversion disorder; subsequent imaging demonstrated a posterior stroke.² Over a 6-year period in an emergency department, Glick and coworkers identified six patients with neurologic pathology who were misdiagnosed with conversion disorder.³ In a study of 4,220 patients presenting to a psychiatric emergency service, three patients complained of extremity paralysis or pain, which was attributed to conversion disorder but later attributed to an organic disease.⁴

These studies emphasize the precarious nature of diagnosing conversion disorder. For that reason, an extensive medical workup is necessary prior to considering a diagnosis of conversion disorder. In Ms. G’s case, a reasonably thorough workup failed to reveal any obvious pathology. Only then was conversion disorder included as a diagnostic possibility.

EVALUATION Childhood abuse

When performing a mental status exam, Ms. G has poor eye contact, but is cooperative with our interview. She is disheveled and overweight, and denies suicidal or homicidal ideation. She displays constricted affect.

During the interview, we note a left facial droop, although Ms. G is able to smile fully. As the interview progresses, her facial droop seems to become more apparent as we discuss her past, including a history of childhood physical and sexual abuse. She has a history of depression and has been seeing an outpatient psychiatrist for the past year. Ms. G describes being hospitalized in a psychiatric unit, but she is unable to provide any details about when and where this occurred.

Ms. G admits to occasional auditory and visual hallucinations, mostly relating to the abuse she experienced as a child by her parents. She exhibits no other signs or symptoms of psychosis; the hallucinations she describes are consistent with flashbacks and vivid memories relating to the abuse. Ms. G also recently lost her job and is experiencing numerous financial stressors.

The authors' observations

There are many examples in the literature of patients with conversion disorder (Table 1),⁴ ranging from pseudoseizures, which are relatively common, to intriguing cases, such as cochlear implant failure.⁵

Some studies estimate that the prevalence of conversion disorder symptoms ranges from 16.1% to 21.9% in the general population.⁶ Somatoform disorders, including conversion disorder, often are comorbid with anxiety and depression. In one study, 26% of somatoform disorder patients also had depression or anxiety, or both.⁷ Patients with conversion disorder often report a history of childhood physical or sexual abuse.⁶ In many patients with conversion disorder, there also appears to be a significant association between the disorder and a recent and distant history of psychosocial stressors.⁸

Ms. G had an extensive history of abuse by her parents. Conversion disorder presenting as a stroke with realistic and convincing physical manifestations is an unusual presentation. There are case reports that detail this presentation, particularly in the emergency department setting.⁶

Clinical considerations

The relative uncertainty that accompanies a diagnosis of conversion disorder can be discomforting for clinicians. As demonstrated by Ms. G, as well as other case reports of conversion disorder, it takes time for the patient to find a clinician who will consider a diagnosis of conversion disorder.⁹ Largely, this is because DSM-5 requires that other medical causes be ruled out (Table 2).¹⁰ This often proves to be problematic because feigning, or the lack thereof, is difficult to prove.⁹

Further complicating the diagnosis is the lack of a diagnostic test. Neurologists can use video EEG or physical exam maneuvers such as the Hoover’s sign to help make a diagnosis of conversion disorder.¹¹ In this sense, the physical exam maneuvers form the basis of making a diagnosis, while imaging and lab work support the diagnosis. Hoover’s sign, for example, has not been well studied in a controlled manner, but is recognized as a test that may aid a conversion disorder diagnosis. Clinicians should not solely rely upon these physical exam maneuvers; interpreting them in the context of the patient’s overall presentation is critical. This demonstrates the importance of using the physical exam as a way to guide the diagnosis in association with other tests.¹²

Despite the lack of pathology, studies demonstrate that patients with conversion disorder may have abnormal brain activity that causes them to perceive motor symptoms as involuntary.¹¹ Therefore, there is a clear need for an increased understanding of psychiatric and neurologic components of diagnosing conversion disorder.⁸

With Ms. G, it was prudent to make a conversion disorder diagnosis to prevent harm to the patient should future stroke-like events occur. Without considering a conversion disorder diagnosis, a patient may continue to receive unnecessary interventions. Basic physical exam maneuvers, such as Hoover’s sign, can be performed quickly in the ED setting before proceeding with other potentially harmful interventions, such as administering tPA.

Treatment. There are few therapies for conversion disorder. This is, in part, because of lack of understanding about the disorder’s neurologic and biologic etiologies. Although there are some studies that support the use of cognitive-behavioral therapy (CBT), there is little evidence advocating the use of a single mechanism to treat conversion disorder.¹³ There is evidence that CBT is an effective treatment for several somatoform disorders, including conversion disorder. Research suggests that patients with somatoform disorder have better outcomes when CBT is added to a traditional follow-up.^14,15

In Ms. G’s case, we provided information about the diagnosis and scheduled visits to continue her outpatient therapy.

Bottom Line

Conversion disorder is difficult to diagnose, and can mimic potentially life- threatening medical conditions. Conduct a thorough medical workup of these patients, even when it is tempting to jump to a diagnosis of conversion disorder. The use of physical exam maneuvers such as Hoover’s sign may help guide the diagnosis when used in conjunction with other testing.

Related Resources

• Conversion disorder. www.nlm.nih.gov/medlineplus/ency/ article/000954.htm.
• Couprie W, Wijdicks EF, Rooijmans HG, et al. Outcome in conver- sion disorder: a follow up study. J Neurol Neurosurg Psychiatry. 1995;58(6):750-752.

Drug Brand Names

Amitriptyline • Elavil       Citalopram • Celexa

Ropinirole • Requip         Valproate • Depakote

Disclosure

The authors report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.

Psychogenic itch—an excessive impulse to scratch, gouge, or pick at skin in the absence of dermatologic cause—is common among psychiatric inpatients, but can be challenging to assess and manage in outpatients. Patients with psychogenic itch predominantly are female, with average age of onset between 30 and 45 years.¹ Psychiatric disorders associated with psychogenic itch include depression, obsessive-compulsive disorder, anxiety, somatoform disorders, mania, psychosis, and substance abuse.² Body dysmorphic disorder, trichotillomania, kleptomania, and borderline personality disorder may be comorbid in patients with psychogenic itch.³

Characteristics of psychogenic itch

Consider psychogenic itch in patients who have recurring physical symptoms and demand examination despite repeated negative results. Other indicators include psychological factors—loss of a loved one, unemployment, relocation, etc.—that may be associated with onset, severity, elicitation, or maintenance of the itching; impairments in the patient’s social or professional life; and marked preoccupation with itching or the state of her (his) skin. Characteristically, itching can be provoked by emotional triggers, most notably during stages of excitement, and also by mechanical or chemical stimuli.

Skin changes associated with psychogenic itch often are found on areas accessible to the patient’s hand: face, arms, legs, abdomen, thighs, upper back, and shoulders. These changes can be seen in varying stages, from discrete superficial excoriations, erosions, and ulcers to thick, darkened nodules and colorless atrophic scars. Patients often complain of burning. In some cases, a patient uses a tool or instrument to autoaggressively manipulate his (her) skin in response to tingling or stabbing sensations. Artificial lesions or eczemas brought on by self-
manipulation can occur. Stress, life changes, or inhibited rage may be evoking the burning sensation and subsequent complaints.

Interventions to consider

After you have ruled out other causes of pruritus and made a diagnosis of psychogenic itch,  educate your patient about the multifactorial etiology. Explain possible associations between skin disorders and unconscious reaction patterns, and the role of emotional and cognitive stimuli.

Moisturizing the skin can help the dryness associated with repetitive scratching. Consider prescribing an antihistamine, moisturizer, topical steroid, antibiotic, or
occlusive dressing.

Some pharmacological properties of antidepressants that are not related to their antidepressant activity—eg, the histamine-1 blocking effect of tricyclic antidepressants—are beneficial for treating psychogenic itch.⁴ Sedating antihistamines (hydroxyzine) and antidepressants (doxepin) may help break cycles of itching and depression or itching and scratching.⁴ Tricyclic antidepressants also are recommended for treating burning, stabbing, or tingling sensations.

Disclosure

Dr. Jain reports no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.

Psychogenic itch—an excessive impulse to scratch, gouge, or pick at skin in the absence of dermatologic cause—is common among psychiatric inpatients, but can be challenging to assess and manage in outpatients. Patients with psychogenic itch predominantly are female, with average age of onset between 30 and 45 years.¹ Psychiatric disorders associated with psychogenic itch include depression, obsessive-compulsive disorder, anxiety, somatoform disorders, mania, psychosis, and substance abuse.² Body dysmorphic disorder, trichotillomania, kleptomania, and borderline personality disorder may be comorbid in patients with psychogenic itch.³

Characteristics of psychogenic itch

Consider psychogenic itch in patients who have recurring physical symptoms and demand examination despite repeated negative results. Other indicators include psychological factors—loss of a loved one, unemployment, relocation, etc.—that may be associated with onset, severity, elicitation, or maintenance of the itching; impairments in the patient’s social or professional life; and marked preoccupation with itching or the state of her (his) skin. Characteristically, itching can be provoked by emotional triggers, most notably during stages of excitement, and also by mechanical or chemical stimuli.

Skin changes associated with psychogenic itch often are found on areas accessible to the patient’s hand: face, arms, legs, abdomen, thighs, upper back, and shoulders. These changes can be seen in varying stages, from discrete superficial excoriations, erosions, and ulcers to thick, darkened nodules and colorless atrophic scars. Patients often complain of burning. In some cases, a patient uses a tool or instrument to autoaggressively manipulate his (her) skin in response to tingling or stabbing sensations. Artificial lesions or eczemas brought on by self-
manipulation can occur. Stress, life changes, or inhibited rage may be evoking the burning sensation and subsequent complaints.

Interventions to consider

After you have ruled out other causes of pruritus and made a diagnosis of psychogenic itch,  educate your patient about the multifactorial etiology. Explain possible associations between skin disorders and unconscious reaction patterns, and the role of emotional and cognitive stimuli.

Moisturizing the skin can help the dryness associated with repetitive scratching. Consider prescribing an antihistamine, moisturizer, topical steroid, antibiotic, or
occlusive dressing.

Some pharmacological properties of antidepressants that are not related to their antidepressant activity—eg, the histamine-1 blocking effect of tricyclic antidepressants—are beneficial for treating psychogenic itch.⁴ Sedating antihistamines (hydroxyzine) and antidepressants (doxepin) may help break cycles of itching and depression or itching and scratching.⁴ Tricyclic antidepressants also are recommended for treating burning, stabbing, or tingling sensations.

Disclosure

Dr. Jain reports no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.

Psychogenic itch—an excessive impulse to scratch, gouge, or pick at skin in the absence of dermatologic cause—is common among psychiatric inpatients, but can be challenging to assess and manage in outpatients. Patients with psychogenic itch predominantly are female, with average age of onset between 30 and 45 years.¹ Psychiatric disorders associated with psychogenic itch include depression, obsessive-compulsive disorder, anxiety, somatoform disorders, mania, psychosis, and substance abuse.² Body dysmorphic disorder, trichotillomania, kleptomania, and borderline personality disorder may be comorbid in patients with psychogenic itch.³

Characteristics of psychogenic itch

Consider psychogenic itch in patients who have recurring physical symptoms and demand examination despite repeated negative results. Other indicators include psychological factors—loss of a loved one, unemployment, relocation, etc.—that may be associated with onset, severity, elicitation, or maintenance of the itching; impairments in the patient’s social or professional life; and marked preoccupation with itching or the state of her (his) skin. Characteristically, itching can be provoked by emotional triggers, most notably during stages of excitement, and also by mechanical or chemical stimuli.

Skin changes associated with psychogenic itch often are found on areas accessible to the patient’s hand: face, arms, legs, abdomen, thighs, upper back, and shoulders. These changes can be seen in varying stages, from discrete superficial excoriations, erosions, and ulcers to thick, darkened nodules and colorless atrophic scars. Patients often complain of burning. In some cases, a patient uses a tool or instrument to autoaggressively manipulate his (her) skin in response to tingling or stabbing sensations. Artificial lesions or eczemas brought on by self-
manipulation can occur. Stress, life changes, or inhibited rage may be evoking the burning sensation and subsequent complaints.

Interventions to consider

After you have ruled out other causes of pruritus and made a diagnosis of psychogenic itch,  educate your patient about the multifactorial etiology. Explain possible associations between skin disorders and unconscious reaction patterns, and the role of emotional and cognitive stimuli.

Moisturizing the skin can help the dryness associated with repetitive scratching. Consider prescribing an antihistamine, moisturizer, topical steroid, antibiotic, or
occlusive dressing.

Some pharmacological properties of antidepressants that are not related to their antidepressant activity—eg, the histamine-1 blocking effect of tricyclic antidepressants—are beneficial for treating psychogenic itch.⁴ Sedating antihistamines (hydroxyzine) and antidepressants (doxepin) may help break cycles of itching and depression or itching and scratching.⁴ Tricyclic antidepressants also are recommended for treating burning, stabbing, or tingling sensations.

Disclosure

Dr. Jain reports no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.

Chimeric antigen receptor-modified T cells represent a new approach to immune therapy in the treatment of hematologic malignancies. The clinical activity of chimeric antigen receptors (CARs) has been published in acute lymphoblastic leukemia (ALL)and chronic lymphocytic leukemia (CLL).¹ The results have been remarkable, although only a very small number of patients have been treated. We are anticipating further clinical trials and further development of this technology for more wide spread treatment opportunities for patients. The CARs that have been the most successful clinically have a similar basic make-up. They are genetically modified T cells. The T cells are collected from the patients through leukapheresis, then they are genetically
modified to express an extracellular recognition domain that is connected in the intracellular signaling domains of the T cells. Various extracellular recognition domains have been engineered, but the target of CD19 has proven most successful in patients with B cell malignancies, and CD19 is widely expressed on CLL and B-cell ALL. The cells are infused back into the patient, sometimes after undergoing chemotherapy to lymphodeplete the patient (which may improve the recovery and persistence of the cells after treatment). The infusion responses have been
dramatic in some patients, with severe cytokine storm described in reports, usually several days after treatment.² This is thought to reflect the very rapid identification of the target protein and response of the T cells to the target. Those patients with acute leukemia who have responded also appear to respond rapidly, with disappearance of blasts from the peripheral blood within a month. The cells have been detectable in some patients for months after treatment.

Please click here to view the PDF.

Chimeric antigen receptor-modified T cells represent a new approach to immune therapy in the treatment of hematologic malignancies. The clinical activity of chimeric antigen receptors (CARs) has been published in acute lymphoblastic leukemia (ALL)and chronic lymphocytic leukemia (CLL).¹ The results have been remarkable, although only a very small number of patients have been treated. We are anticipating further clinical trials and further development of this technology for more wide spread treatment opportunities for patients. The CARs that have been the most successful clinically have a similar basic make-up. They are genetically modified T cells. The T cells are collected from the patients through leukapheresis, then they are genetically
modified to express an extracellular recognition domain that is connected in the intracellular signaling domains of the T cells. Various extracellular recognition domains have been engineered, but the target of CD19 has proven most successful in patients with B cell malignancies, and CD19 is widely expressed on CLL and B-cell ALL. The cells are infused back into the patient, sometimes after undergoing chemotherapy to lymphodeplete the patient (which may improve the recovery and persistence of the cells after treatment). The infusion responses have been
dramatic in some patients, with severe cytokine storm described in reports, usually several days after treatment.² This is thought to reflect the very rapid identification of the target protein and response of the T cells to the target. Those patients with acute leukemia who have responded also appear to respond rapidly, with disappearance of blasts from the peripheral blood within a month. The cells have been detectable in some patients for months after treatment.

Please click here to view the PDF.

Chimeric antigen receptor-modified T cells represent a new approach to immune therapy in the treatment of hematologic malignancies. The clinical activity of chimeric antigen receptors (CARs) has been published in acute lymphoblastic leukemia (ALL)and chronic lymphocytic leukemia (CLL).¹ The results have been remarkable, although only a very small number of patients have been treated. We are anticipating further clinical trials and further development of this technology for more wide spread treatment opportunities for patients. The CARs that have been the most successful clinically have a similar basic make-up. They are genetically modified T cells. The T cells are collected from the patients through leukapheresis, then they are genetically
modified to express an extracellular recognition domain that is connected in the intracellular signaling domains of the T cells. Various extracellular recognition domains have been engineered, but the target of CD19 has proven most successful in patients with B cell malignancies, and CD19 is widely expressed on CLL and B-cell ALL. The cells are infused back into the patient, sometimes after undergoing chemotherapy to lymphodeplete the patient (which may improve the recovery and persistence of the cells after treatment). The infusion responses have been
dramatic in some patients, with severe cytokine storm described in reports, usually several days after treatment.² This is thought to reflect the very rapid identification of the target protein and response of the T cells to the target. Those patients with acute leukemia who have responded also appear to respond rapidly, with disappearance of blasts from the peripheral blood within a month. The cells have been detectable in some patients for months after treatment.

Please click here to view the PDF.

A new report that shows double-digit gains in hospitals’ electronic health information exchanges with other providers is a boon to healthcare, says one of SHM’s leading health information technology experts.

Published last month at HealthAffairs.org, “Hospital Electronic Health Information Exchange Grew Substantially in 2008-2012,” found that nearly 6 in 10 hospitals actively exchanged electronic health information with providers and hospitals outside of their own organization in 2012, a 41% jump since 2008.

Kendall Rogers, MD, FACP, SFHM, chief of the division of hospital medicine at the University of New Mexico Health Sciences Center in Albuquerque, says in an email to The Hospitalist that the growth is a good thing.

“Obviously, flow of information is never a bad thing for hospital medicine,” writes Dr. Rogers, chair of SHM’s Information Technology Executive Committee. “I think we have made more progress getting information back out to providers in the community, [and] helping with a safer transition (though we still have a long way to go), but we still lack significantly [in] getting info from providers or other hospitals on admission.”

The report notes that while more information has flowed among hospitals and providers, exchanges of clinical-care summaries and medication lists remain limited. The authors suggest that “new and ongoing policy initiatives and payment reforms may accelerate” the process.

Dr. Rogers adds that making systems more user-friendly may also encourage meaningful participation. “We have a health information exchange here in New Mexico that includes most hospitals”; however, he writes, “it is cumbersome and not routinely used, but definitely a step in the right direction.”

Visit our website for more information on health information technology.

A new report that shows double-digit gains in hospitals’ electronic health information exchanges with other providers is a boon to healthcare, says one of SHM’s leading health information technology experts.

Published last month at HealthAffairs.org, “Hospital Electronic Health Information Exchange Grew Substantially in 2008-2012,” found that nearly 6 in 10 hospitals actively exchanged electronic health information with providers and hospitals outside of their own organization in 2012, a 41% jump since 2008.

Kendall Rogers, MD, FACP, SFHM, chief of the division of hospital medicine at the University of New Mexico Health Sciences Center in Albuquerque, says in an email to The Hospitalist that the growth is a good thing.

“Obviously, flow of information is never a bad thing for hospital medicine,” writes Dr. Rogers, chair of SHM’s Information Technology Executive Committee. “I think we have made more progress getting information back out to providers in the community, [and] helping with a safer transition (though we still have a long way to go), but we still lack significantly [in] getting info from providers or other hospitals on admission.”

The report notes that while more information has flowed among hospitals and providers, exchanges of clinical-care summaries and medication lists remain limited. The authors suggest that “new and ongoing policy initiatives and payment reforms may accelerate” the process.

Dr. Rogers adds that making systems more user-friendly may also encourage meaningful participation. “We have a health information exchange here in New Mexico that includes most hospitals”; however, he writes, “it is cumbersome and not routinely used, but definitely a step in the right direction.”

Visit our website for more information on health information technology.

A new report that shows double-digit gains in hospitals’ electronic health information exchanges with other providers is a boon to healthcare, says one of SHM’s leading health information technology experts.

Published last month at HealthAffairs.org, “Hospital Electronic Health Information Exchange Grew Substantially in 2008-2012,” found that nearly 6 in 10 hospitals actively exchanged electronic health information with providers and hospitals outside of their own organization in 2012, a 41% jump since 2008.

Kendall Rogers, MD, FACP, SFHM, chief of the division of hospital medicine at the University of New Mexico Health Sciences Center in Albuquerque, says in an email to The Hospitalist that the growth is a good thing.

“Obviously, flow of information is never a bad thing for hospital medicine,” writes Dr. Rogers, chair of SHM’s Information Technology Executive Committee. “I think we have made more progress getting information back out to providers in the community, [and] helping with a safer transition (though we still have a long way to go), but we still lack significantly [in] getting info from providers or other hospitals on admission.”

The report notes that while more information has flowed among hospitals and providers, exchanges of clinical-care summaries and medication lists remain limited. The authors suggest that “new and ongoing policy initiatives and payment reforms may accelerate” the process.

Dr. Rogers adds that making systems more user-friendly may also encourage meaningful participation. “We have a health information exchange here in New Mexico that includes most hospitals”; however, he writes, “it is cumbersome and not routinely used, but definitely a step in the right direction.”

Visit our website for more information on health information technology.