"How have you been treating this?" I asked Ivan. He had a rash on his shin.

"Plantain leaves," he explained.

Plantains, of course. Fry ’em or apply ’em.

Home remedies have always intrigued me. Take Preparation H ointment. Good for bags under the eyes, they say. Also good for hemorrhoids. Really good for people who have trouble telling the difference.

Or tea tree oil. I’ve heard about that for years, but never took the time to find out what a tea tree is. A tree shaped like a "T"? A tree that grows tea? A tree made out of tea?

Turns out it is Melaleuca alternifolia, a source of traditional remedies among the indigenous Bundjalung people of Eastern Australia. (Thank you, Wikipedia.) It may kill viruses, bacteria, and fungi. And it makes a dandy shampoo.

Got poison ivy? Try jewelweed (if you can find it). Or rat vein tea (not sure I want to find that). Or boiled sweet fern. Or (of course) tea tree oil.

Do home remedies work? Truth be told, I don’t claim to know one way or the other. Anyhow, I find a different question more interesting – not whether home remedies work, but why people think they do.

The answer to that seems straightforward. People think home remedies work because other people say so. Vicks VapoRub ointment for toenail fungus? Hank says it cleared him right up! His buddy, Frankie, on the other hand, swears by apple cider vinegar for his own toenails. He’s also sure it got rid of Frankie Jr.’s head lice, although back at school, other kids complained that Frankie Jr. smelled like a salad. And his wife Franchette uses it to help reverse the signs of aging.

Which points to something about the popularity of home remedies: There is a big difference between the way patients think and the way doctors do. Many of these cures – most nowadays are either traditional, natural, or both – are supposed to be good for ... well, just about anything. The list of uses for plantains, for instance, includes rashes, wounds, ulcerations, cuts, swelling, sprains, bruises, burns, eczema, cracked lips, poison ivy, mosquito bites, diaper rash, boils, hemorrhoids, blisters, snake bites, spider bites, splinters, and thorns.

Or take another popular item, jojoba oil (that’s ho-HO-ba to you). Named by the Tohono O’odham people of the Sonoran desert (repositories of ancient wisdom, presumably), jojoba is recommended for the treatment of wrinkles; hair loss; joint pain; hemorrhoids (take note, Preparation H nonresponders!); smoker’s cough; and constipation. It also lubricates locks and engines, and it is good for covering homemade cucumbers. Look it up.

Lists like these might make a physician skeptical, prone to wonder which mechanism of action could possibly explain such disparate effects and what studies could be designed to support or refute them. Considerations like these do not generally trouble patients. If something is good, well, it’s just good, for one thing or for many. Doctors split. Patients lump.

I thought I’d heard every folk remedy there is, earnest or whimsical, until Tibor came by last month. A well-spoken gent with a thick, Hungarian accent, Tibor pulled up his shirt and showed me a lot of eczema.

"Two things make it better," he explained. "The first thing, I swim every day in a chlorinated pool to cool it off."

That was a surprise, considering how many eczema patients are convinced that chlorine makes them worse.

And the second?

"Yogurt," he said. "I put on nonfat yogurt." But not just any nonfat yogurt.

"I tried all different kinds," Tibor went on. "I tried flavored yogurt, I tried Greek yogurt. But the best is plain nonfat yogurt."

A controlled experiment!

I asked Tibor where he got the idea for applying yogurt to his rash.

"My mother suggested some kind of peasant remedy when I was a kid," he said. "It may have been sour cream."

So it was some kind of rash, treated with something dairy. I tried to picture little Tibor covered with sour cream. I couldn’t.

"I put the yogurt on last night," said Tibor, proudly rolling up his sleeve to show me an almost eczema-free arm. "See how well it works!"

Anecdotal, perhaps, but still impressive. It cures eczema! It lowers cholesterol! It’s on sale!

Take that, tea tree oil.

Dr. Rockoff practices dermatology in Brookline, Mass.

"How have you been treating this?" I asked Ivan. He had a rash on his shin.

"Plantain leaves," he explained.

Plantains, of course. Fry ’em or apply ’em.

Home remedies have always intrigued me. Take Preparation H ointment. Good for bags under the eyes, they say. Also good for hemorrhoids. Really good for people who have trouble telling the difference.

Or tea tree oil. I’ve heard about that for years, but never took the time to find out what a tea tree is. A tree shaped like a "T"? A tree that grows tea? A tree made out of tea?

Turns out it is Melaleuca alternifolia, a source of traditional remedies among the indigenous Bundjalung people of Eastern Australia. (Thank you, Wikipedia.) It may kill viruses, bacteria, and fungi. And it makes a dandy shampoo.

Got poison ivy? Try jewelweed (if you can find it). Or rat vein tea (not sure I want to find that). Or boiled sweet fern. Or (of course) tea tree oil.

Do home remedies work? Truth be told, I don’t claim to know one way or the other. Anyhow, I find a different question more interesting – not whether home remedies work, but why people think they do.

The answer to that seems straightforward. People think home remedies work because other people say so. Vicks VapoRub ointment for toenail fungus? Hank says it cleared him right up! His buddy, Frankie, on the other hand, swears by apple cider vinegar for his own toenails. He’s also sure it got rid of Frankie Jr.’s head lice, although back at school, other kids complained that Frankie Jr. smelled like a salad. And his wife Franchette uses it to help reverse the signs of aging.

Which points to something about the popularity of home remedies: There is a big difference between the way patients think and the way doctors do. Many of these cures – most nowadays are either traditional, natural, or both – are supposed to be good for ... well, just about anything. The list of uses for plantains, for instance, includes rashes, wounds, ulcerations, cuts, swelling, sprains, bruises, burns, eczema, cracked lips, poison ivy, mosquito bites, diaper rash, boils, hemorrhoids, blisters, snake bites, spider bites, splinters, and thorns.

Or take another popular item, jojoba oil (that’s ho-HO-ba to you). Named by the Tohono O’odham people of the Sonoran desert (repositories of ancient wisdom, presumably), jojoba is recommended for the treatment of wrinkles; hair loss; joint pain; hemorrhoids (take note, Preparation H nonresponders!); smoker’s cough; and constipation. It also lubricates locks and engines, and it is good for covering homemade cucumbers. Look it up.

Lists like these might make a physician skeptical, prone to wonder which mechanism of action could possibly explain such disparate effects and what studies could be designed to support or refute them. Considerations like these do not generally trouble patients. If something is good, well, it’s just good, for one thing or for many. Doctors split. Patients lump.

I thought I’d heard every folk remedy there is, earnest or whimsical, until Tibor came by last month. A well-spoken gent with a thick, Hungarian accent, Tibor pulled up his shirt and showed me a lot of eczema.

"Two things make it better," he explained. "The first thing, I swim every day in a chlorinated pool to cool it off."

That was a surprise, considering how many eczema patients are convinced that chlorine makes them worse.

And the second?

"Yogurt," he said. "I put on nonfat yogurt." But not just any nonfat yogurt.

"I tried all different kinds," Tibor went on. "I tried flavored yogurt, I tried Greek yogurt. But the best is plain nonfat yogurt."

A controlled experiment!

I asked Tibor where he got the idea for applying yogurt to his rash.

"My mother suggested some kind of peasant remedy when I was a kid," he said. "It may have been sour cream."

So it was some kind of rash, treated with something dairy. I tried to picture little Tibor covered with sour cream. I couldn’t.

"I put the yogurt on last night," said Tibor, proudly rolling up his sleeve to show me an almost eczema-free arm. "See how well it works!"

Anecdotal, perhaps, but still impressive. It cures eczema! It lowers cholesterol! It’s on sale!

Take that, tea tree oil.

Dr. Rockoff practices dermatology in Brookline, Mass.

"How have you been treating this?" I asked Ivan. He had a rash on his shin.

"Plantain leaves," he explained.

Plantains, of course. Fry ’em or apply ’em.

Home remedies have always intrigued me. Take Preparation H ointment. Good for bags under the eyes, they say. Also good for hemorrhoids. Really good for people who have trouble telling the difference.

Or tea tree oil. I’ve heard about that for years, but never took the time to find out what a tea tree is. A tree shaped like a "T"? A tree that grows tea? A tree made out of tea?

Turns out it is Melaleuca alternifolia, a source of traditional remedies among the indigenous Bundjalung people of Eastern Australia. (Thank you, Wikipedia.) It may kill viruses, bacteria, and fungi. And it makes a dandy shampoo.

Got poison ivy? Try jewelweed (if you can find it). Or rat vein tea (not sure I want to find that). Or boiled sweet fern. Or (of course) tea tree oil.

Do home remedies work? Truth be told, I don’t claim to know one way or the other. Anyhow, I find a different question more interesting – not whether home remedies work, but why people think they do.

The answer to that seems straightforward. People think home remedies work because other people say so. Vicks VapoRub ointment for toenail fungus? Hank says it cleared him right up! His buddy, Frankie, on the other hand, swears by apple cider vinegar for his own toenails. He’s also sure it got rid of Frankie Jr.’s head lice, although back at school, other kids complained that Frankie Jr. smelled like a salad. And his wife Franchette uses it to help reverse the signs of aging.

Which points to something about the popularity of home remedies: There is a big difference between the way patients think and the way doctors do. Many of these cures – most nowadays are either traditional, natural, or both – are supposed to be good for ... well, just about anything. The list of uses for plantains, for instance, includes rashes, wounds, ulcerations, cuts, swelling, sprains, bruises, burns, eczema, cracked lips, poison ivy, mosquito bites, diaper rash, boils, hemorrhoids, blisters, snake bites, spider bites, splinters, and thorns.

Or take another popular item, jojoba oil (that’s ho-HO-ba to you). Named by the Tohono O’odham people of the Sonoran desert (repositories of ancient wisdom, presumably), jojoba is recommended for the treatment of wrinkles; hair loss; joint pain; hemorrhoids (take note, Preparation H nonresponders!); smoker’s cough; and constipation. It also lubricates locks and engines, and it is good for covering homemade cucumbers. Look it up.

Lists like these might make a physician skeptical, prone to wonder which mechanism of action could possibly explain such disparate effects and what studies could be designed to support or refute them. Considerations like these do not generally trouble patients. If something is good, well, it’s just good, for one thing or for many. Doctors split. Patients lump.

I thought I’d heard every folk remedy there is, earnest or whimsical, until Tibor came by last month. A well-spoken gent with a thick, Hungarian accent, Tibor pulled up his shirt and showed me a lot of eczema.

"Two things make it better," he explained. "The first thing, I swim every day in a chlorinated pool to cool it off."

That was a surprise, considering how many eczema patients are convinced that chlorine makes them worse.

And the second?

"Yogurt," he said. "I put on nonfat yogurt." But not just any nonfat yogurt.

"I tried all different kinds," Tibor went on. "I tried flavored yogurt, I tried Greek yogurt. But the best is plain nonfat yogurt."

A controlled experiment!

I asked Tibor where he got the idea for applying yogurt to his rash.

"My mother suggested some kind of peasant remedy when I was a kid," he said. "It may have been sour cream."

So it was some kind of rash, treated with something dairy. I tried to picture little Tibor covered with sour cream. I couldn’t.

"I put the yogurt on last night," said Tibor, proudly rolling up his sleeve to show me an almost eczema-free arm. "See how well it works!"

Anecdotal, perhaps, but still impressive. It cures eczema! It lowers cholesterol! It’s on sale!

Take that, tea tree oil.

Dr. Rockoff practices dermatology in Brookline, Mass.

When I first started with this practice, our local imaging facilities took care of obtaining authorizations for the CT scans and MRI studies that I ordered. It is easy for them; they know just what to say to get insurance providers to pay for these costly tests.

But of course, this is exactly the kind of conflict of interest that we try to avoid in medicine, so about 2 years ago the largest private insurer in Rhode Island changed the rules. This is an entirely reasonable change. But it is also quite inconvenient and time consuming, and, ultimately, it is not clear that it is saving the health care industry all that much money.

Today, if I want an imaging procedure done, I need to get approval for it myself. This usually means my secretary fills out the initial paperwork, the request gets denied, and then, after a series of faxes and phone tag that can take days to weeks, I get on the phone with a physician somewhere else in the world who is purportedly helping me make better patient-care decisions.

Some months ago I was trying to get an approval for a CT scan of the chest for a patient whom I suspected of having sarcoidosis. After an initial denial by the insurance company, I finally got hold of a physician for a "peer-to-peer" evaluation. The person on the other end of the line was a radiologist. He denied my request for a CT scan because the chest x-ray had not shown any evidence of sarcoidosis. Of course, I argued, that was precisely the reason I needed the CT scan. I also respectfully suggested that, being a radiologist, he ought to know.

If it were truly a peer-to-peer evaluation, the person on the other end of the line would have the ability to understand my reasoning, and would have sound counterarguments. If the idea is to reduce the cost of health care, then it is the job of the person on the other end of the line to educate me about why I might be wrong or let me know of alternatives that are cheaper, but no less valuable, that I may have overlooked. It’s either that or recognize that there aren’t any alternatives, and that I have exercised careful decision making.

Instead, all they do is pose questions to me, and then, after having made the patient, my staff, and myself go through all the trouble, finally approve my request. The goal ought to be thoughtful collaboration that ultimately drives health care costs down. Instead, it feels like the goal is to actively discourage me from making more requests by making the process too onerous.

My so-called peers would understand that my elderly patient on Coumadin might be better off with a Lidoderm patch than with some other systemic alternatives. If they were truly my peers, they would understand why it is royally unreasonable to withhold infliximab from a patient who has been doing well on it for years. More recently, because Blue Cross & Blue Shield of Rhode Island started using a new pharmacy benefits manager, we’ve even had to fill out prior authorization requests for methotrexate and prednisone. Do they really think we’re cavalier about writing prescriptions for such toxic medications?

Also, how much money are they saving, exactly? They probably spend a lot more money employing people to do this work than they are saving by denying these prescriptions, some of which are generic. In addition, there’s the cost to my patients’ productivity when they take time out of work. Certainly, it would be cheaper for the insurance company to pay for the cost of Voltaren gel rather than pay for a GI bleed requiring hospitalization, blood transfusions, and possible invasive interventions.

The rising cost of health care in the United States has not led to improved patient outcomes. It begs the question: How much of the increased cost is because of the increasing administrative hurdles?

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

When I first started with this practice, our local imaging facilities took care of obtaining authorizations for the CT scans and MRI studies that I ordered. It is easy for them; they know just what to say to get insurance providers to pay for these costly tests.

But of course, this is exactly the kind of conflict of interest that we try to avoid in medicine, so about 2 years ago the largest private insurer in Rhode Island changed the rules. This is an entirely reasonable change. But it is also quite inconvenient and time consuming, and, ultimately, it is not clear that it is saving the health care industry all that much money.

Today, if I want an imaging procedure done, I need to get approval for it myself. This usually means my secretary fills out the initial paperwork, the request gets denied, and then, after a series of faxes and phone tag that can take days to weeks, I get on the phone with a physician somewhere else in the world who is purportedly helping me make better patient-care decisions.

Some months ago I was trying to get an approval for a CT scan of the chest for a patient whom I suspected of having sarcoidosis. After an initial denial by the insurance company, I finally got hold of a physician for a "peer-to-peer" evaluation. The person on the other end of the line was a radiologist. He denied my request for a CT scan because the chest x-ray had not shown any evidence of sarcoidosis. Of course, I argued, that was precisely the reason I needed the CT scan. I also respectfully suggested that, being a radiologist, he ought to know.

If it were truly a peer-to-peer evaluation, the person on the other end of the line would have the ability to understand my reasoning, and would have sound counterarguments. If the idea is to reduce the cost of health care, then it is the job of the person on the other end of the line to educate me about why I might be wrong or let me know of alternatives that are cheaper, but no less valuable, that I may have overlooked. It’s either that or recognize that there aren’t any alternatives, and that I have exercised careful decision making.

Instead, all they do is pose questions to me, and then, after having made the patient, my staff, and myself go through all the trouble, finally approve my request. The goal ought to be thoughtful collaboration that ultimately drives health care costs down. Instead, it feels like the goal is to actively discourage me from making more requests by making the process too onerous.

My so-called peers would understand that my elderly patient on Coumadin might be better off with a Lidoderm patch than with some other systemic alternatives. If they were truly my peers, they would understand why it is royally unreasonable to withhold infliximab from a patient who has been doing well on it for years. More recently, because Blue Cross & Blue Shield of Rhode Island started using a new pharmacy benefits manager, we’ve even had to fill out prior authorization requests for methotrexate and prednisone. Do they really think we’re cavalier about writing prescriptions for such toxic medications?

Also, how much money are they saving, exactly? They probably spend a lot more money employing people to do this work than they are saving by denying these prescriptions, some of which are generic. In addition, there’s the cost to my patients’ productivity when they take time out of work. Certainly, it would be cheaper for the insurance company to pay for the cost of Voltaren gel rather than pay for a GI bleed requiring hospitalization, blood transfusions, and possible invasive interventions.

The rising cost of health care in the United States has not led to improved patient outcomes. It begs the question: How much of the increased cost is because of the increasing administrative hurdles?

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

When I first started with this practice, our local imaging facilities took care of obtaining authorizations for the CT scans and MRI studies that I ordered. It is easy for them; they know just what to say to get insurance providers to pay for these costly tests.

But of course, this is exactly the kind of conflict of interest that we try to avoid in medicine, so about 2 years ago the largest private insurer in Rhode Island changed the rules. This is an entirely reasonable change. But it is also quite inconvenient and time consuming, and, ultimately, it is not clear that it is saving the health care industry all that much money.

Today, if I want an imaging procedure done, I need to get approval for it myself. This usually means my secretary fills out the initial paperwork, the request gets denied, and then, after a series of faxes and phone tag that can take days to weeks, I get on the phone with a physician somewhere else in the world who is purportedly helping me make better patient-care decisions.

Some months ago I was trying to get an approval for a CT scan of the chest for a patient whom I suspected of having sarcoidosis. After an initial denial by the insurance company, I finally got hold of a physician for a "peer-to-peer" evaluation. The person on the other end of the line was a radiologist. He denied my request for a CT scan because the chest x-ray had not shown any evidence of sarcoidosis. Of course, I argued, that was precisely the reason I needed the CT scan. I also respectfully suggested that, being a radiologist, he ought to know.

If it were truly a peer-to-peer evaluation, the person on the other end of the line would have the ability to understand my reasoning, and would have sound counterarguments. If the idea is to reduce the cost of health care, then it is the job of the person on the other end of the line to educate me about why I might be wrong or let me know of alternatives that are cheaper, but no less valuable, that I may have overlooked. It’s either that or recognize that there aren’t any alternatives, and that I have exercised careful decision making.

Instead, all they do is pose questions to me, and then, after having made the patient, my staff, and myself go through all the trouble, finally approve my request. The goal ought to be thoughtful collaboration that ultimately drives health care costs down. Instead, it feels like the goal is to actively discourage me from making more requests by making the process too onerous.

My so-called peers would understand that my elderly patient on Coumadin might be better off with a Lidoderm patch than with some other systemic alternatives. If they were truly my peers, they would understand why it is royally unreasonable to withhold infliximab from a patient who has been doing well on it for years. More recently, because Blue Cross & Blue Shield of Rhode Island started using a new pharmacy benefits manager, we’ve even had to fill out prior authorization requests for methotrexate and prednisone. Do they really think we’re cavalier about writing prescriptions for such toxic medications?

Also, how much money are they saving, exactly? They probably spend a lot more money employing people to do this work than they are saving by denying these prescriptions, some of which are generic. In addition, there’s the cost to my patients’ productivity when they take time out of work. Certainly, it would be cheaper for the insurance company to pay for the cost of Voltaren gel rather than pay for a GI bleed requiring hospitalization, blood transfusions, and possible invasive interventions.

The rising cost of health care in the United States has not led to improved patient outcomes. It begs the question: How much of the increased cost is because of the increasing administrative hurdles?

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

MAUI, HAWAII – "Slow Mohs" has gained near-universal acceptance among skin cancer specialists as a definitive surgical technique for complete removal of lentigo maligna melanoma while simultaneously sparing normal tissue, according to Dr. Ellen Marmur of Mount Sinai School of Medicine, New York.

The big advantage that slow Mohs has over standard wide local excision with 0.5- to 1-cm margins is a 5-year cure rate approaching 100%. In contrast, standard excision has a recurrence rate of up to 20%, she said at the Hawaii Dermatology Seminar, sponsored by Global Academy for Medical Education/Skin Disease Education Foundation.

Bruce C. Jancin/IMNG Medical Media

Slow Mohs is a modified form of Mohs micrographic surgery. The surgery compares with conventional Mohs: It is staged, margin-controlled excision. But in slow Mohs, rush permanent sections are sent off to the pathologist rather than the frozen sections integral to conventional Mohs.

Dr. Marmur relies upon slow Mohs, with "bread-loafing" of the central tumor by the pathologist, because the permanent sections better preserve the tumor’s microscopic features. Interpreting atypical melanocytes in frozen sections can be quite a challenge. However, she added, some Mohs surgeons have found that using rapid immunostains also markedly improves the sensitivity and specificity of frozen sections in lentigo maligna surgery.

Slow Mohs takes place over the course of days, she said. "Basically, you do your Wood’s lamp to define the lesion diameter, you measure out your margins, you excise the tumor, pack the area with a bandage, and send the patient home. You rush your pathology, and you don’t do any reconstruction until you get the margins clear."

A pathology report that comes back stating narrow margins are present is "a heart stopper," she added.

"You have the option of observing the area if the margin is clear but the tumor was close to the margin. That’s a good approach for an elderly patient or when the lentigo maligna was in a cosmetically important area."

Lentigo maligna melanoma accounts for 4% of all cases of melanoma. It typically arises on sun-damaged skin in individuals in their 70s or older. Common sites include the malar area, forehead, nose, and temple. The differential diagnosis includes seborrheic keratosis, pigmented actinic keratosis, and pigmented nevus.

Lentigo maligna becomes lentigo maligna melanoma when malignant melanoma cells invade the dermis and deeper appendages. Roughly 5% of lentigo malignas eventually progress to invasive melanoma, according to Dr. Marmur. Typically, a lentigo maligna undergoes extended gradual horizontal growth before beginning a vertical growth phase.

"It spreads like an oil slick for many years," Dr. Marmur said at the seminar.

Established treatment modalities for patients who aren’t surgical candidates include cryotherapy, radiotherapy, and topical imiquimod 5%. All have disadvantages, including high 5-year recurrence rates.

Dr. Marmur noted that a newer nonsurgical therapy drawing considerable interest involves off-label use of topical combination therapy with imiquimod and tazarotene gel. The concept is to use the topical retinoid to disrupt the stratum corneum in order to enhance imiquimod penetration, thereby achieving a greater inflammatory response than possible with imiquimod alone.

Initial data have been published by researchers at the University of Utah, Salt Lake City. They randomized 90 patients with 91 lentigo malignas to imiquimod 5% cream applied 5 days per week for 3 months or to the imiquimod regimen plus tazarotene 0.1% gel on the other 2 days per week. After 3 months of topical therapy, patients underwent conservative staged excision with frozen section analysis with Melan A immunostaining to confirm negative margins.

Of those treated with dual topical therapy for 3 months, 29 of 37 lesions (78%) had complete responses with no residual lentigo maligna at the time of staged excision. So did 27 of 42 (64%) treated with imiquimod alone (Arch. Dermatol. 2012;148:592-6).

The modest difference in outcome was not significant (P = .17). Nevertheless, the Utah investigators wrote that topical pretreatment appears to reduce surgical defect sizes, an important consideration in lentigo maligna because the lesions are often large and located on cosmetically sensitive facial sites. At the patient’s first visit, the researchers saucerize the entire tumor to remove all visible evidence of lentigo maligna and nip in the bud any invasive element that might be present. One month later, after the wound has healed by secondary intention, the patient begins topical imiquimod therapy 5 days per week. If no inflammation is observed, tazarotene gel is added on the other 2 days per week. After 3 months of topical therapy, the patient goes off treatment for 2 months so the inflammatory response can subside. Then a staged excision is performed with 2-mm margins around the perimeter of the original tumor outline.

"This is an interesting thought, but it’s still not considered standard of care," Dr. Marmur commented in describing the Utah research.

Bruce C. Jancin/IMNG Medical Media

Session chair Dr. Allan C. Halpern, chief of the dermatology service at Memorial Sloan-Kettering Cancer Center in New York, said he and his colleagues, like the Utah group, are using a lot of topical imiquimod as adjunctive therapy for lentigo maligna.

"Because we’re a referral center, we see all those patients whose melanomas unfortunately do recur at the edge of large surgeries. We see a lot of patients whose local surgeons have chased around their faces for a certain amount of time. So I think the general concept of the cure rates of surgery is a bit overstated. I’m not trying to sell an off-label use of a drug, but I think sometimes imiquimod can be very helpful," Dr. Halpern said.

He offered a clinical pearl in diagnosing lentigo maligna: Consider a broad shave biopsy of a suspicious lesion rather than a deeper, smaller-diameter biopsy.

"Sampling errors are a real problem with lentigo maligna. We learned early on that if you take a large lentigo maligna and do multiple biopsies of the same lesion and send them to what we think are our very expert pathologists, on average, we get two or three back that were melanoma and two or three back that were pigmented actinic keratoses. The sampling error tends to be more in the horizontal than in the depth for these very early lesions," according to Dr. Halpern.

Dr. Marmur and Dr. Halpern reported having no relevant financial interests. SDEF and this news organization are owned by the same parent company.

[email protected]

MAUI, HAWAII – "Slow Mohs" has gained near-universal acceptance among skin cancer specialists as a definitive surgical technique for complete removal of lentigo maligna melanoma while simultaneously sparing normal tissue, according to Dr. Ellen Marmur of Mount Sinai School of Medicine, New York.

The big advantage that slow Mohs has over standard wide local excision with 0.5- to 1-cm margins is a 5-year cure rate approaching 100%. In contrast, standard excision has a recurrence rate of up to 20%, she said at the Hawaii Dermatology Seminar, sponsored by Global Academy for Medical Education/Skin Disease Education Foundation.

Bruce C. Jancin/IMNG Medical Media

Slow Mohs is a modified form of Mohs micrographic surgery. The surgery compares with conventional Mohs: It is staged, margin-controlled excision. But in slow Mohs, rush permanent sections are sent off to the pathologist rather than the frozen sections integral to conventional Mohs.

Dr. Marmur relies upon slow Mohs, with "bread-loafing" of the central tumor by the pathologist, because the permanent sections better preserve the tumor’s microscopic features. Interpreting atypical melanocytes in frozen sections can be quite a challenge. However, she added, some Mohs surgeons have found that using rapid immunostains also markedly improves the sensitivity and specificity of frozen sections in lentigo maligna surgery.

Slow Mohs takes place over the course of days, she said. "Basically, you do your Wood’s lamp to define the lesion diameter, you measure out your margins, you excise the tumor, pack the area with a bandage, and send the patient home. You rush your pathology, and you don’t do any reconstruction until you get the margins clear."

A pathology report that comes back stating narrow margins are present is "a heart stopper," she added.

"You have the option of observing the area if the margin is clear but the tumor was close to the margin. That’s a good approach for an elderly patient or when the lentigo maligna was in a cosmetically important area."

Lentigo maligna melanoma accounts for 4% of all cases of melanoma. It typically arises on sun-damaged skin in individuals in their 70s or older. Common sites include the malar area, forehead, nose, and temple. The differential diagnosis includes seborrheic keratosis, pigmented actinic keratosis, and pigmented nevus.

Lentigo maligna becomes lentigo maligna melanoma when malignant melanoma cells invade the dermis and deeper appendages. Roughly 5% of lentigo malignas eventually progress to invasive melanoma, according to Dr. Marmur. Typically, a lentigo maligna undergoes extended gradual horizontal growth before beginning a vertical growth phase.

"It spreads like an oil slick for many years," Dr. Marmur said at the seminar.

Established treatment modalities for patients who aren’t surgical candidates include cryotherapy, radiotherapy, and topical imiquimod 5%. All have disadvantages, including high 5-year recurrence rates.

Dr. Marmur noted that a newer nonsurgical therapy drawing considerable interest involves off-label use of topical combination therapy with imiquimod and tazarotene gel. The concept is to use the topical retinoid to disrupt the stratum corneum in order to enhance imiquimod penetration, thereby achieving a greater inflammatory response than possible with imiquimod alone.

Initial data have been published by researchers at the University of Utah, Salt Lake City. They randomized 90 patients with 91 lentigo malignas to imiquimod 5% cream applied 5 days per week for 3 months or to the imiquimod regimen plus tazarotene 0.1% gel on the other 2 days per week. After 3 months of topical therapy, patients underwent conservative staged excision with frozen section analysis with Melan A immunostaining to confirm negative margins.

Of those treated with dual topical therapy for 3 months, 29 of 37 lesions (78%) had complete responses with no residual lentigo maligna at the time of staged excision. So did 27 of 42 (64%) treated with imiquimod alone (Arch. Dermatol. 2012;148:592-6).

The modest difference in outcome was not significant (P = .17). Nevertheless, the Utah investigators wrote that topical pretreatment appears to reduce surgical defect sizes, an important consideration in lentigo maligna because the lesions are often large and located on cosmetically sensitive facial sites. At the patient’s first visit, the researchers saucerize the entire tumor to remove all visible evidence of lentigo maligna and nip in the bud any invasive element that might be present. One month later, after the wound has healed by secondary intention, the patient begins topical imiquimod therapy 5 days per week. If no inflammation is observed, tazarotene gel is added on the other 2 days per week. After 3 months of topical therapy, the patient goes off treatment for 2 months so the inflammatory response can subside. Then a staged excision is performed with 2-mm margins around the perimeter of the original tumor outline.

"This is an interesting thought, but it’s still not considered standard of care," Dr. Marmur commented in describing the Utah research.

Bruce C. Jancin/IMNG Medical Media

Session chair Dr. Allan C. Halpern, chief of the dermatology service at Memorial Sloan-Kettering Cancer Center in New York, said he and his colleagues, like the Utah group, are using a lot of topical imiquimod as adjunctive therapy for lentigo maligna.

"Because we’re a referral center, we see all those patients whose melanomas unfortunately do recur at the edge of large surgeries. We see a lot of patients whose local surgeons have chased around their faces for a certain amount of time. So I think the general concept of the cure rates of surgery is a bit overstated. I’m not trying to sell an off-label use of a drug, but I think sometimes imiquimod can be very helpful," Dr. Halpern said.

He offered a clinical pearl in diagnosing lentigo maligna: Consider a broad shave biopsy of a suspicious lesion rather than a deeper, smaller-diameter biopsy.

"Sampling errors are a real problem with lentigo maligna. We learned early on that if you take a large lentigo maligna and do multiple biopsies of the same lesion and send them to what we think are our very expert pathologists, on average, we get two or three back that were melanoma and two or three back that were pigmented actinic keratoses. The sampling error tends to be more in the horizontal than in the depth for these very early lesions," according to Dr. Halpern.

Dr. Marmur and Dr. Halpern reported having no relevant financial interests. SDEF and this news organization are owned by the same parent company.

[email protected]

MAUI, HAWAII – "Slow Mohs" has gained near-universal acceptance among skin cancer specialists as a definitive surgical technique for complete removal of lentigo maligna melanoma while simultaneously sparing normal tissue, according to Dr. Ellen Marmur of Mount Sinai School of Medicine, New York.

The big advantage that slow Mohs has over standard wide local excision with 0.5- to 1-cm margins is a 5-year cure rate approaching 100%. In contrast, standard excision has a recurrence rate of up to 20%, she said at the Hawaii Dermatology Seminar, sponsored by Global Academy for Medical Education/Skin Disease Education Foundation.

Bruce C. Jancin/IMNG Medical Media

Slow Mohs is a modified form of Mohs micrographic surgery. The surgery compares with conventional Mohs: It is staged, margin-controlled excision. But in slow Mohs, rush permanent sections are sent off to the pathologist rather than the frozen sections integral to conventional Mohs.

Dr. Marmur relies upon slow Mohs, with "bread-loafing" of the central tumor by the pathologist, because the permanent sections better preserve the tumor’s microscopic features. Interpreting atypical melanocytes in frozen sections can be quite a challenge. However, she added, some Mohs surgeons have found that using rapid immunostains also markedly improves the sensitivity and specificity of frozen sections in lentigo maligna surgery.

Slow Mohs takes place over the course of days, she said. "Basically, you do your Wood’s lamp to define the lesion diameter, you measure out your margins, you excise the tumor, pack the area with a bandage, and send the patient home. You rush your pathology, and you don’t do any reconstruction until you get the margins clear."

A pathology report that comes back stating narrow margins are present is "a heart stopper," she added.

"You have the option of observing the area if the margin is clear but the tumor was close to the margin. That’s a good approach for an elderly patient or when the lentigo maligna was in a cosmetically important area."

Lentigo maligna melanoma accounts for 4% of all cases of melanoma. It typically arises on sun-damaged skin in individuals in their 70s or older. Common sites include the malar area, forehead, nose, and temple. The differential diagnosis includes seborrheic keratosis, pigmented actinic keratosis, and pigmented nevus.

Lentigo maligna becomes lentigo maligna melanoma when malignant melanoma cells invade the dermis and deeper appendages. Roughly 5% of lentigo malignas eventually progress to invasive melanoma, according to Dr. Marmur. Typically, a lentigo maligna undergoes extended gradual horizontal growth before beginning a vertical growth phase.

"It spreads like an oil slick for many years," Dr. Marmur said at the seminar.

Established treatment modalities for patients who aren’t surgical candidates include cryotherapy, radiotherapy, and topical imiquimod 5%. All have disadvantages, including high 5-year recurrence rates.

Dr. Marmur noted that a newer nonsurgical therapy drawing considerable interest involves off-label use of topical combination therapy with imiquimod and tazarotene gel. The concept is to use the topical retinoid to disrupt the stratum corneum in order to enhance imiquimod penetration, thereby achieving a greater inflammatory response than possible with imiquimod alone.

Initial data have been published by researchers at the University of Utah, Salt Lake City. They randomized 90 patients with 91 lentigo malignas to imiquimod 5% cream applied 5 days per week for 3 months or to the imiquimod regimen plus tazarotene 0.1% gel on the other 2 days per week. After 3 months of topical therapy, patients underwent conservative staged excision with frozen section analysis with Melan A immunostaining to confirm negative margins.

Of those treated with dual topical therapy for 3 months, 29 of 37 lesions (78%) had complete responses with no residual lentigo maligna at the time of staged excision. So did 27 of 42 (64%) treated with imiquimod alone (Arch. Dermatol. 2012;148:592-6).

The modest difference in outcome was not significant (P = .17). Nevertheless, the Utah investigators wrote that topical pretreatment appears to reduce surgical defect sizes, an important consideration in lentigo maligna because the lesions are often large and located on cosmetically sensitive facial sites. At the patient’s first visit, the researchers saucerize the entire tumor to remove all visible evidence of lentigo maligna and nip in the bud any invasive element that might be present. One month later, after the wound has healed by secondary intention, the patient begins topical imiquimod therapy 5 days per week. If no inflammation is observed, tazarotene gel is added on the other 2 days per week. After 3 months of topical therapy, the patient goes off treatment for 2 months so the inflammatory response can subside. Then a staged excision is performed with 2-mm margins around the perimeter of the original tumor outline.

"This is an interesting thought, but it’s still not considered standard of care," Dr. Marmur commented in describing the Utah research.

Bruce C. Jancin/IMNG Medical Media

Session chair Dr. Allan C. Halpern, chief of the dermatology service at Memorial Sloan-Kettering Cancer Center in New York, said he and his colleagues, like the Utah group, are using a lot of topical imiquimod as adjunctive therapy for lentigo maligna.

"Because we’re a referral center, we see all those patients whose melanomas unfortunately do recur at the edge of large surgeries. We see a lot of patients whose local surgeons have chased around their faces for a certain amount of time. So I think the general concept of the cure rates of surgery is a bit overstated. I’m not trying to sell an off-label use of a drug, but I think sometimes imiquimod can be very helpful," Dr. Halpern said.

He offered a clinical pearl in diagnosing lentigo maligna: Consider a broad shave biopsy of a suspicious lesion rather than a deeper, smaller-diameter biopsy.

"Sampling errors are a real problem with lentigo maligna. We learned early on that if you take a large lentigo maligna and do multiple biopsies of the same lesion and send them to what we think are our very expert pathologists, on average, we get two or three back that were melanoma and two or three back that were pigmented actinic keratoses. The sampling error tends to be more in the horizontal than in the depth for these very early lesions," according to Dr. Halpern.

Dr. Marmur and Dr. Halpern reported having no relevant financial interests. SDEF and this news organization are owned by the same parent company.

[email protected]

Nonsteroidal anti-inflammatory drugs (NSAIDs) have therapeutic applications that "have spanned several centuries," according to Rao and Knaus (J. Pharm. Pharm. Sci. 2008;11:81s-110s). NSAIDs are among the increasing number of anti-inflammatory agents used to target bioactive lipids produced from arachidonic acid. Although this drug class is one of the most often used in practice and has been well studied by investigators, the role of NSAIDs for cutaneous purposes has been relatively limited (J. Cutan. Med. Surg. 2002;6:241-56). Indeed, only three topical NSAIDs are approved for use in the United States, for a narrow range of conditions.

Diclofenac sodium 1.5% topical solution (containing dimethyl sulfoxide to enhance penetration) and diclofenac sodium gel 1% are currently approved in the United States for hand and knee osteoarthritis (Postgrad. Med. 2010;122:98-106). The diclofenac hydroxyethylpyrrolidine (epolamine) 1.3% patch was approved by the U.S. Food and Drug Administration for soft-tissue injuries in January 2007, although it has long been available in more than 40 countries (Int. J. Clin. Pract. 2010;64:1546-53; Clin. Ther. 2010;32:1001-14).

A winning adverse event profile

Significantly, topical NSAIDs have not been associated with the adverse events resulting from oral NSAIDs, which engender various dose-related side effects (Semin. Arthritis. Rheum. 2009;39:203-12). Mild and self-limiting local skin reactions are the most common adverse side effects from topical NSAID products. The diclofenac products are approved in the European Union, as are ibuprofen creams and gels, ketoprofen gel, felbinac gel and cutaneous foam, and piroxicam gel.

The efficacy and safety of these products have been established through meta-analyses. In a recent study, researchers cautioned that the patient, the drug, and the drug delivery mechanism should be considered in topical NSAID selection, because the pharmacokinetic absorption from topical preparations can vary with different formulations of the same drug, depending on the agent, the underlying disorder, and the application site (Am. J. Ther. 2012 Feb 22 [Epub ahead of print]).

Easing osteoarthritis

Although oral NSAIDs have been the mainstays of hand and knee osteoarthritis treatment regimens, their dose- and age-related side effect profiles (including adverse effects on the cardiovascular, renal, and gastrointestinal systems) have prompted the use of topical NSAIDs, which yield comparable efficacy with far less systemic risk. Results of a Jan. 1, 2005, to March 31, 2010, literature review showed that topical products exhibited superior efficacy compared with placebo, with similar adverse event profiles. Topicals also showed efficacy comparable to that of oral diclofenac, with side effects seen primarily at the application site and no ulcers, perforations, or bleeding (Postgrad. Med. 2010;122(6):98-106).

In 2009, Barthel et al. evaluated the efficacy and safety of topical diclofenac sodium gel (DSG) 1% in a randomized, double-blind, vehicle-controlled trial of 492 adults (aged 35 years and older) with mild to moderate symptomatic knee osteoarthritis lasting at least 6 months. Patients received 4 g of topical treatment of DSG or vehicle four times daily for 12 weeks. The investigators noted significant reductions in the DSG group compared with the vehicle group according to the Western Ontario and McMaster Universities Osteoarthritis Index (WOMAC) pain and physical function subscales, as well as global rating of disease. They also observed significantly better efficacy results with DSG as early as week 1 of treatment. Gastrointestinal reactions occurred in 5.9% of the DSG group and 5.0% of the vehicle group, and application site reactions emerged in 5.1% of the DSG group and 2.5% of the vehicle group (Semin. Arthritis Rheum. 2009;39:203-12).

In 2010, Baraf et al. also conducted a 12-week efficacy and safety study of topical DSG 1% for symptomatic knee osteoarthritis. This randomized, double-blind, parallel-group, multicenter trial of patients at least 35 years of age with symptomatic Kellgren-Lawrence grade (KLG) 1 to 3 osteoarthritis in one or both knees for at least 6 months assigned 208 subjects to DSG treatment and 212 to vehicle. The investigators found significant improvement according to WOMAC metrics in the DSG patients compared with placebo patients. Unlike the Barthel report, no gastrointestinal upset was noted in this study. Application site reactions were the most common side effect, occurring in 4.8% of the DSG group and 0% of the vehicle group (Phys. Sportsmed. 2010;38:19-28).

In 2012, Baraf et al. extended their previous work and assessed the safety of topical DSG 1% for the treatment of knee and hand osteoarthritis in older and younger patients. They also compared the treatment in those with or without comorbid hypertension, type 2 diabetes, or cerebrovascular or cardiovascular disease. This post hoc analysis of pooled data from five randomized, double-blind, placebo-controlled trials included 1,426 patients 35 years of age and older with mild to moderate osteoarthritis of the knee and 783 patients 40 years of age and older with mild to moderate osteoarthritis of the hand. Participants applied 4 g of DSG or vehicle to affected knees q.i.d. for 12 weeks or 2 g of DSG or vehicle to affected hands q.i.d. for 8 weeks. The investigators found that the adverse event profile was similar across comparisons of patients with knee osteoarthritis. Among patients with hand osteoarthritis, the only differences were that the adverse event profile was lower in patients with type 2 diabetes than in patients without the condition, and higher in patients with cerebrovascular or cardiovascular disease than in patients without those conditions. The authors concluded that the rates of adverse side effects were similar and low between the two groups (Am. J. Geriatr. Pharmacother. 2012;10:47-60).

To further examine the efficacy and tolerability of the diclofenac epolamine topical patch (DETP), investigators reviewed data from eight studies from 1984 to 2009, including data on patients with acute pain from soft-tissue injuries or localized periarticular disorders. Significant reductions in spontaneous pain from baseline due to DETP were seen (range, 26%-88% on day 7 and 56%-61% on day 14). In addition, significant decreases in pain scores were linked to DETP use compared with a placebo patch in two studies and compared with diclofenac diethylammonium topical gel in one study. Adverse events were low across studies; reactions at the application site and nausea were the most common events (Clin. Ther. 2010;32:1001-14).

Oral ibuprofen and combination therapy

Notably, ibuprofen has demonstrated effectiveness in the treatment of acne, as inflammatory acne lesions are infiltrated with neutrophils and ibuprofen suppresses leukocyte chemotaxis (Dermatology. 2003;206:68-73). Ibuprofen is generally considered safe, with low potential for causing gastrointestinal, cardiovascular, or renal risks compared with other NSAIDs and selective cyclooxygenase-2 inhibitors (coxibs), which have been removed from the market (Inflammopharmacology 2009;17:275-342; J. Pharm. Pharm. Sci. 2008;11:81s-110s).

In a double-blind study of 60 patients aged 15-35 years with acne vulgaris, patients were randomly assigned to one of four groups: oral ibuprofen (600 mg) plus tetracycline (250 mg) four times daily; ibuprofen (600 mg) plus placebo four times daily; tetracycline (250 mg) plus placebo four times daily; and two placebos four times daily. Interestingly, the combination therapy was the only approach that yielded an effect statistically superior to that of placebo in reducing total lesion counts. The use of ibuprofen alone netted improvements comparable to those afforded by tetracycline but with fewer side effects (J. Am. Acad. Dermatol. 1984;11:1076-81).

NSAIDs are also used for the treatment of sunburn. In 1992, Hughes et al. investigated ameliorating UVB-induced skin injury by nonsteroidal drugs (oral ibuprofen or indomethacin) plus topical betamethasone dipropionate in 24 subjects. Measurements of erythema and increased skin blood flow, performed serially, revealed a synergistic effect of oral NSAIDs combined with topical corticosteroids to repair UVB-induced skin damage (Dermatology 1992;184:54-8).

Conclusion

An ideal anti-inflammatory agent has not yet been developed, but topical NSAIDs appear to fit the bill in terms of reducing or eliminating the adverse side effects associated with oral NSAID regimens. However, topical NSAIDs are approved for only a narrow range of indications, and more research is necessary to determine whether they are appropriate for a wider array of dermatologic conditions.

Dr. Baumann is in private practice in Miami Beach. She did not disclose any conflicts of interest. 

Nonsteroidal anti-inflammatory drugs (NSAIDs) have therapeutic applications that "have spanned several centuries," according to Rao and Knaus (J. Pharm. Pharm. Sci. 2008;11:81s-110s). NSAIDs are among the increasing number of anti-inflammatory agents used to target bioactive lipids produced from arachidonic acid. Although this drug class is one of the most often used in practice and has been well studied by investigators, the role of NSAIDs for cutaneous purposes has been relatively limited (J. Cutan. Med. Surg. 2002;6:241-56). Indeed, only three topical NSAIDs are approved for use in the United States, for a narrow range of conditions.

Diclofenac sodium 1.5% topical solution (containing dimethyl sulfoxide to enhance penetration) and diclofenac sodium gel 1% are currently approved in the United States for hand and knee osteoarthritis (Postgrad. Med. 2010;122:98-106). The diclofenac hydroxyethylpyrrolidine (epolamine) 1.3% patch was approved by the U.S. Food and Drug Administration for soft-tissue injuries in January 2007, although it has long been available in more than 40 countries (Int. J. Clin. Pract. 2010;64:1546-53; Clin. Ther. 2010;32:1001-14).

A winning adverse event profile

Significantly, topical NSAIDs have not been associated with the adverse events resulting from oral NSAIDs, which engender various dose-related side effects (Semin. Arthritis. Rheum. 2009;39:203-12). Mild and self-limiting local skin reactions are the most common adverse side effects from topical NSAID products. The diclofenac products are approved in the European Union, as are ibuprofen creams and gels, ketoprofen gel, felbinac gel and cutaneous foam, and piroxicam gel.

The efficacy and safety of these products have been established through meta-analyses. In a recent study, researchers cautioned that the patient, the drug, and the drug delivery mechanism should be considered in topical NSAID selection, because the pharmacokinetic absorption from topical preparations can vary with different formulations of the same drug, depending on the agent, the underlying disorder, and the application site (Am. J. Ther. 2012 Feb 22 [Epub ahead of print]).

Easing osteoarthritis

Although oral NSAIDs have been the mainstays of hand and knee osteoarthritis treatment regimens, their dose- and age-related side effect profiles (including adverse effects on the cardiovascular, renal, and gastrointestinal systems) have prompted the use of topical NSAIDs, which yield comparable efficacy with far less systemic risk. Results of a Jan. 1, 2005, to March 31, 2010, literature review showed that topical products exhibited superior efficacy compared with placebo, with similar adverse event profiles. Topicals also showed efficacy comparable to that of oral diclofenac, with side effects seen primarily at the application site and no ulcers, perforations, or bleeding (Postgrad. Med. 2010;122(6):98-106).

In 2009, Barthel et al. evaluated the efficacy and safety of topical diclofenac sodium gel (DSG) 1% in a randomized, double-blind, vehicle-controlled trial of 492 adults (aged 35 years and older) with mild to moderate symptomatic knee osteoarthritis lasting at least 6 months. Patients received 4 g of topical treatment of DSG or vehicle four times daily for 12 weeks. The investigators noted significant reductions in the DSG group compared with the vehicle group according to the Western Ontario and McMaster Universities Osteoarthritis Index (WOMAC) pain and physical function subscales, as well as global rating of disease. They also observed significantly better efficacy results with DSG as early as week 1 of treatment. Gastrointestinal reactions occurred in 5.9% of the DSG group and 5.0% of the vehicle group, and application site reactions emerged in 5.1% of the DSG group and 2.5% of the vehicle group (Semin. Arthritis Rheum. 2009;39:203-12).

In 2010, Baraf et al. also conducted a 12-week efficacy and safety study of topical DSG 1% for symptomatic knee osteoarthritis. This randomized, double-blind, parallel-group, multicenter trial of patients at least 35 years of age with symptomatic Kellgren-Lawrence grade (KLG) 1 to 3 osteoarthritis in one or both knees for at least 6 months assigned 208 subjects to DSG treatment and 212 to vehicle. The investigators found significant improvement according to WOMAC metrics in the DSG patients compared with placebo patients. Unlike the Barthel report, no gastrointestinal upset was noted in this study. Application site reactions were the most common side effect, occurring in 4.8% of the DSG group and 0% of the vehicle group (Phys. Sportsmed. 2010;38:19-28).

In 2012, Baraf et al. extended their previous work and assessed the safety of topical DSG 1% for the treatment of knee and hand osteoarthritis in older and younger patients. They also compared the treatment in those with or without comorbid hypertension, type 2 diabetes, or cerebrovascular or cardiovascular disease. This post hoc analysis of pooled data from five randomized, double-blind, placebo-controlled trials included 1,426 patients 35 years of age and older with mild to moderate osteoarthritis of the knee and 783 patients 40 years of age and older with mild to moderate osteoarthritis of the hand. Participants applied 4 g of DSG or vehicle to affected knees q.i.d. for 12 weeks or 2 g of DSG or vehicle to affected hands q.i.d. for 8 weeks. The investigators found that the adverse event profile was similar across comparisons of patients with knee osteoarthritis. Among patients with hand osteoarthritis, the only differences were that the adverse event profile was lower in patients with type 2 diabetes than in patients without the condition, and higher in patients with cerebrovascular or cardiovascular disease than in patients without those conditions. The authors concluded that the rates of adverse side effects were similar and low between the two groups (Am. J. Geriatr. Pharmacother. 2012;10:47-60).

To further examine the efficacy and tolerability of the diclofenac epolamine topical patch (DETP), investigators reviewed data from eight studies from 1984 to 2009, including data on patients with acute pain from soft-tissue injuries or localized periarticular disorders. Significant reductions in spontaneous pain from baseline due to DETP were seen (range, 26%-88% on day 7 and 56%-61% on day 14). In addition, significant decreases in pain scores were linked to DETP use compared with a placebo patch in two studies and compared with diclofenac diethylammonium topical gel in one study. Adverse events were low across studies; reactions at the application site and nausea were the most common events (Clin. Ther. 2010;32:1001-14).

Oral ibuprofen and combination therapy

Notably, ibuprofen has demonstrated effectiveness in the treatment of acne, as inflammatory acne lesions are infiltrated with neutrophils and ibuprofen suppresses leukocyte chemotaxis (Dermatology. 2003;206:68-73). Ibuprofen is generally considered safe, with low potential for causing gastrointestinal, cardiovascular, or renal risks compared with other NSAIDs and selective cyclooxygenase-2 inhibitors (coxibs), which have been removed from the market (Inflammopharmacology 2009;17:275-342; J. Pharm. Pharm. Sci. 2008;11:81s-110s).

In a double-blind study of 60 patients aged 15-35 years with acne vulgaris, patients were randomly assigned to one of four groups: oral ibuprofen (600 mg) plus tetracycline (250 mg) four times daily; ibuprofen (600 mg) plus placebo four times daily; tetracycline (250 mg) plus placebo four times daily; and two placebos four times daily. Interestingly, the combination therapy was the only approach that yielded an effect statistically superior to that of placebo in reducing total lesion counts. The use of ibuprofen alone netted improvements comparable to those afforded by tetracycline but with fewer side effects (J. Am. Acad. Dermatol. 1984;11:1076-81).

NSAIDs are also used for the treatment of sunburn. In 1992, Hughes et al. investigated ameliorating UVB-induced skin injury by nonsteroidal drugs (oral ibuprofen or indomethacin) plus topical betamethasone dipropionate in 24 subjects. Measurements of erythema and increased skin blood flow, performed serially, revealed a synergistic effect of oral NSAIDs combined with topical corticosteroids to repair UVB-induced skin damage (Dermatology 1992;184:54-8).

Conclusion

An ideal anti-inflammatory agent has not yet been developed, but topical NSAIDs appear to fit the bill in terms of reducing or eliminating the adverse side effects associated with oral NSAID regimens. However, topical NSAIDs are approved for only a narrow range of indications, and more research is necessary to determine whether they are appropriate for a wider array of dermatologic conditions.

Dr. Baumann is in private practice in Miami Beach. She did not disclose any conflicts of interest. 

Nonsteroidal anti-inflammatory drugs (NSAIDs) have therapeutic applications that "have spanned several centuries," according to Rao and Knaus (J. Pharm. Pharm. Sci. 2008;11:81s-110s). NSAIDs are among the increasing number of anti-inflammatory agents used to target bioactive lipids produced from arachidonic acid. Although this drug class is one of the most often used in practice and has been well studied by investigators, the role of NSAIDs for cutaneous purposes has been relatively limited (J. Cutan. Med. Surg. 2002;6:241-56). Indeed, only three topical NSAIDs are approved for use in the United States, for a narrow range of conditions.

Diclofenac sodium 1.5% topical solution (containing dimethyl sulfoxide to enhance penetration) and diclofenac sodium gel 1% are currently approved in the United States for hand and knee osteoarthritis (Postgrad. Med. 2010;122:98-106). The diclofenac hydroxyethylpyrrolidine (epolamine) 1.3% patch was approved by the U.S. Food and Drug Administration for soft-tissue injuries in January 2007, although it has long been available in more than 40 countries (Int. J. Clin. Pract. 2010;64:1546-53; Clin. Ther. 2010;32:1001-14).

A winning adverse event profile

Significantly, topical NSAIDs have not been associated with the adverse events resulting from oral NSAIDs, which engender various dose-related side effects (Semin. Arthritis. Rheum. 2009;39:203-12). Mild and self-limiting local skin reactions are the most common adverse side effects from topical NSAID products. The diclofenac products are approved in the European Union, as are ibuprofen creams and gels, ketoprofen gel, felbinac gel and cutaneous foam, and piroxicam gel.

The efficacy and safety of these products have been established through meta-analyses. In a recent study, researchers cautioned that the patient, the drug, and the drug delivery mechanism should be considered in topical NSAID selection, because the pharmacokinetic absorption from topical preparations can vary with different formulations of the same drug, depending on the agent, the underlying disorder, and the application site (Am. J. Ther. 2012 Feb 22 [Epub ahead of print]).

Easing osteoarthritis

Although oral NSAIDs have been the mainstays of hand and knee osteoarthritis treatment regimens, their dose- and age-related side effect profiles (including adverse effects on the cardiovascular, renal, and gastrointestinal systems) have prompted the use of topical NSAIDs, which yield comparable efficacy with far less systemic risk. Results of a Jan. 1, 2005, to March 31, 2010, literature review showed that topical products exhibited superior efficacy compared with placebo, with similar adverse event profiles. Topicals also showed efficacy comparable to that of oral diclofenac, with side effects seen primarily at the application site and no ulcers, perforations, or bleeding (Postgrad. Med. 2010;122(6):98-106).

In 2009, Barthel et al. evaluated the efficacy and safety of topical diclofenac sodium gel (DSG) 1% in a randomized, double-blind, vehicle-controlled trial of 492 adults (aged 35 years and older) with mild to moderate symptomatic knee osteoarthritis lasting at least 6 months. Patients received 4 g of topical treatment of DSG or vehicle four times daily for 12 weeks. The investigators noted significant reductions in the DSG group compared with the vehicle group according to the Western Ontario and McMaster Universities Osteoarthritis Index (WOMAC) pain and physical function subscales, as well as global rating of disease. They also observed significantly better efficacy results with DSG as early as week 1 of treatment. Gastrointestinal reactions occurred in 5.9% of the DSG group and 5.0% of the vehicle group, and application site reactions emerged in 5.1% of the DSG group and 2.5% of the vehicle group (Semin. Arthritis Rheum. 2009;39:203-12).

In 2010, Baraf et al. also conducted a 12-week efficacy and safety study of topical DSG 1% for symptomatic knee osteoarthritis. This randomized, double-blind, parallel-group, multicenter trial of patients at least 35 years of age with symptomatic Kellgren-Lawrence grade (KLG) 1 to 3 osteoarthritis in one or both knees for at least 6 months assigned 208 subjects to DSG treatment and 212 to vehicle. The investigators found significant improvement according to WOMAC metrics in the DSG patients compared with placebo patients. Unlike the Barthel report, no gastrointestinal upset was noted in this study. Application site reactions were the most common side effect, occurring in 4.8% of the DSG group and 0% of the vehicle group (Phys. Sportsmed. 2010;38:19-28).

In 2012, Baraf et al. extended their previous work and assessed the safety of topical DSG 1% for the treatment of knee and hand osteoarthritis in older and younger patients. They also compared the treatment in those with or without comorbid hypertension, type 2 diabetes, or cerebrovascular or cardiovascular disease. This post hoc analysis of pooled data from five randomized, double-blind, placebo-controlled trials included 1,426 patients 35 years of age and older with mild to moderate osteoarthritis of the knee and 783 patients 40 years of age and older with mild to moderate osteoarthritis of the hand. Participants applied 4 g of DSG or vehicle to affected knees q.i.d. for 12 weeks or 2 g of DSG or vehicle to affected hands q.i.d. for 8 weeks. The investigators found that the adverse event profile was similar across comparisons of patients with knee osteoarthritis. Among patients with hand osteoarthritis, the only differences were that the adverse event profile was lower in patients with type 2 diabetes than in patients without the condition, and higher in patients with cerebrovascular or cardiovascular disease than in patients without those conditions. The authors concluded that the rates of adverse side effects were similar and low between the two groups (Am. J. Geriatr. Pharmacother. 2012;10:47-60).

To further examine the efficacy and tolerability of the diclofenac epolamine topical patch (DETP), investigators reviewed data from eight studies from 1984 to 2009, including data on patients with acute pain from soft-tissue injuries or localized periarticular disorders. Significant reductions in spontaneous pain from baseline due to DETP were seen (range, 26%-88% on day 7 and 56%-61% on day 14). In addition, significant decreases in pain scores were linked to DETP use compared with a placebo patch in two studies and compared with diclofenac diethylammonium topical gel in one study. Adverse events were low across studies; reactions at the application site and nausea were the most common events (Clin. Ther. 2010;32:1001-14).

Oral ibuprofen and combination therapy

Notably, ibuprofen has demonstrated effectiveness in the treatment of acne, as inflammatory acne lesions are infiltrated with neutrophils and ibuprofen suppresses leukocyte chemotaxis (Dermatology. 2003;206:68-73). Ibuprofen is generally considered safe, with low potential for causing gastrointestinal, cardiovascular, or renal risks compared with other NSAIDs and selective cyclooxygenase-2 inhibitors (coxibs), which have been removed from the market (Inflammopharmacology 2009;17:275-342; J. Pharm. Pharm. Sci. 2008;11:81s-110s).

In a double-blind study of 60 patients aged 15-35 years with acne vulgaris, patients were randomly assigned to one of four groups: oral ibuprofen (600 mg) plus tetracycline (250 mg) four times daily; ibuprofen (600 mg) plus placebo four times daily; tetracycline (250 mg) plus placebo four times daily; and two placebos four times daily. Interestingly, the combination therapy was the only approach that yielded an effect statistically superior to that of placebo in reducing total lesion counts. The use of ibuprofen alone netted improvements comparable to those afforded by tetracycline but with fewer side effects (J. Am. Acad. Dermatol. 1984;11:1076-81).

NSAIDs are also used for the treatment of sunburn. In 1992, Hughes et al. investigated ameliorating UVB-induced skin injury by nonsteroidal drugs (oral ibuprofen or indomethacin) plus topical betamethasone dipropionate in 24 subjects. Measurements of erythema and increased skin blood flow, performed serially, revealed a synergistic effect of oral NSAIDs combined with topical corticosteroids to repair UVB-induced skin damage (Dermatology 1992;184:54-8).

Conclusion

An ideal anti-inflammatory agent has not yet been developed, but topical NSAIDs appear to fit the bill in terms of reducing or eliminating the adverse side effects associated with oral NSAID regimens. However, topical NSAIDs are approved for only a narrow range of indications, and more research is necessary to determine whether they are appropriate for a wider array of dermatologic conditions.

Dr. Baumann is in private practice in Miami Beach. She did not disclose any conflicts of interest. 

A recent Agency for Healthcare Research and Quality (AHRQ) report, “Making Health Care Safer II: An Updated Critical Analysis of the Evidence for Patient Safety Practices,” holds nearly 1,000 pages of practice-management tips for improving outcomes. But where does a hospitalist begin when reviewing such a massive playbook for progress?

Jim Battles, PhD, an AHRQ social science analyst for patient safety who worked on the report, says the best place to start is by asking yourself: “What keeps you up at night? … What scares the heck out of you?”

The report, a follow-up to the influential and controversial 2001 report “Making Health Care Safer: A Critical Analysis of Patient Safety Practices,” is viewed by its authors as the next step in the continuum of improving patient outcomes. The latest research culled a list of more than 100 patient-safety practices (PSPs) down to 10 that should be “strongly encouraged” and another dozen that are “encouraged.” Battles looks at the 2001 report as more about pushing physicians to think about PSPs, with the updated version as a guidebook on how to think about it.

Listen to AHRQ analyst Jim Battles, PhD, talk about how hospitalists and others should view the new report

Paul Shekelle, MD, PhD, director of the Southern California Evidence-Based Practice Center site of RAND Corp., which AHRQ commissioned to produce the report, says that some might look at safety initiatives since the landmark Institute of Medicine report “To Err is Human” in 1999 and question whether enough progress has been made. But all progress is meaningful to individual patients, and the improvements of the past decade and a half have been important, he adds.

“What I believe is that we’ve made a lot of progress in certain areas,” Dr. Shekelle says, “but this can't be seen when we look at aggregate data, because the improvements we have seen don't account for a sufficiently large proportion in aggregate of the overall patient safety problem.”

Dr. Shekelle—one of three co-principal investigators on the report, along with Peter Pronovost, MD, PhD, FCCM, of Johns Hopkins School of Medicine in Baltimore and HM pioneer Robert Wachter, MD, MHM, chief of the division of hospital medicine at the University of California at San Francisco—says he hopes physicians realize that while the report’s recommendations are evidence-based, they’re not a magic bullet.

“One of the main messages of our report is this is not like writing a prescription for a statin,” Dr. Shekelle says. “This is going to take work. It’s going to take local adaptation, and it’s going to take talking to your front-line clinicians to try and find out how to make this thing work.”

Dr. Wachter, who helped craft both the 2001 and 2013 reports, says patient safety “can be one of those things that is so compelling and so dramatic that you develop a little bit of Nike syndrome—let’s just do it, let’s just computerize, let’s just do teamwork training, let’s do simulation.” However, the healthcare system has a much better, deeper understanding of patient safety and “the role of context, the role of the setting, the role of collateral interventions. It’s generally not going to be one thing that’s the magic bullet, but it’s going to be one thing embedded in a series of other activities that are designed to make sure that you have the right design and the right culture.”

Drs. Wachter and Shekelle and Battles agree that much of the difficulty with patient safety practices is rooted in healthcare system cultures. Each uses different terms to describe the roadblock, as Dr. Wachter discusses implementation science and Battles highlights the difference between the technical work of PSPs and their “social adoption.” But all concur that unless PSPs are committed for the long haul, implementation might be little more than lip service.

“It’s a responsibility of the CEO, the CMO, the CNO, and environmental services, all the way down,” Battles says. “You have to develop around these practices the shared ownership of the risk you’re trying to mitigate. Otherwise, this list of practices, OK, it’s a nice list. But you’ve got to say, ‘What are the risks and hazards to my organization, and how can I apply these evidence practices to the problem?’” TH

Richard Quinn is a freelance writer in New Jersey.

A recent Agency for Healthcare Research and Quality (AHRQ) report, “Making Health Care Safer II: An Updated Critical Analysis of the Evidence for Patient Safety Practices,” holds nearly 1,000 pages of practice-management tips for improving outcomes. But where does a hospitalist begin when reviewing such a massive playbook for progress?

Jim Battles, PhD, an AHRQ social science analyst for patient safety who worked on the report, says the best place to start is by asking yourself: “What keeps you up at night? … What scares the heck out of you?”

The report, a follow-up to the influential and controversial 2001 report “Making Health Care Safer: A Critical Analysis of Patient Safety Practices,” is viewed by its authors as the next step in the continuum of improving patient outcomes. The latest research culled a list of more than 100 patient-safety practices (PSPs) down to 10 that should be “strongly encouraged” and another dozen that are “encouraged.” Battles looks at the 2001 report as more about pushing physicians to think about PSPs, with the updated version as a guidebook on how to think about it.

Listen to AHRQ analyst Jim Battles, PhD, talk about how hospitalists and others should view the new report

Paul Shekelle, MD, PhD, director of the Southern California Evidence-Based Practice Center site of RAND Corp., which AHRQ commissioned to produce the report, says that some might look at safety initiatives since the landmark Institute of Medicine report “To Err is Human” in 1999 and question whether enough progress has been made. But all progress is meaningful to individual patients, and the improvements of the past decade and a half have been important, he adds.

“What I believe is that we’ve made a lot of progress in certain areas,” Dr. Shekelle says, “but this can't be seen when we look at aggregate data, because the improvements we have seen don't account for a sufficiently large proportion in aggregate of the overall patient safety problem.”

Dr. Shekelle—one of three co-principal investigators on the report, along with Peter Pronovost, MD, PhD, FCCM, of Johns Hopkins School of Medicine in Baltimore and HM pioneer Robert Wachter, MD, MHM, chief of the division of hospital medicine at the University of California at San Francisco—says he hopes physicians realize that while the report’s recommendations are evidence-based, they’re not a magic bullet.

“One of the main messages of our report is this is not like writing a prescription for a statin,” Dr. Shekelle says. “This is going to take work. It’s going to take local adaptation, and it’s going to take talking to your front-line clinicians to try and find out how to make this thing work.”

Dr. Wachter, who helped craft both the 2001 and 2013 reports, says patient safety “can be one of those things that is so compelling and so dramatic that you develop a little bit of Nike syndrome—let’s just do it, let’s just computerize, let’s just do teamwork training, let’s do simulation.” However, the healthcare system has a much better, deeper understanding of patient safety and “the role of context, the role of the setting, the role of collateral interventions. It’s generally not going to be one thing that’s the magic bullet, but it’s going to be one thing embedded in a series of other activities that are designed to make sure that you have the right design and the right culture.”

Drs. Wachter and Shekelle and Battles agree that much of the difficulty with patient safety practices is rooted in healthcare system cultures. Each uses different terms to describe the roadblock, as Dr. Wachter discusses implementation science and Battles highlights the difference between the technical work of PSPs and their “social adoption.” But all concur that unless PSPs are committed for the long haul, implementation might be little more than lip service.

“It’s a responsibility of the CEO, the CMO, the CNO, and environmental services, all the way down,” Battles says. “You have to develop around these practices the shared ownership of the risk you’re trying to mitigate. Otherwise, this list of practices, OK, it’s a nice list. But you’ve got to say, ‘What are the risks and hazards to my organization, and how can I apply these evidence practices to the problem?’” TH

Richard Quinn is a freelance writer in New Jersey.

A recent Agency for Healthcare Research and Quality (AHRQ) report, “Making Health Care Safer II: An Updated Critical Analysis of the Evidence for Patient Safety Practices,” holds nearly 1,000 pages of practice-management tips for improving outcomes. But where does a hospitalist begin when reviewing such a massive playbook for progress?

Jim Battles, PhD, an AHRQ social science analyst for patient safety who worked on the report, says the best place to start is by asking yourself: “What keeps you up at night? … What scares the heck out of you?”

The report, a follow-up to the influential and controversial 2001 report “Making Health Care Safer: A Critical Analysis of Patient Safety Practices,” is viewed by its authors as the next step in the continuum of improving patient outcomes. The latest research culled a list of more than 100 patient-safety practices (PSPs) down to 10 that should be “strongly encouraged” and another dozen that are “encouraged.” Battles looks at the 2001 report as more about pushing physicians to think about PSPs, with the updated version as a guidebook on how to think about it.

Listen to AHRQ analyst Jim Battles, PhD, talk about how hospitalists and others should view the new report

Paul Shekelle, MD, PhD, director of the Southern California Evidence-Based Practice Center site of RAND Corp., which AHRQ commissioned to produce the report, says that some might look at safety initiatives since the landmark Institute of Medicine report “To Err is Human” in 1999 and question whether enough progress has been made. But all progress is meaningful to individual patients, and the improvements of the past decade and a half have been important, he adds.

“What I believe is that we’ve made a lot of progress in certain areas,” Dr. Shekelle says, “but this can't be seen when we look at aggregate data, because the improvements we have seen don't account for a sufficiently large proportion in aggregate of the overall patient safety problem.”

Dr. Shekelle—one of three co-principal investigators on the report, along with Peter Pronovost, MD, PhD, FCCM, of Johns Hopkins School of Medicine in Baltimore and HM pioneer Robert Wachter, MD, MHM, chief of the division of hospital medicine at the University of California at San Francisco—says he hopes physicians realize that while the report’s recommendations are evidence-based, they’re not a magic bullet.

“One of the main messages of our report is this is not like writing a prescription for a statin,” Dr. Shekelle says. “This is going to take work. It’s going to take local adaptation, and it’s going to take talking to your front-line clinicians to try and find out how to make this thing work.”

Dr. Wachter, who helped craft both the 2001 and 2013 reports, says patient safety “can be one of those things that is so compelling and so dramatic that you develop a little bit of Nike syndrome—let’s just do it, let’s just computerize, let’s just do teamwork training, let’s do simulation.” However, the healthcare system has a much better, deeper understanding of patient safety and “the role of context, the role of the setting, the role of collateral interventions. It’s generally not going to be one thing that’s the magic bullet, but it’s going to be one thing embedded in a series of other activities that are designed to make sure that you have the right design and the right culture.”

Drs. Wachter and Shekelle and Battles agree that much of the difficulty with patient safety practices is rooted in healthcare system cultures. Each uses different terms to describe the roadblock, as Dr. Wachter discusses implementation science and Battles highlights the difference between the technical work of PSPs and their “social adoption.” But all concur that unless PSPs are committed for the long haul, implementation might be little more than lip service.

“It’s a responsibility of the CEO, the CMO, the CNO, and environmental services, all the way down,” Battles says. “You have to develop around these practices the shared ownership of the risk you’re trying to mitigate. Otherwise, this list of practices, OK, it’s a nice list. But you’ve got to say, ‘What are the risks and hazards to my organization, and how can I apply these evidence practices to the problem?’” TH

Richard Quinn is a freelance writer in New Jersey.

Click here to listen to Dr. Agarwal-Antal

Click here to listen to Dr. Agarwal-Antal

Click here to listen to Dr. Agarwal-Antal

Click here to listen to Paul Stander

Click here to listen to Paul Stander

Click here to listen to Paul Stander

In July 2010, 443-bed Mary Washington Hospital in Fredericksburg, Va., decided to end its contract for hospitalist services with a local private practice, the Fredericksburg Hospitalist Group (FGH), and to contract instead with national management company HMG (now Cogent HMG).

“We thought the local group might fold and leave, even though they retained a contract with our smaller affiliated hospital,” the 100-bed Stafford Hospital in nearby Stafford, Va., says Rebecca Bigoney, MD, vice president of medical affairs at Mary Washington Hospital. But FHG chose to stay and started aggressively marketing its services to local physicians.

“Today, we have two hospitalist groups that are similar in size, with an almost identical number of patients. They are both competitive and collegial, and it works far better than we thought it would,” Dr. Bigoney says. “We have seen many benefits from having two hospitalist groups; it makes both of them try harder. They have good leaders and aligned incentives.”

The groups also work together on such projects as developing order sets, managing lengths of hospital stay, and implementing computerized physician order entry.

Both groups are represented on hospital committees and within the recently formed division of hospital medicine. Rules of engagement were negotiated with the leadership of the two groups, including a policy on hospitalist admissions and transfers, protocols for handling unassigned patients, a process for local medical groups and physicians to designate their preference for hospitalist coverage, and what to do if the patient is admitted to the wrong group because the primary-care physician is not known at time of admission. If no preference for hospitalist group is given by the primary-care physician, the referral goes to Cogent HMG.

Dr. Bigoney acknowledges FHG physicians had some hard feelings at first. That sentiment is confirmed by FHG founder and hospitalist Feroz Tamana, MD.

“Of course, there was some confusion and anxiety [over the transfer],” Dr. Tamana says. “But from Day One, it has worked pretty well.”

FHG initially downsized from 24 physicians to eight, but has since grown back to 14.

Kerry Lecky, MD, joined Mary Washington in November 2011 to lead the contracting Cogent HMG practice. Everyone was in agreement as to the rules of engagement at that time “and how to align with the hospital’s goals,” said Dr. Lecky, who has since moved on to another position. “The competition has been an opportunity to improve quality. It could be a problem if there were too many hospitalist groups. But two is a very manageable number.”

Is this approach sustainable for the long haul?

“With two groups, we keep each other on our toes,” she says. And the ability to offer a choice of hospitalists to primary-care physicians has been a plus. TH

Larry Beresford is a freelance writer in Oakland, Calif.

In July 2010, 443-bed Mary Washington Hospital in Fredericksburg, Va., decided to end its contract for hospitalist services with a local private practice, the Fredericksburg Hospitalist Group (FGH), and to contract instead with national management company HMG (now Cogent HMG).

“We thought the local group might fold and leave, even though they retained a contract with our smaller affiliated hospital,” the 100-bed Stafford Hospital in nearby Stafford, Va., says Rebecca Bigoney, MD, vice president of medical affairs at Mary Washington Hospital. But FHG chose to stay and started aggressively marketing its services to local physicians.

“Today, we have two hospitalist groups that are similar in size, with an almost identical number of patients. They are both competitive and collegial, and it works far better than we thought it would,” Dr. Bigoney says. “We have seen many benefits from having two hospitalist groups; it makes both of them try harder. They have good leaders and aligned incentives.”

The groups also work together on such projects as developing order sets, managing lengths of hospital stay, and implementing computerized physician order entry.

Both groups are represented on hospital committees and within the recently formed division of hospital medicine. Rules of engagement were negotiated with the leadership of the two groups, including a policy on hospitalist admissions and transfers, protocols for handling unassigned patients, a process for local medical groups and physicians to designate their preference for hospitalist coverage, and what to do if the patient is admitted to the wrong group because the primary-care physician is not known at time of admission. If no preference for hospitalist group is given by the primary-care physician, the referral goes to Cogent HMG.

Dr. Bigoney acknowledges FHG physicians had some hard feelings at first. That sentiment is confirmed by FHG founder and hospitalist Feroz Tamana, MD.

“Of course, there was some confusion and anxiety [over the transfer],” Dr. Tamana says. “But from Day One, it has worked pretty well.”

FHG initially downsized from 24 physicians to eight, but has since grown back to 14.

Kerry Lecky, MD, joined Mary Washington in November 2011 to lead the contracting Cogent HMG practice. Everyone was in agreement as to the rules of engagement at that time “and how to align with the hospital’s goals,” said Dr. Lecky, who has since moved on to another position. “The competition has been an opportunity to improve quality. It could be a problem if there were too many hospitalist groups. But two is a very manageable number.”

Is this approach sustainable for the long haul?

“With two groups, we keep each other on our toes,” she says. And the ability to offer a choice of hospitalists to primary-care physicians has been a plus. TH

Larry Beresford is a freelance writer in Oakland, Calif.

In July 2010, 443-bed Mary Washington Hospital in Fredericksburg, Va., decided to end its contract for hospitalist services with a local private practice, the Fredericksburg Hospitalist Group (FGH), and to contract instead with national management company HMG (now Cogent HMG).

“We thought the local group might fold and leave, even though they retained a contract with our smaller affiliated hospital,” the 100-bed Stafford Hospital in nearby Stafford, Va., says Rebecca Bigoney, MD, vice president of medical affairs at Mary Washington Hospital. But FHG chose to stay and started aggressively marketing its services to local physicians.

“Today, we have two hospitalist groups that are similar in size, with an almost identical number of patients. They are both competitive and collegial, and it works far better than we thought it would,” Dr. Bigoney says. “We have seen many benefits from having two hospitalist groups; it makes both of them try harder. They have good leaders and aligned incentives.”

The groups also work together on such projects as developing order sets, managing lengths of hospital stay, and implementing computerized physician order entry.

Both groups are represented on hospital committees and within the recently formed division of hospital medicine. Rules of engagement were negotiated with the leadership of the two groups, including a policy on hospitalist admissions and transfers, protocols for handling unassigned patients, a process for local medical groups and physicians to designate their preference for hospitalist coverage, and what to do if the patient is admitted to the wrong group because the primary-care physician is not known at time of admission. If no preference for hospitalist group is given by the primary-care physician, the referral goes to Cogent HMG.

Dr. Bigoney acknowledges FHG physicians had some hard feelings at first. That sentiment is confirmed by FHG founder and hospitalist Feroz Tamana, MD.

“Of course, there was some confusion and anxiety [over the transfer],” Dr. Tamana says. “But from Day One, it has worked pretty well.”

FHG initially downsized from 24 physicians to eight, but has since grown back to 14.

Kerry Lecky, MD, joined Mary Washington in November 2011 to lead the contracting Cogent HMG practice. Everyone was in agreement as to the rules of engagement at that time “and how to align with the hospital’s goals,” said Dr. Lecky, who has since moved on to another position. “The competition has been an opportunity to improve quality. It could be a problem if there were too many hospitalist groups. But two is a very manageable number.”

Is this approach sustainable for the long haul?

“With two groups, we keep each other on our toes,” she says. And the ability to offer a choice of hospitalists to primary-care physicians has been a plus. TH

Larry Beresford is a freelance writer in Oakland, Calif.

Hospitalists sometimes come across skin problems in pediatric patients, and some of these issues fall outside the scope of their expertise.

“I find lesions incidentally that I recommend be referred to dermatologists for evaluation on an outpatient basis” more often than in inpatient dermatologic situations, says Logan Murray, MD, a pediatric hospitalist at the Barbara Bush Children’s Hospital at Maine Medical Center in Portland. “I recently managed a newborn with a 6 cm diameter brown patch in the lumbar area with fine, dark, vellus hair, which I suspect is a congenital giant melanocytic nevus,” he says. To properly evaluate the birthmark, he referred the patient’s parents to a dermatologist.

In these instances, it makes sense for a hospitalist to request that a dermatologist see the child and talk with the parents during hospitalization.

“We get many consults [that] are appropriate,” says Susan Bayliss, MD, a pediatric dermatologist at St. Louis Children’s Hospital. If a hospitalist can’t identify a particular skin issue and reassure parents, it’s time to call a dermatologist.

Distinguishing between acute and chronic dermatologic conditions is important. “The skin is often overlooked among hospitalists,” who are managing sicker patients nowadays, says Neera Agarwal-Antal, MD, head of the division of dermatology at Akron Children’s Hospital in Akron, Ohio.

One of the most dangerous and potentially fatal dermatologic emergencies is Stevens-Johnson syndrome, known in later stages as toxic epidermal necrolysis. Usually triggered by a drug-related reaction, the disease can cause large areas of skin to detach and lesions to develop in the mucous membranes. However, “the good news is most skin conditions are not acute or deadly,” Dr. Agarwal-Antal says.

Warts are very common and often can wait for examination in an outpatient setting. If an adolescent has significant acne, a hospitalist may ask gently, “Are you interested in doing something about your complexion?” To a patient who answers “yes,” a hospitalist could suggest over-the-counter benzoyl peroxide, says Dr. Bayliss, who is also professor of dermatology and pediatrics at Washington University School of Medicine in St. Louis.

“Pediatric dermatology is basically an outpatient specialty,” she adds. “Many kids have skin issues, but most of them do not need to be addressed by a hospitalist.” TH

Susan Kreimer is a freelance writer in New York.

Hospitalists sometimes come across skin problems in pediatric patients, and some of these issues fall outside the scope of their expertise.

“I find lesions incidentally that I recommend be referred to dermatologists for evaluation on an outpatient basis” more often than in inpatient dermatologic situations, says Logan Murray, MD, a pediatric hospitalist at the Barbara Bush Children’s Hospital at Maine Medical Center in Portland. “I recently managed a newborn with a 6 cm diameter brown patch in the lumbar area with fine, dark, vellus hair, which I suspect is a congenital giant melanocytic nevus,” he says. To properly evaluate the birthmark, he referred the patient’s parents to a dermatologist.

In these instances, it makes sense for a hospitalist to request that a dermatologist see the child and talk with the parents during hospitalization.

“We get many consults [that] are appropriate,” says Susan Bayliss, MD, a pediatric dermatologist at St. Louis Children’s Hospital. If a hospitalist can’t identify a particular skin issue and reassure parents, it’s time to call a dermatologist.

Distinguishing between acute and chronic dermatologic conditions is important. “The skin is often overlooked among hospitalists,” who are managing sicker patients nowadays, says Neera Agarwal-Antal, MD, head of the division of dermatology at Akron Children’s Hospital in Akron, Ohio.

One of the most dangerous and potentially fatal dermatologic emergencies is Stevens-Johnson syndrome, known in later stages as toxic epidermal necrolysis. Usually triggered by a drug-related reaction, the disease can cause large areas of skin to detach and lesions to develop in the mucous membranes. However, “the good news is most skin conditions are not acute or deadly,” Dr. Agarwal-Antal says.

Warts are very common and often can wait for examination in an outpatient setting. If an adolescent has significant acne, a hospitalist may ask gently, “Are you interested in doing something about your complexion?” To a patient who answers “yes,” a hospitalist could suggest over-the-counter benzoyl peroxide, says Dr. Bayliss, who is also professor of dermatology and pediatrics at Washington University School of Medicine in St. Louis.

“Pediatric dermatology is basically an outpatient specialty,” she adds. “Many kids have skin issues, but most of them do not need to be addressed by a hospitalist.” TH

Susan Kreimer is a freelance writer in New York.

Hospitalists sometimes come across skin problems in pediatric patients, and some of these issues fall outside the scope of their expertise.

“I find lesions incidentally that I recommend be referred to dermatologists for evaluation on an outpatient basis” more often than in inpatient dermatologic situations, says Logan Murray, MD, a pediatric hospitalist at the Barbara Bush Children’s Hospital at Maine Medical Center in Portland. “I recently managed a newborn with a 6 cm diameter brown patch in the lumbar area with fine, dark, vellus hair, which I suspect is a congenital giant melanocytic nevus,” he says. To properly evaluate the birthmark, he referred the patient’s parents to a dermatologist.

In these instances, it makes sense for a hospitalist to request that a dermatologist see the child and talk with the parents during hospitalization.

“We get many consults [that] are appropriate,” says Susan Bayliss, MD, a pediatric dermatologist at St. Louis Children’s Hospital. If a hospitalist can’t identify a particular skin issue and reassure parents, it’s time to call a dermatologist.

Distinguishing between acute and chronic dermatologic conditions is important. “The skin is often overlooked among hospitalists,” who are managing sicker patients nowadays, says Neera Agarwal-Antal, MD, head of the division of dermatology at Akron Children’s Hospital in Akron, Ohio.

One of the most dangerous and potentially fatal dermatologic emergencies is Stevens-Johnson syndrome, known in later stages as toxic epidermal necrolysis. Usually triggered by a drug-related reaction, the disease can cause large areas of skin to detach and lesions to develop in the mucous membranes. However, “the good news is most skin conditions are not acute or deadly,” Dr. Agarwal-Antal says.

Warts are very common and often can wait for examination in an outpatient setting. If an adolescent has significant acne, a hospitalist may ask gently, “Are you interested in doing something about your complexion?” To a patient who answers “yes,” a hospitalist could suggest over-the-counter benzoyl peroxide, says Dr. Bayliss, who is also professor of dermatology and pediatrics at Washington University School of Medicine in St. Louis.

“Pediatric dermatology is basically an outpatient specialty,” she adds. “Many kids have skin issues, but most of them do not need to be addressed by a hospitalist.” TH

Susan Kreimer is a freelance writer in New York.

Not infrequently, less than 90 day old infants have fever and irritability and are more sleepy than usual, but have no apparent focus of infection. The sepsis evaluation is usually negative. It is frustrating for parents and providers when we report that we don’t really know what caused the febrile illness.

In summer/autumn season, some infants have enterovirus, with the predominate serotypes varying year to year. The enterovirus genus has several species, i.e., polio, enterovirus, echovirus, and Coxsackie A and Coxsackie B viruses. Echovirus is an acronym for enteric, cytopathic, human, orphan virus. Coxsackie is named from the city where it was first reported. Recently discovered enteroviruses have numbers starting at 68, and include a strain causing severe disease in Asia, enterovirus 71.

Sometimes clinicians can tell that enterovirus is in the community without laboratory tests because children present with hand, foot, and mouth (and sometimes buttock) disease. or herpangina. Enteroviruses also cause pericarditis, myocarditis, or pleurodynia (a.k.a. the "devil’s grippe").

But enteroviruses also cause aseptic meningitis. A modest pleocytosis with a mononuclear predominance and near-normal CSF glucose/protein values, plus negative bacterial cultures, is commonly called "aseptic meningitis."

Enteroviruses cause modest CSF pleocytosis (50-400 WBC), usually with mononuclear predominance and relatively normal CSF chemistries. While there can initially be a CSF neutrophil predominance, the differential usually shifts to mostly mononuclear cells less than 24 hours later. In the 1970s and 1980s (before polymerase chain reaction [PCR]), we used a "double tap" strategy to allow early discontinuation of antibiotics and hospital discharge. If the second CSF obtained within 24 hours of the first CSF had reasonably normal chemistries plus fewer WBCs or shifted to almost all mononuclear cells, children were discharged before final culture results. While hypoglycorrhachia is seen rarely with enterovirus (as low as 10 mg/dL), low CSF glucose values are usually due to bacterial or tuberculous meningitis. CSF protein concentrations with enteroviral meningitis are rarely greater than 80 mg/dL, the usual values for bacterial meningitis.

But consider this caveat: When "aseptic meningitis" seems present but CSF chemistries are abnormal (elevated protein or low glucose), check for tuberculosis risk factors and/or indolent neurological findings that could indicate tuberculous meningitis. In infants less than 2 months of age, consider neonatal herpes simplex virus (HSV) disease, particularly if the CSF protein is elevated.

These days "double taps" are not routine. Instead, CSF PCR is used. HSV and enterovirus PCR on CSF is available at most institutions with results available before bacteria cultures are final. A positive CSF enterovirus PCR (J. Pediatr. 1997;131:393-7) allows discontinuing antibacterials and acyclovir, if it was started empirically, plus early discharge. A positive HSV PCR also clarifies management: Continue acyclovir but discontinue antibacterial drugs. Keep in mind that enteroviral meningitis outbreaks are quite seasonal, with the majority of disease noted in the summer and early fall.

So we know the answer if the enterovirus or HSV PCR is positive. But what if these PCRs and bacterial cultures are negative in a child not pretreated with antibiotics? Well, the new kid on the block for aseptic meningitis is human parechovirus (HPeV). The first viruses classified as HPeV (HPeV1 and HPeV2) were previously called echovirus 22 and echovirus 23. But clinical and genome differences from enteroviruses led to reclassification as HPeVs. Now there are 16 HPeV serotypes. So why do we care?

In the past 6 years, HPeV3 emerged as the most common definable cause of sepsis-like syndrome in young infants with negative bacterial cultures (J. Clin. Virol. 2011;52:187-91; Pediatr. Infect. Dis. J. 2013;32:213-6). Interestingly, HPeV3-infected infants have more frequent peripheral leukopenia and lymphopenia plus more febrile days and higher fevers than those with enteroviruses. HPeV3 has a nearly every-other-year cycle (May-November). HPeV was as frequent or more frequent than all enteroviruses combined.

HPEV is not detected by enterovirus PCR, but is confirmed by HPeV-specific PCR. Like enteroviruses, PCR of blood is usually positive in HPeV-infected infants.

An important difference from HSV or enteroviruses is that almost no HPeV3 CNS-infected infants have CSF pleocytosis. That’s right. CSF in HPeV CNS infection is like HHV-6 (minimal CSF WBCs despite CNS infection). At our institution, HPeV3 PCR is performed routinely on CSF from all infants less than 90 days of age undergoing sepsis evaluations in summer/autumn.

If cultures and PCRs are negative in young infants with sepsis-like syndrome, your laboratory can likely perform or send out HPeV3 PCR. When HPeV3 CSF PCRs are positive, antibacterials can be stopped and patients discharged. Clinicians may be reluctant to discharge before final negative bacterial cultures because these infants can still "look ill," and providers are just learning about HPeV3. But based on our multiyear experience, it appears safe. We saw only three concurrent bacterial infections when HPeV3 was detected in CSF – all urinary tract infections that were easily detected during the sepsis evaluation and treated as such.

There have been no defined sequelae of HPeV CNS infection to date in the United States, although long-term follow-up is lacking for this emerging pathogen. There have been rare CNS sequelae, including white matter changes or seizures outside the United States, but these were apparent during the acute illness. We recommend outpatient follow-up soon after discharge, particularly if fever persists at discharge.

If we add HPeV3 PCR to our testing for infant sepsis-like syndrome during summer/fall, particularly when there is no or minimal CSF pleocytosis plus peripheral leuko/lymphopenia, there will fewer times when we lack a confirmed cause.

Dr. Harrison is a professor of pediatrics and pediatric infectious diseases at Children’s Mercy Hospitals and Clinics, Kansas City, Mo. Dr. Harrison said he has no relevant financial disclosures.

Not infrequently, less than 90 day old infants have fever and irritability and are more sleepy than usual, but have no apparent focus of infection. The sepsis evaluation is usually negative. It is frustrating for parents and providers when we report that we don’t really know what caused the febrile illness.

In summer/autumn season, some infants have enterovirus, with the predominate serotypes varying year to year. The enterovirus genus has several species, i.e., polio, enterovirus, echovirus, and Coxsackie A and Coxsackie B viruses. Echovirus is an acronym for enteric, cytopathic, human, orphan virus. Coxsackie is named from the city where it was first reported. Recently discovered enteroviruses have numbers starting at 68, and include a strain causing severe disease in Asia, enterovirus 71.

Sometimes clinicians can tell that enterovirus is in the community without laboratory tests because children present with hand, foot, and mouth (and sometimes buttock) disease. or herpangina. Enteroviruses also cause pericarditis, myocarditis, or pleurodynia (a.k.a. the "devil’s grippe").

But enteroviruses also cause aseptic meningitis. A modest pleocytosis with a mononuclear predominance and near-normal CSF glucose/protein values, plus negative bacterial cultures, is commonly called "aseptic meningitis."

Enteroviruses cause modest CSF pleocytosis (50-400 WBC), usually with mononuclear predominance and relatively normal CSF chemistries. While there can initially be a CSF neutrophil predominance, the differential usually shifts to mostly mononuclear cells less than 24 hours later. In the 1970s and 1980s (before polymerase chain reaction [PCR]), we used a "double tap" strategy to allow early discontinuation of antibiotics and hospital discharge. If the second CSF obtained within 24 hours of the first CSF had reasonably normal chemistries plus fewer WBCs or shifted to almost all mononuclear cells, children were discharged before final culture results. While hypoglycorrhachia is seen rarely with enterovirus (as low as 10 mg/dL), low CSF glucose values are usually due to bacterial or tuberculous meningitis. CSF protein concentrations with enteroviral meningitis are rarely greater than 80 mg/dL, the usual values for bacterial meningitis.

But consider this caveat: When "aseptic meningitis" seems present but CSF chemistries are abnormal (elevated protein or low glucose), check for tuberculosis risk factors and/or indolent neurological findings that could indicate tuberculous meningitis. In infants less than 2 months of age, consider neonatal herpes simplex virus (HSV) disease, particularly if the CSF protein is elevated.

These days "double taps" are not routine. Instead, CSF PCR is used. HSV and enterovirus PCR on CSF is available at most institutions with results available before bacteria cultures are final. A positive CSF enterovirus PCR (J. Pediatr. 1997;131:393-7) allows discontinuing antibacterials and acyclovir, if it was started empirically, plus early discharge. A positive HSV PCR also clarifies management: Continue acyclovir but discontinue antibacterial drugs. Keep in mind that enteroviral meningitis outbreaks are quite seasonal, with the majority of disease noted in the summer and early fall.

So we know the answer if the enterovirus or HSV PCR is positive. But what if these PCRs and bacterial cultures are negative in a child not pretreated with antibiotics? Well, the new kid on the block for aseptic meningitis is human parechovirus (HPeV). The first viruses classified as HPeV (HPeV1 and HPeV2) were previously called echovirus 22 and echovirus 23. But clinical and genome differences from enteroviruses led to reclassification as HPeVs. Now there are 16 HPeV serotypes. So why do we care?

In the past 6 years, HPeV3 emerged as the most common definable cause of sepsis-like syndrome in young infants with negative bacterial cultures (J. Clin. Virol. 2011;52:187-91; Pediatr. Infect. Dis. J. 2013;32:213-6). Interestingly, HPeV3-infected infants have more frequent peripheral leukopenia and lymphopenia plus more febrile days and higher fevers than those with enteroviruses. HPeV3 has a nearly every-other-year cycle (May-November). HPeV was as frequent or more frequent than all enteroviruses combined.

HPEV is not detected by enterovirus PCR, but is confirmed by HPeV-specific PCR. Like enteroviruses, PCR of blood is usually positive in HPeV-infected infants.

An important difference from HSV or enteroviruses is that almost no HPeV3 CNS-infected infants have CSF pleocytosis. That’s right. CSF in HPeV CNS infection is like HHV-6 (minimal CSF WBCs despite CNS infection). At our institution, HPeV3 PCR is performed routinely on CSF from all infants less than 90 days of age undergoing sepsis evaluations in summer/autumn.

If cultures and PCRs are negative in young infants with sepsis-like syndrome, your laboratory can likely perform or send out HPeV3 PCR. When HPeV3 CSF PCRs are positive, antibacterials can be stopped and patients discharged. Clinicians may be reluctant to discharge before final negative bacterial cultures because these infants can still "look ill," and providers are just learning about HPeV3. But based on our multiyear experience, it appears safe. We saw only three concurrent bacterial infections when HPeV3 was detected in CSF – all urinary tract infections that were easily detected during the sepsis evaluation and treated as such.

There have been no defined sequelae of HPeV CNS infection to date in the United States, although long-term follow-up is lacking for this emerging pathogen. There have been rare CNS sequelae, including white matter changes or seizures outside the United States, but these were apparent during the acute illness. We recommend outpatient follow-up soon after discharge, particularly if fever persists at discharge.

If we add HPeV3 PCR to our testing for infant sepsis-like syndrome during summer/fall, particularly when there is no or minimal CSF pleocytosis plus peripheral leuko/lymphopenia, there will fewer times when we lack a confirmed cause.

Dr. Harrison is a professor of pediatrics and pediatric infectious diseases at Children’s Mercy Hospitals and Clinics, Kansas City, Mo. Dr. Harrison said he has no relevant financial disclosures.

Not infrequently, less than 90 day old infants have fever and irritability and are more sleepy than usual, but have no apparent focus of infection. The sepsis evaluation is usually negative. It is frustrating for parents and providers when we report that we don’t really know what caused the febrile illness.

In summer/autumn season, some infants have enterovirus, with the predominate serotypes varying year to year. The enterovirus genus has several species, i.e., polio, enterovirus, echovirus, and Coxsackie A and Coxsackie B viruses. Echovirus is an acronym for enteric, cytopathic, human, orphan virus. Coxsackie is named from the city where it was first reported. Recently discovered enteroviruses have numbers starting at 68, and include a strain causing severe disease in Asia, enterovirus 71.

Sometimes clinicians can tell that enterovirus is in the community without laboratory tests because children present with hand, foot, and mouth (and sometimes buttock) disease. or herpangina. Enteroviruses also cause pericarditis, myocarditis, or pleurodynia (a.k.a. the "devil’s grippe").

But enteroviruses also cause aseptic meningitis. A modest pleocytosis with a mononuclear predominance and near-normal CSF glucose/protein values, plus negative bacterial cultures, is commonly called "aseptic meningitis."

Enteroviruses cause modest CSF pleocytosis (50-400 WBC), usually with mononuclear predominance and relatively normal CSF chemistries. While there can initially be a CSF neutrophil predominance, the differential usually shifts to mostly mononuclear cells less than 24 hours later. In the 1970s and 1980s (before polymerase chain reaction [PCR]), we used a "double tap" strategy to allow early discontinuation of antibiotics and hospital discharge. If the second CSF obtained within 24 hours of the first CSF had reasonably normal chemistries plus fewer WBCs or shifted to almost all mononuclear cells, children were discharged before final culture results. While hypoglycorrhachia is seen rarely with enterovirus (as low as 10 mg/dL), low CSF glucose values are usually due to bacterial or tuberculous meningitis. CSF protein concentrations with enteroviral meningitis are rarely greater than 80 mg/dL, the usual values for bacterial meningitis.

But consider this caveat: When "aseptic meningitis" seems present but CSF chemistries are abnormal (elevated protein or low glucose), check for tuberculosis risk factors and/or indolent neurological findings that could indicate tuberculous meningitis. In infants less than 2 months of age, consider neonatal herpes simplex virus (HSV) disease, particularly if the CSF protein is elevated.

These days "double taps" are not routine. Instead, CSF PCR is used. HSV and enterovirus PCR on CSF is available at most institutions with results available before bacteria cultures are final. A positive CSF enterovirus PCR (J. Pediatr. 1997;131:393-7) allows discontinuing antibacterials and acyclovir, if it was started empirically, plus early discharge. A positive HSV PCR also clarifies management: Continue acyclovir but discontinue antibacterial drugs. Keep in mind that enteroviral meningitis outbreaks are quite seasonal, with the majority of disease noted in the summer and early fall.

So we know the answer if the enterovirus or HSV PCR is positive. But what if these PCRs and bacterial cultures are negative in a child not pretreated with antibiotics? Well, the new kid on the block for aseptic meningitis is human parechovirus (HPeV). The first viruses classified as HPeV (HPeV1 and HPeV2) were previously called echovirus 22 and echovirus 23. But clinical and genome differences from enteroviruses led to reclassification as HPeVs. Now there are 16 HPeV serotypes. So why do we care?

In the past 6 years, HPeV3 emerged as the most common definable cause of sepsis-like syndrome in young infants with negative bacterial cultures (J. Clin. Virol. 2011;52:187-91; Pediatr. Infect. Dis. J. 2013;32:213-6). Interestingly, HPeV3-infected infants have more frequent peripheral leukopenia and lymphopenia plus more febrile days and higher fevers than those with enteroviruses. HPeV3 has a nearly every-other-year cycle (May-November). HPeV was as frequent or more frequent than all enteroviruses combined.

HPEV is not detected by enterovirus PCR, but is confirmed by HPeV-specific PCR. Like enteroviruses, PCR of blood is usually positive in HPeV-infected infants.

An important difference from HSV or enteroviruses is that almost no HPeV3 CNS-infected infants have CSF pleocytosis. That’s right. CSF in HPeV CNS infection is like HHV-6 (minimal CSF WBCs despite CNS infection). At our institution, HPeV3 PCR is performed routinely on CSF from all infants less than 90 days of age undergoing sepsis evaluations in summer/autumn.

If cultures and PCRs are negative in young infants with sepsis-like syndrome, your laboratory can likely perform or send out HPeV3 PCR. When HPeV3 CSF PCRs are positive, antibacterials can be stopped and patients discharged. Clinicians may be reluctant to discharge before final negative bacterial cultures because these infants can still "look ill," and providers are just learning about HPeV3. But based on our multiyear experience, it appears safe. We saw only three concurrent bacterial infections when HPeV3 was detected in CSF – all urinary tract infections that were easily detected during the sepsis evaluation and treated as such.

There have been no defined sequelae of HPeV CNS infection to date in the United States, although long-term follow-up is lacking for this emerging pathogen. There have been rare CNS sequelae, including white matter changes or seizures outside the United States, but these were apparent during the acute illness. We recommend outpatient follow-up soon after discharge, particularly if fever persists at discharge.

If we add HPeV3 PCR to our testing for infant sepsis-like syndrome during summer/fall, particularly when there is no or minimal CSF pleocytosis plus peripheral leuko/lymphopenia, there will fewer times when we lack a confirmed cause.

Dr. Harrison is a professor of pediatrics and pediatric infectious diseases at Children’s Mercy Hospitals and Clinics, Kansas City, Mo. Dr. Harrison said he has no relevant financial disclosures.