The Society of Hospital Medicine recently opened the 2018 State of Hospital Medicine (SoHM) Survey and is now seeking participants from hospital medicine groups to contribute to the collective understanding of the state of the specialty.

Results from the biennial survey will be analyzed and compiled into the 2018 SoHM Report to provide current data on hospitalist compensation and production, as well as cutting-edge knowledge covering practice demographics, staffing levels, turnover, staff growth, and financial support. The SoHM Survey closes on Feb. 16, 2018.

“The SoHM Survey lays the foundation for the creation of one of the most expansive tools for hospital medicine professionals,” said Beth Hawley, MBA, FACHE, chief operating officer of SHM. “With the help of participants from hospital medicine groups nationwide, it creates an up-to-date snapshot of trends in the specialty to help inform staffing and management decisions.”

The 2018 SoHM Survey includes new questions about open hospitalist physician positions during the year, including what percentage of approved staffing was unfilled and how the group filled the coverage. Other new topics ask about the number of work Relative Value Units generated by participating hospital medicine groups and who selects the billing codes for the groups.

Over the past year and a half, five distinct efforts were completed to collect user feedback for both the survey and report development processes. Efforts ranged from in-person focus groups at SHM’s Annual Conference to online user surveys. After information was collected and summarized, SHM’s Practice Analysis Committee ranked every question to trim down the Survey from 70 questions in 2016 to 52 questions in 2018.

The 2018 SoHM Report will be available this fall in print only, as a bundle of print and digital, or as digital only, with special discounts available for SHM members.

Committee members are available for one-on-one guidance as participants complete the Survey. For more information and to participate, visit www.hospitalmedicine.org/sohm.




 

The Society of Hospital Medicine recently opened the 2018 State of Hospital Medicine (SoHM) Survey and is now seeking participants from hospital medicine groups to contribute to the collective understanding of the state of the specialty.

Results from the biennial survey will be analyzed and compiled into the 2018 SoHM Report to provide current data on hospitalist compensation and production, as well as cutting-edge knowledge covering practice demographics, staffing levels, turnover, staff growth, and financial support. The SoHM Survey closes on Feb. 16, 2018.

“The SoHM Survey lays the foundation for the creation of one of the most expansive tools for hospital medicine professionals,” said Beth Hawley, MBA, FACHE, chief operating officer of SHM. “With the help of participants from hospital medicine groups nationwide, it creates an up-to-date snapshot of trends in the specialty to help inform staffing and management decisions.”

The 2018 SoHM Survey includes new questions about open hospitalist physician positions during the year, including what percentage of approved staffing was unfilled and how the group filled the coverage. Other new topics ask about the number of work Relative Value Units generated by participating hospital medicine groups and who selects the billing codes for the groups.

Over the past year and a half, five distinct efforts were completed to collect user feedback for both the survey and report development processes. Efforts ranged from in-person focus groups at SHM’s Annual Conference to online user surveys. After information was collected and summarized, SHM’s Practice Analysis Committee ranked every question to trim down the Survey from 70 questions in 2016 to 52 questions in 2018.

The 2018 SoHM Report will be available this fall in print only, as a bundle of print and digital, or as digital only, with special discounts available for SHM members.

Committee members are available for one-on-one guidance as participants complete the Survey. For more information and to participate, visit www.hospitalmedicine.org/sohm.




 

The Society of Hospital Medicine recently opened the 2018 State of Hospital Medicine (SoHM) Survey and is now seeking participants from hospital medicine groups to contribute to the collective understanding of the state of the specialty.

Results from the biennial survey will be analyzed and compiled into the 2018 SoHM Report to provide current data on hospitalist compensation and production, as well as cutting-edge knowledge covering practice demographics, staffing levels, turnover, staff growth, and financial support. The SoHM Survey closes on Feb. 16, 2018.

“The SoHM Survey lays the foundation for the creation of one of the most expansive tools for hospital medicine professionals,” said Beth Hawley, MBA, FACHE, chief operating officer of SHM. “With the help of participants from hospital medicine groups nationwide, it creates an up-to-date snapshot of trends in the specialty to help inform staffing and management decisions.”

The 2018 SoHM Survey includes new questions about open hospitalist physician positions during the year, including what percentage of approved staffing was unfilled and how the group filled the coverage. Other new topics ask about the number of work Relative Value Units generated by participating hospital medicine groups and who selects the billing codes for the groups.

Over the past year and a half, five distinct efforts were completed to collect user feedback for both the survey and report development processes. Efforts ranged from in-person focus groups at SHM’s Annual Conference to online user surveys. After information was collected and summarized, SHM’s Practice Analysis Committee ranked every question to trim down the Survey from 70 questions in 2016 to 52 questions in 2018.

The 2018 SoHM Report will be available this fall in print only, as a bundle of print and digital, or as digital only, with special discounts available for SHM members.

Committee members are available for one-on-one guidance as participants complete the Survey. For more information and to participate, visit www.hospitalmedicine.org/sohm.




 

This is the first article in a series on the cost of medications.

While it’s not news that some pharmaceuticals are exorbitantly expensive and therefore unavailable to our patients, I have learned that there are ways around the obstacle of cost for at least some medications. I want to tell you what I’ve learned about the high cost of two medications: aripiprazole, the generic of Abilify, and modafinil, the generic of Provigil, but the lessons learned may apply to other psychotropics – and Smokey Robinson and the Miracles said it best in a line from their 1960 hit song, “You’d better shop around.”

Gina L. Henderson/Frontline Medical News

Dr. Miller is coauthor with Annette Hanson, MD, of “Committed: The Battle Over Involuntary Psychiatric Care” (Baltimore: Johns Hopkins University Press, 2016).

This is the first article in a series on the cost of medications.

While it’s not news that some pharmaceuticals are exorbitantly expensive and therefore unavailable to our patients, I have learned that there are ways around the obstacle of cost for at least some medications. I want to tell you what I’ve learned about the high cost of two medications: aripiprazole, the generic of Abilify, and modafinil, the generic of Provigil, but the lessons learned may apply to other psychotropics – and Smokey Robinson and the Miracles said it best in a line from their 1960 hit song, “You’d better shop around.”

Gina L. Henderson/Frontline Medical News

Dr. Miller is coauthor with Annette Hanson, MD, of “Committed: The Battle Over Involuntary Psychiatric Care” (Baltimore: Johns Hopkins University Press, 2016).

This is the first article in a series on the cost of medications.

While it’s not news that some pharmaceuticals are exorbitantly expensive and therefore unavailable to our patients, I have learned that there are ways around the obstacle of cost for at least some medications. I want to tell you what I’ve learned about the high cost of two medications: aripiprazole, the generic of Abilify, and modafinil, the generic of Provigil, but the lessons learned may apply to other psychotropics – and Smokey Robinson and the Miracles said it best in a line from their 1960 hit song, “You’d better shop around.”

Gina L. Henderson/Frontline Medical News

Dr. Miller is coauthor with Annette Hanson, MD, of “Committed: The Battle Over Involuntary Psychiatric Care” (Baltimore: Johns Hopkins University Press, 2016).

The prior authorization approval process required by health insurance companies for patients’ medical treatments, also called preapproval, eats up countless hours of time and costs, over $80,000 per year, per provider. The average provider deals with 35 of these prior authorization requests per day, and each request takes an average of 20 minutes. Physicians, pharmacists, hospitals, medical groups, and health insurance companies are working together to come up with a solution.

The American Hospital Association, America’s Health Insurance Plans, American Medical Association, American Pharmacists Association, Blue Cross Blue Shield Association, and Medical Group Management Association announced a consensus statement delineating where they agree the health care industry can improve the prior authorization process.

Most of the solutions outlined in the document are intuitive – they include reducing the number of health care professionals subject to prior authorization requirements based on their performance; adherence to evidence-based medical practices or participation in a value-based agreement with the health insurance provider; reviewing the services and medications that require prior authorization and eliminating requirements for therapies that no longer warrant them; improving communications between health insurance providers, health care professionals, and patients to provide clarity on prior authorization requirements and changes; protecting continuity of care for patients; improving formulary information and coverage restrictions at point-of-care; and adopting national electronic standards for prior authorization.

Jack Resneck Jr., MD, chair-elect of the AMA board of trustees, described the document as a “good initial step” toward reducing the difficulties imposed by prior authorizations.

Prior authorization requests are particularly burdensome for medications that are expensive, a headache that doctors working with patients who have rheumatoid arthritis or lupus know well.

As insurance and provider groups work to improve the prior authorization process “it will be vital that they consider the issue from the perspective of general practitioners as well as specialists, the latter of whom prescribe more of the specialty tier medications that are subject to more protocols before patients can access these often life-improving medications,” Stephen Marmaras, director of policy and advocacy at Global Healthy Living Foundation, said in an interview. “Ultimately, improved communication between both parties – the physician offices and the payers – will allow us to identify barriers existing in current appeals processes and work toward collectively building solutions that benefit patients, particularly those with chronic disease who rely on stable access to medications.”

Sean Fahey, MD, chair of the American College of Rheumatology’s insurance subcommittee, said that, while the consensus statement is “a step in the right direction, like a lot of things, the devil is in the details.

“There’s good concepts in the statement without a whole lot of specifics,” Dr. Fahey said. Most changes will be addressed at the state level, because the federal legislature is very hesitant to legislate decisions for nongovernment insurance.

“A lot of the ideas set forth in this consensus statement are wonderful,” said Dr. Fahey. “Unfortunately for our patients, many of their medications are ludicrously expensive. … Every time you write a prescription for one of these medications, after appropriate therapy, you have to do [a preauthorization] just to get the medicine that people want and need. It’s frustrating that the issue of drug cost is driving the whole process. For a $60,000 a year price you’re going to have to do a preauthorization every single time, as opposed to a drug that’s $100 a year.”

Still, the statement is “an important step” toward ultimately making vital medications “more accessible for patients,” Dr. Fahey said.

[email protected]

The prior authorization approval process required by health insurance companies for patients’ medical treatments, also called preapproval, eats up countless hours of time and costs, over $80,000 per year, per provider. The average provider deals with 35 of these prior authorization requests per day, and each request takes an average of 20 minutes. Physicians, pharmacists, hospitals, medical groups, and health insurance companies are working together to come up with a solution.

The American Hospital Association, America’s Health Insurance Plans, American Medical Association, American Pharmacists Association, Blue Cross Blue Shield Association, and Medical Group Management Association announced a consensus statement delineating where they agree the health care industry can improve the prior authorization process.

Most of the solutions outlined in the document are intuitive – they include reducing the number of health care professionals subject to prior authorization requirements based on their performance; adherence to evidence-based medical practices or participation in a value-based agreement with the health insurance provider; reviewing the services and medications that require prior authorization and eliminating requirements for therapies that no longer warrant them; improving communications between health insurance providers, health care professionals, and patients to provide clarity on prior authorization requirements and changes; protecting continuity of care for patients; improving formulary information and coverage restrictions at point-of-care; and adopting national electronic standards for prior authorization.

Jack Resneck Jr., MD, chair-elect of the AMA board of trustees, described the document as a “good initial step” toward reducing the difficulties imposed by prior authorizations.

Prior authorization requests are particularly burdensome for medications that are expensive, a headache that doctors working with patients who have rheumatoid arthritis or lupus know well.

As insurance and provider groups work to improve the prior authorization process “it will be vital that they consider the issue from the perspective of general practitioners as well as specialists, the latter of whom prescribe more of the specialty tier medications that are subject to more protocols before patients can access these often life-improving medications,” Stephen Marmaras, director of policy and advocacy at Global Healthy Living Foundation, said in an interview. “Ultimately, improved communication between both parties – the physician offices and the payers – will allow us to identify barriers existing in current appeals processes and work toward collectively building solutions that benefit patients, particularly those with chronic disease who rely on stable access to medications.”

Sean Fahey, MD, chair of the American College of Rheumatology’s insurance subcommittee, said that, while the consensus statement is “a step in the right direction, like a lot of things, the devil is in the details.

“There’s good concepts in the statement without a whole lot of specifics,” Dr. Fahey said. Most changes will be addressed at the state level, because the federal legislature is very hesitant to legislate decisions for nongovernment insurance.

“A lot of the ideas set forth in this consensus statement are wonderful,” said Dr. Fahey. “Unfortunately for our patients, many of their medications are ludicrously expensive. … Every time you write a prescription for one of these medications, after appropriate therapy, you have to do [a preauthorization] just to get the medicine that people want and need. It’s frustrating that the issue of drug cost is driving the whole process. For a $60,000 a year price you’re going to have to do a preauthorization every single time, as opposed to a drug that’s $100 a year.”

Still, the statement is “an important step” toward ultimately making vital medications “more accessible for patients,” Dr. Fahey said.

[email protected]

The prior authorization approval process required by health insurance companies for patients’ medical treatments, also called preapproval, eats up countless hours of time and costs, over $80,000 per year, per provider. The average provider deals with 35 of these prior authorization requests per day, and each request takes an average of 20 minutes. Physicians, pharmacists, hospitals, medical groups, and health insurance companies are working together to come up with a solution.

The American Hospital Association, America’s Health Insurance Plans, American Medical Association, American Pharmacists Association, Blue Cross Blue Shield Association, and Medical Group Management Association announced a consensus statement delineating where they agree the health care industry can improve the prior authorization process.

Most of the solutions outlined in the document are intuitive – they include reducing the number of health care professionals subject to prior authorization requirements based on their performance; adherence to evidence-based medical practices or participation in a value-based agreement with the health insurance provider; reviewing the services and medications that require prior authorization and eliminating requirements for therapies that no longer warrant them; improving communications between health insurance providers, health care professionals, and patients to provide clarity on prior authorization requirements and changes; protecting continuity of care for patients; improving formulary information and coverage restrictions at point-of-care; and adopting national electronic standards for prior authorization.

Jack Resneck Jr., MD, chair-elect of the AMA board of trustees, described the document as a “good initial step” toward reducing the difficulties imposed by prior authorizations.

Prior authorization requests are particularly burdensome for medications that are expensive, a headache that doctors working with patients who have rheumatoid arthritis or lupus know well.

As insurance and provider groups work to improve the prior authorization process “it will be vital that they consider the issue from the perspective of general practitioners as well as specialists, the latter of whom prescribe more of the specialty tier medications that are subject to more protocols before patients can access these often life-improving medications,” Stephen Marmaras, director of policy and advocacy at Global Healthy Living Foundation, said in an interview. “Ultimately, improved communication between both parties – the physician offices and the payers – will allow us to identify barriers existing in current appeals processes and work toward collectively building solutions that benefit patients, particularly those with chronic disease who rely on stable access to medications.”

Sean Fahey, MD, chair of the American College of Rheumatology’s insurance subcommittee, said that, while the consensus statement is “a step in the right direction, like a lot of things, the devil is in the details.

“There’s good concepts in the statement without a whole lot of specifics,” Dr. Fahey said. Most changes will be addressed at the state level, because the federal legislature is very hesitant to legislate decisions for nongovernment insurance.

“A lot of the ideas set forth in this consensus statement are wonderful,” said Dr. Fahey. “Unfortunately for our patients, many of their medications are ludicrously expensive. … Every time you write a prescription for one of these medications, after appropriate therapy, you have to do [a preauthorization] just to get the medicine that people want and need. It’s frustrating that the issue of drug cost is driving the whole process. For a $60,000 a year price you’re going to have to do a preauthorization every single time, as opposed to a drug that’s $100 a year.”

Still, the statement is “an important step” toward ultimately making vital medications “more accessible for patients,” Dr. Fahey said.

[email protected]

The Diagnosis: Nevus Sebaceous

The patient presented with a typical solitary scalp lesion characteristic of nevus sebaceous (NS). The lesion was present at birth as a flat and smooth hairless plaque; however, over time it became more thickened and noticeable, which prompted the parents to seek medical advice.

Nevus sebaceous, also known as NS of Jadassohn, is a benign congenital hamartoma of the sebaceous gland that usually is present at birth and frequently involves the scalp and/or the face. The classic NS lesion is solitary and appears as a well-circumscribed, waxy, yellow-orange or tan, hairless plaque. Despite the presence of these lesions at birth, they may not be noted until early childhood or rarely until adulthood. Generally, the lesion tends to thicken and become more verrucous and velvety over time, particularly around the time of reaching puberty.¹ Clinically, NS lesions vary in size from 1 cm to several centimeters. Lesions initially tend to grow proportionately with the child until puberty when they become notably thicker, greasier, and verrucous or nodular under hormonal influences. The yellow discoloration of the lesion is due to sebaceous gland secretion, and the characteristic color usually becomes less evident with age.

Nevus sebaceous occurs in approximately 0.3% of newborns and tends to be sporadic in nature; however, rare familial forms have been reported.^2,3 Nevus sebaceous can present as multiple nevi that tend to be extensive and distributed along the Blaschko lines, and they usually are associated with neurologic, ocular, or skeletal defects. Involvement of the central nervous system frequently is associated with large sebaceous nevi located on the face or scalp. This association has been termed NS syndrome.⁴ Neurologic abnormalities associated with NS syndrome include seizures, mental retardation, and hemimegalencephaly.⁵ Ocular findings most communally associated with the syndrome are choristomas and colobomas.^6-8

There are several benign and malignant epithelial neoplasms that may develop within sebaceous nevi. Benign tumors include trichoblastoma, syringocystadenoma papilliferum, trichilemmoma, sebaceoma, nodular hidradenoma, and hidrocystoma.^1,8,9 Malignant neoplasms include basal cell carcinoma (BCC), apocrine carcinoma, sebaceous carcinoma, and squamous cell carcinoma. The lifetime risk of malignancy in NS is unknown. In an extensive literature review by Moody et al¹⁰ of 4923 cases of NS for the development of secondary benign and malignant neoplasms, 16% developed benign tumors while 8% developed malignant tumors such as BCC. However, subsequent studies suggested that the incidence of BCC may have been overestimated due to misinterpretation of trichoblastoma and may be less than 1%.^11-13

Usually the diagnosis of NS is made clinically and rarely a biopsy for histopathologic confirmation may be needed when the diagnosis is uncertain. Typically, these histopathologic findings include immature hair follicles, hyperplastic immature sebaceous glands, dilated apocrine glands, and epidermal hyperplasia.⁹ For patients with suspected NS syndrome, additional neurologic and ophthalmologic evaluations should be performed including neuroimaging studies, skeletal radiography, and analysis of liver and renal function.¹⁴

The current standard of care in treating NS is full-thickness excision. However, the decision should be individualized based on patient age, extension and location of the lesion, concerns about the cosmetic appearance, and the risk for malignancy. 

The 2 main reasons to excise NS include concern about malignancy and undesirable cosmetic appearance. Once a malignant lesion develops within NS, it generally is agreed that the tumor and the entire nevus should be removed; however, recommendations vary for excising NS prophylactically to decrease the risk for malignant growths. Because the risk for malignant transformation seems to be lower than previously thought, observation can be a reasonable choice for lesions that are not associated with cosmetic concern.^12,13

Photodynamic therapy, CO2 laser resurfacing, and dermabrasion have been reported as alternative therapeutic approaches. However, there is a growing concern on how effective these treatment modalities are in completely removing the lesion and whether the risk for recurrence and potential for neoplasm development remains.^1,9

This patient was healthy with normal development and growth and no signs of neurologic or ocular involvement. The parents were counseled about the risk for malignancy and the long-term cosmetic appearance of the lesion. They opted for surgical excision of the lesion at 18 months of age.

The Diagnosis: Nevus Sebaceous

The patient presented with a typical solitary scalp lesion characteristic of nevus sebaceous (NS). The lesion was present at birth as a flat and smooth hairless plaque; however, over time it became more thickened and noticeable, which prompted the parents to seek medical advice.

Nevus sebaceous, also known as NS of Jadassohn, is a benign congenital hamartoma of the sebaceous gland that usually is present at birth and frequently involves the scalp and/or the face. The classic NS lesion is solitary and appears as a well-circumscribed, waxy, yellow-orange or tan, hairless plaque. Despite the presence of these lesions at birth, they may not be noted until early childhood or rarely until adulthood. Generally, the lesion tends to thicken and become more verrucous and velvety over time, particularly around the time of reaching puberty.¹ Clinically, NS lesions vary in size from 1 cm to several centimeters. Lesions initially tend to grow proportionately with the child until puberty when they become notably thicker, greasier, and verrucous or nodular under hormonal influences. The yellow discoloration of the lesion is due to sebaceous gland secretion, and the characteristic color usually becomes less evident with age.

Nevus sebaceous occurs in approximately 0.3% of newborns and tends to be sporadic in nature; however, rare familial forms have been reported.^2,3 Nevus sebaceous can present as multiple nevi that tend to be extensive and distributed along the Blaschko lines, and they usually are associated with neurologic, ocular, or skeletal defects. Involvement of the central nervous system frequently is associated with large sebaceous nevi located on the face or scalp. This association has been termed NS syndrome.⁴ Neurologic abnormalities associated with NS syndrome include seizures, mental retardation, and hemimegalencephaly.⁵ Ocular findings most communally associated with the syndrome are choristomas and colobomas.^6-8

There are several benign and malignant epithelial neoplasms that may develop within sebaceous nevi. Benign tumors include trichoblastoma, syringocystadenoma papilliferum, trichilemmoma, sebaceoma, nodular hidradenoma, and hidrocystoma.^1,8,9 Malignant neoplasms include basal cell carcinoma (BCC), apocrine carcinoma, sebaceous carcinoma, and squamous cell carcinoma. The lifetime risk of malignancy in NS is unknown. In an extensive literature review by Moody et al¹⁰ of 4923 cases of NS for the development of secondary benign and malignant neoplasms, 16% developed benign tumors while 8% developed malignant tumors such as BCC. However, subsequent studies suggested that the incidence of BCC may have been overestimated due to misinterpretation of trichoblastoma and may be less than 1%.^11-13

Usually the diagnosis of NS is made clinically and rarely a biopsy for histopathologic confirmation may be needed when the diagnosis is uncertain. Typically, these histopathologic findings include immature hair follicles, hyperplastic immature sebaceous glands, dilated apocrine glands, and epidermal hyperplasia.⁹ For patients with suspected NS syndrome, additional neurologic and ophthalmologic evaluations should be performed including neuroimaging studies, skeletal radiography, and analysis of liver and renal function.¹⁴

The current standard of care in treating NS is full-thickness excision. However, the decision should be individualized based on patient age, extension and location of the lesion, concerns about the cosmetic appearance, and the risk for malignancy. 

The 2 main reasons to excise NS include concern about malignancy and undesirable cosmetic appearance. Once a malignant lesion develops within NS, it generally is agreed that the tumor and the entire nevus should be removed; however, recommendations vary for excising NS prophylactically to decrease the risk for malignant growths. Because the risk for malignant transformation seems to be lower than previously thought, observation can be a reasonable choice for lesions that are not associated with cosmetic concern.^12,13

Photodynamic therapy, CO2 laser resurfacing, and dermabrasion have been reported as alternative therapeutic approaches. However, there is a growing concern on how effective these treatment modalities are in completely removing the lesion and whether the risk for recurrence and potential for neoplasm development remains.^1,9

This patient was healthy with normal development and growth and no signs of neurologic or ocular involvement. The parents were counseled about the risk for malignancy and the long-term cosmetic appearance of the lesion. They opted for surgical excision of the lesion at 18 months of age.

The Diagnosis: Nevus Sebaceous

The patient presented with a typical solitary scalp lesion characteristic of nevus sebaceous (NS). The lesion was present at birth as a flat and smooth hairless plaque; however, over time it became more thickened and noticeable, which prompted the parents to seek medical advice.

Nevus sebaceous, also known as NS of Jadassohn, is a benign congenital hamartoma of the sebaceous gland that usually is present at birth and frequently involves the scalp and/or the face. The classic NS lesion is solitary and appears as a well-circumscribed, waxy, yellow-orange or tan, hairless plaque. Despite the presence of these lesions at birth, they may not be noted until early childhood or rarely until adulthood. Generally, the lesion tends to thicken and become more verrucous and velvety over time, particularly around the time of reaching puberty.¹ Clinically, NS lesions vary in size from 1 cm to several centimeters. Lesions initially tend to grow proportionately with the child until puberty when they become notably thicker, greasier, and verrucous or nodular under hormonal influences. The yellow discoloration of the lesion is due to sebaceous gland secretion, and the characteristic color usually becomes less evident with age.

Nevus sebaceous occurs in approximately 0.3% of newborns and tends to be sporadic in nature; however, rare familial forms have been reported.^2,3 Nevus sebaceous can present as multiple nevi that tend to be extensive and distributed along the Blaschko lines, and they usually are associated with neurologic, ocular, or skeletal defects. Involvement of the central nervous system frequently is associated with large sebaceous nevi located on the face or scalp. This association has been termed NS syndrome.⁴ Neurologic abnormalities associated with NS syndrome include seizures, mental retardation, and hemimegalencephaly.⁵ Ocular findings most communally associated with the syndrome are choristomas and colobomas.^6-8

There are several benign and malignant epithelial neoplasms that may develop within sebaceous nevi. Benign tumors include trichoblastoma, syringocystadenoma papilliferum, trichilemmoma, sebaceoma, nodular hidradenoma, and hidrocystoma.^1,8,9 Malignant neoplasms include basal cell carcinoma (BCC), apocrine carcinoma, sebaceous carcinoma, and squamous cell carcinoma. The lifetime risk of malignancy in NS is unknown. In an extensive literature review by Moody et al¹⁰ of 4923 cases of NS for the development of secondary benign and malignant neoplasms, 16% developed benign tumors while 8% developed malignant tumors such as BCC. However, subsequent studies suggested that the incidence of BCC may have been overestimated due to misinterpretation of trichoblastoma and may be less than 1%.^11-13

Usually the diagnosis of NS is made clinically and rarely a biopsy for histopathologic confirmation may be needed when the diagnosis is uncertain. Typically, these histopathologic findings include immature hair follicles, hyperplastic immature sebaceous glands, dilated apocrine glands, and epidermal hyperplasia.⁹ For patients with suspected NS syndrome, additional neurologic and ophthalmologic evaluations should be performed including neuroimaging studies, skeletal radiography, and analysis of liver and renal function.¹⁴

The current standard of care in treating NS is full-thickness excision. However, the decision should be individualized based on patient age, extension and location of the lesion, concerns about the cosmetic appearance, and the risk for malignancy. 

The 2 main reasons to excise NS include concern about malignancy and undesirable cosmetic appearance. Once a malignant lesion develops within NS, it generally is agreed that the tumor and the entire nevus should be removed; however, recommendations vary for excising NS prophylactically to decrease the risk for malignant growths. Because the risk for malignant transformation seems to be lower than previously thought, observation can be a reasonable choice for lesions that are not associated with cosmetic concern.^12,13

Photodynamic therapy, CO2 laser resurfacing, and dermabrasion have been reported as alternative therapeutic approaches. However, there is a growing concern on how effective these treatment modalities are in completely removing the lesion and whether the risk for recurrence and potential for neoplasm development remains.^1,9

This patient was healthy with normal development and growth and no signs of neurologic or ocular involvement. The parents were counseled about the risk for malignancy and the long-term cosmetic appearance of the lesion. They opted for surgical excision of the lesion at 18 months of age.

Surgical left atrial appendage occlusion may be just as good as anticoagulation at preventing thromboembolic events in older people with atrial fibrillation, with less risk of bleeding into the brain, according to a database review of more than 10,000 patients.

Among elderly atrial fibrillation patients who underwent heart surgery with no oral follow-up oral anticoagulation, those who had the left atrial appendage surgically occluded were 74% less likely than were those who did not to be readmitted for a major thromboembolic event within 3 years, and 68% less likely to be readmitted for a hemorrhagic stroke, researchers at Duke University in Durham, N.C., found.

“The current study demonstrated that S-LAAO [surgical left atrial appendage occlusion] was associated with a significantly lower rate of thromboembolism among patients without oral anticoagulation. In the cohort of patients discharged with oral anticoagulation, S-LAAO was not associated with [reduced] thromboembolism but was associated with a lower risk for hemorrhagic stroke presumably related to eventual discontinuation of oral anticoagulation among S-LAAO patients,” reported Daniel Friedman, MD, and his coinvestigators. The study was published Jan. 23 in JAMA.

In short, the findings suggest that shutting down the left atrial appendage in older patients offers the same stroke protection as anticoagulation, but without the bleeding risk. Given the low rates of anticoagulant use, physicians have been considering that approach for a while. Even so, it’s only been a weak (IIb) recommendation so far in AF guidelines because of the lack of evidence.

That might change soon, but “additional randomized studies comparing S-LAAO without anticoagulation [versus] systemic anticoagulation alone will be needed to define the optimal use of S-LAAO,” said Dr. Friedman, a cardiothoracic surgeon at Duke, and his colleagues. Those studies are in the works.

The team found 10,524 older patients in the Society of Thoracic Surgeons Adult Cardiac Surgery Database during 2011-2012, and linked them to Medicare data so they could be followed for up to 3 years. About a third of the subjects had stand-alone coronary artery bypass grafting; the rest had mitral or aortic valve repairs with or without CABG.

The investigators compared outcomes among the 37% (3,892) who had S-LAAO with outcomes among those who did not. Participants were a median of 76 years of age, 61% were men, and they were all at high risk for AF stroke.

After a mean follow-up of 2.6 years, subjects who received S-LAAO without postoperative anticoagulation had a significantly lower risk of readmission for thromboembolism – stroke, transient ischemic attack, or systemic embolism – compared with those who received neither S-LAAO nor anticoagulation (unadjusted rate 4.2% versus 6.0%; adjusted subdistribution hazard ratio [sHR] 0.26, 95% CI, 0.17-0.40, P less than .001).

There was no extra embolic stroke protection from S-LAAO in patients who were discharged on anticoagulation (sHR 0.88, 95% CI, 0.56-1.39; P = .59), but the risk of returning with a hemorrhagic stroke was considerably less (sHR 0.32, 95% CI, 0.17-0.57, P less than .001).

The S-LAAO group more commonly had nonparoxysmal AF, a higher ejection fraction, a lower mortality risk score, and lower rates of common stroke risks, such as diabetes, hypertension, and prior stroke. The Duke team adjusted for those and a long list of other confounders, including smoking, age, preoperative warfarin, and academic hospital status.

There were important limitations. No one knows what surgeons did to close the LAA, or how well it worked, and most patients discharged on anticoagulation were sent home on warfarin, not the newer direct oral anticoagulants.

The investigators noted that “the strongest data to date for LAAO come from randomized trials comparing warfarin with percutaneous LAAO using the WATCHMAN device” from Boston Scientific.

The reduction in cardiovascular mortality in those trials appeared to be driven by a reduction in hemorrhagic stroke and occurred despite increased rates of ischemic stroke, they said.

The current study, however, showed that S-LAAO was associated with a significantly lower rate of thromboembolism in patients without oral anticoagulation, the authors said.

The work was funded, in part, by the Food and Drug Administration. Dr. Friedman reported grants from Boston Scientific and Abbott. Other authors reported financial relations with those and several other companies.

[email protected]

SOURCE: Friedman DJ, et. al. JAMA. 2018;319(4):365-74. doi: 10.1001/jama.2017.20125.

Surgical left atrial appendage occlusion may be just as good as anticoagulation at preventing thromboembolic events in older people with atrial fibrillation, with less risk of bleeding into the brain, according to a database review of more than 10,000 patients.

Among elderly atrial fibrillation patients who underwent heart surgery with no oral follow-up oral anticoagulation, those who had the left atrial appendage surgically occluded were 74% less likely than were those who did not to be readmitted for a major thromboembolic event within 3 years, and 68% less likely to be readmitted for a hemorrhagic stroke, researchers at Duke University in Durham, N.C., found.

“The current study demonstrated that S-LAAO [surgical left atrial appendage occlusion] was associated with a significantly lower rate of thromboembolism among patients without oral anticoagulation. In the cohort of patients discharged with oral anticoagulation, S-LAAO was not associated with [reduced] thromboembolism but was associated with a lower risk for hemorrhagic stroke presumably related to eventual discontinuation of oral anticoagulation among S-LAAO patients,” reported Daniel Friedman, MD, and his coinvestigators. The study was published Jan. 23 in JAMA.

In short, the findings suggest that shutting down the left atrial appendage in older patients offers the same stroke protection as anticoagulation, but without the bleeding risk. Given the low rates of anticoagulant use, physicians have been considering that approach for a while. Even so, it’s only been a weak (IIb) recommendation so far in AF guidelines because of the lack of evidence.

That might change soon, but “additional randomized studies comparing S-LAAO without anticoagulation [versus] systemic anticoagulation alone will be needed to define the optimal use of S-LAAO,” said Dr. Friedman, a cardiothoracic surgeon at Duke, and his colleagues. Those studies are in the works.

The team found 10,524 older patients in the Society of Thoracic Surgeons Adult Cardiac Surgery Database during 2011-2012, and linked them to Medicare data so they could be followed for up to 3 years. About a third of the subjects had stand-alone coronary artery bypass grafting; the rest had mitral or aortic valve repairs with or without CABG.

The investigators compared outcomes among the 37% (3,892) who had S-LAAO with outcomes among those who did not. Participants were a median of 76 years of age, 61% were men, and they were all at high risk for AF stroke.

After a mean follow-up of 2.6 years, subjects who received S-LAAO without postoperative anticoagulation had a significantly lower risk of readmission for thromboembolism – stroke, transient ischemic attack, or systemic embolism – compared with those who received neither S-LAAO nor anticoagulation (unadjusted rate 4.2% versus 6.0%; adjusted subdistribution hazard ratio [sHR] 0.26, 95% CI, 0.17-0.40, P less than .001).

There was no extra embolic stroke protection from S-LAAO in patients who were discharged on anticoagulation (sHR 0.88, 95% CI, 0.56-1.39; P = .59), but the risk of returning with a hemorrhagic stroke was considerably less (sHR 0.32, 95% CI, 0.17-0.57, P less than .001).

The S-LAAO group more commonly had nonparoxysmal AF, a higher ejection fraction, a lower mortality risk score, and lower rates of common stroke risks, such as diabetes, hypertension, and prior stroke. The Duke team adjusted for those and a long list of other confounders, including smoking, age, preoperative warfarin, and academic hospital status.

There were important limitations. No one knows what surgeons did to close the LAA, or how well it worked, and most patients discharged on anticoagulation were sent home on warfarin, not the newer direct oral anticoagulants.

The investigators noted that “the strongest data to date for LAAO come from randomized trials comparing warfarin with percutaneous LAAO using the WATCHMAN device” from Boston Scientific.

The reduction in cardiovascular mortality in those trials appeared to be driven by a reduction in hemorrhagic stroke and occurred despite increased rates of ischemic stroke, they said.

The current study, however, showed that S-LAAO was associated with a significantly lower rate of thromboembolism in patients without oral anticoagulation, the authors said.

The work was funded, in part, by the Food and Drug Administration. Dr. Friedman reported grants from Boston Scientific and Abbott. Other authors reported financial relations with those and several other companies.

[email protected]

SOURCE: Friedman DJ, et. al. JAMA. 2018;319(4):365-74. doi: 10.1001/jama.2017.20125.

Surgical left atrial appendage occlusion may be just as good as anticoagulation at preventing thromboembolic events in older people with atrial fibrillation, with less risk of bleeding into the brain, according to a database review of more than 10,000 patients.

Among elderly atrial fibrillation patients who underwent heart surgery with no oral follow-up oral anticoagulation, those who had the left atrial appendage surgically occluded were 74% less likely than were those who did not to be readmitted for a major thromboembolic event within 3 years, and 68% less likely to be readmitted for a hemorrhagic stroke, researchers at Duke University in Durham, N.C., found.

“The current study demonstrated that S-LAAO [surgical left atrial appendage occlusion] was associated with a significantly lower rate of thromboembolism among patients without oral anticoagulation. In the cohort of patients discharged with oral anticoagulation, S-LAAO was not associated with [reduced] thromboembolism but was associated with a lower risk for hemorrhagic stroke presumably related to eventual discontinuation of oral anticoagulation among S-LAAO patients,” reported Daniel Friedman, MD, and his coinvestigators. The study was published Jan. 23 in JAMA.

In short, the findings suggest that shutting down the left atrial appendage in older patients offers the same stroke protection as anticoagulation, but without the bleeding risk. Given the low rates of anticoagulant use, physicians have been considering that approach for a while. Even so, it’s only been a weak (IIb) recommendation so far in AF guidelines because of the lack of evidence.

That might change soon, but “additional randomized studies comparing S-LAAO without anticoagulation [versus] systemic anticoagulation alone will be needed to define the optimal use of S-LAAO,” said Dr. Friedman, a cardiothoracic surgeon at Duke, and his colleagues. Those studies are in the works.

The team found 10,524 older patients in the Society of Thoracic Surgeons Adult Cardiac Surgery Database during 2011-2012, and linked them to Medicare data so they could be followed for up to 3 years. About a third of the subjects had stand-alone coronary artery bypass grafting; the rest had mitral or aortic valve repairs with or without CABG.

The investigators compared outcomes among the 37% (3,892) who had S-LAAO with outcomes among those who did not. Participants were a median of 76 years of age, 61% were men, and they were all at high risk for AF stroke.

After a mean follow-up of 2.6 years, subjects who received S-LAAO without postoperative anticoagulation had a significantly lower risk of readmission for thromboembolism – stroke, transient ischemic attack, or systemic embolism – compared with those who received neither S-LAAO nor anticoagulation (unadjusted rate 4.2% versus 6.0%; adjusted subdistribution hazard ratio [sHR] 0.26, 95% CI, 0.17-0.40, P less than .001).

There was no extra embolic stroke protection from S-LAAO in patients who were discharged on anticoagulation (sHR 0.88, 95% CI, 0.56-1.39; P = .59), but the risk of returning with a hemorrhagic stroke was considerably less (sHR 0.32, 95% CI, 0.17-0.57, P less than .001).

The S-LAAO group more commonly had nonparoxysmal AF, a higher ejection fraction, a lower mortality risk score, and lower rates of common stroke risks, such as diabetes, hypertension, and prior stroke. The Duke team adjusted for those and a long list of other confounders, including smoking, age, preoperative warfarin, and academic hospital status.

There were important limitations. No one knows what surgeons did to close the LAA, or how well it worked, and most patients discharged on anticoagulation were sent home on warfarin, not the newer direct oral anticoagulants.

The investigators noted that “the strongest data to date for LAAO come from randomized trials comparing warfarin with percutaneous LAAO using the WATCHMAN device” from Boston Scientific.

The reduction in cardiovascular mortality in those trials appeared to be driven by a reduction in hemorrhagic stroke and occurred despite increased rates of ischemic stroke, they said.

The current study, however, showed that S-LAAO was associated with a significantly lower rate of thromboembolism in patients without oral anticoagulation, the authors said.

The work was funded, in part, by the Food and Drug Administration. Dr. Friedman reported grants from Boston Scientific and Abbott. Other authors reported financial relations with those and several other companies.

[email protected]

SOURCE: Friedman DJ, et. al. JAMA. 2018;319(4):365-74. doi: 10.1001/jama.2017.20125.

To the Editor:

Trigeminal motor neuropathy is a rare condition presenting with muscle weakness and atrophy in the distribution of the trigeminal nerve without sensory changes. We present a challenging case with clinical features that mimic progressive hemifacial atrophy (PHA), a disease characterized by slowly progressive, unilateral facial atrophy that can be accompanied by inflammation and sclerosis as early features.

A 55-year-old man presented with right-sided ptosis and progressive right-sided facial atrophy of 4 years’ duration. A clinical diagnosis of PHA was made by the rheumatology department, and the patient was referred to the dermatology department for further evaluation. Examination at presentation revealed right-sided subcutaneous atrophy of the cheek, temple, and forehead extending to the scalp with absence of sclerosis, pigmentary alteration, or typical linear morphea lesions (Figures 1 and 2). The patient had no sensory changes in the affected area.

Workup by the dermatology department included magnetic resonance imaging (MRI) of the face and scalp, which demonstrated denervation muscle atrophy exclusively in the distribution of the third branch of the right trigeminal nerve, including severe atrophy of the right temporalis and masseter muscles and moderate atrophy of the pterygoid muscles. No signs of inflammation, fibrosis, or atrophy of the skin or subcutaneous fat were found, ruling out a diagnosis of PHA.

The patient was referred to the neurology department where he was found to have a normal neurologic examination with the exception of right-sided ptosis and temporalis and masseter muscle atrophy. Notably, the patient had normal sensation in the distribution of the trigeminal nerve and normal strength of the masseter and temporalis muscles.

An extensive workup by the neurology department was completed, including magnetic resonance angiography, eyeblink testing, and testing for causes of neuropathies (eg, infectious, autoimmune, vitamin deficiencies, toxin related). Of note, magnetic resonance angiography showed no abnormalities within the cavernous sinus or trigeminal cave but showed potential vascular compression of the trigeminal nerve, which was believed to be an incidental finding. The remainder of the workup was unremarkable. Based on muscle denervation atrophy in the distribution of the third branch of the trigeminal nerve in the absence of sensory symptoms or deficits, the patient’s presentation was consistent with trigeminal motor neuropathy.

In reported cases, the pathogenesis of trigeminal motor neuropathy is attributed to tumors, trauma, stroke, viral infection, and autoimmune reaction.^1-6 In other reported cases the cause is unknown,^6-8 as was the case in our patient. Magnetic resonance angiography revealed potential vascular compression of the trigeminal nerve, which has been previously reported to cause trigeminal neuropathy.⁹ However, patients with trigeminal neuropathy presented with sensory changes in the distribution of the trigeminal nerve as opposed to motor symptoms and muscle atrophy.

We present a case of trigeminal motor neuropathy presenting as PHA. Progressive hemifacial atrophy is a rare, slowly progressive disease characterized by unilateral atrophy of the skin, subcutis, muscle, and bony structures of the face. Onset usually is during childhood, though later onset has been reported.¹⁰ The pathogenesis of PHA is not well understood, though trauma, infection, immune-mediated causes, sympathetic dysfunction, and metabolic dysfunction have been proposed.¹¹ Diagnosis of PHA typically is based on clinical presentation, but histology and imaging are useful. In contrast to trigeminal motor neuropathy, MRI findings in PHA demonstrate involvement of the skin.¹²

Differentiation between PHA and trigeminal motor neuropathy is important because treatment differs. Treatment of trigeminal motor neuropathy depends on the etiology and may include removal of underlying neoplasms, while treatment of PHA depends on disease activity. The initial goal when treating PHA is to improve symptoms and slow disease progression; immunosuppressants may be considered. Facial reconstruction is an option when PHA is stable.

In this case, the features differentiating trigeminal motor neuropathy from PHA include age of onset and MRI as well as clinical findings of muscle atrophy limited to the distribution of the third branch of the trigeminal nerve. Although PHA is a rare disorder, this case demonstrates the importance of including trigeminal motor neuropathy in the differential diagnosis.

To the Editor:

Trigeminal motor neuropathy is a rare condition presenting with muscle weakness and atrophy in the distribution of the trigeminal nerve without sensory changes. We present a challenging case with clinical features that mimic progressive hemifacial atrophy (PHA), a disease characterized by slowly progressive, unilateral facial atrophy that can be accompanied by inflammation and sclerosis as early features.

A 55-year-old man presented with right-sided ptosis and progressive right-sided facial atrophy of 4 years’ duration. A clinical diagnosis of PHA was made by the rheumatology department, and the patient was referred to the dermatology department for further evaluation. Examination at presentation revealed right-sided subcutaneous atrophy of the cheek, temple, and forehead extending to the scalp with absence of sclerosis, pigmentary alteration, or typical linear morphea lesions (Figures 1 and 2). The patient had no sensory changes in the affected area.

Workup by the dermatology department included magnetic resonance imaging (MRI) of the face and scalp, which demonstrated denervation muscle atrophy exclusively in the distribution of the third branch of the right trigeminal nerve, including severe atrophy of the right temporalis and masseter muscles and moderate atrophy of the pterygoid muscles. No signs of inflammation, fibrosis, or atrophy of the skin or subcutaneous fat were found, ruling out a diagnosis of PHA.

The patient was referred to the neurology department where he was found to have a normal neurologic examination with the exception of right-sided ptosis and temporalis and masseter muscle atrophy. Notably, the patient had normal sensation in the distribution of the trigeminal nerve and normal strength of the masseter and temporalis muscles.

An extensive workup by the neurology department was completed, including magnetic resonance angiography, eyeblink testing, and testing for causes of neuropathies (eg, infectious, autoimmune, vitamin deficiencies, toxin related). Of note, magnetic resonance angiography showed no abnormalities within the cavernous sinus or trigeminal cave but showed potential vascular compression of the trigeminal nerve, which was believed to be an incidental finding. The remainder of the workup was unremarkable. Based on muscle denervation atrophy in the distribution of the third branch of the trigeminal nerve in the absence of sensory symptoms or deficits, the patient’s presentation was consistent with trigeminal motor neuropathy.

In reported cases, the pathogenesis of trigeminal motor neuropathy is attributed to tumors, trauma, stroke, viral infection, and autoimmune reaction.^1-6 In other reported cases the cause is unknown,^6-8 as was the case in our patient. Magnetic resonance angiography revealed potential vascular compression of the trigeminal nerve, which has been previously reported to cause trigeminal neuropathy.⁹ However, patients with trigeminal neuropathy presented with sensory changes in the distribution of the trigeminal nerve as opposed to motor symptoms and muscle atrophy.

We present a case of trigeminal motor neuropathy presenting as PHA. Progressive hemifacial atrophy is a rare, slowly progressive disease characterized by unilateral atrophy of the skin, subcutis, muscle, and bony structures of the face. Onset usually is during childhood, though later onset has been reported.¹⁰ The pathogenesis of PHA is not well understood, though trauma, infection, immune-mediated causes, sympathetic dysfunction, and metabolic dysfunction have been proposed.¹¹ Diagnosis of PHA typically is based on clinical presentation, but histology and imaging are useful. In contrast to trigeminal motor neuropathy, MRI findings in PHA demonstrate involvement of the skin.¹²

Differentiation between PHA and trigeminal motor neuropathy is important because treatment differs. Treatment of trigeminal motor neuropathy depends on the etiology and may include removal of underlying neoplasms, while treatment of PHA depends on disease activity. The initial goal when treating PHA is to improve symptoms and slow disease progression; immunosuppressants may be considered. Facial reconstruction is an option when PHA is stable.

In this case, the features differentiating trigeminal motor neuropathy from PHA include age of onset and MRI as well as clinical findings of muscle atrophy limited to the distribution of the third branch of the trigeminal nerve. Although PHA is a rare disorder, this case demonstrates the importance of including trigeminal motor neuropathy in the differential diagnosis.

To the Editor:

Trigeminal motor neuropathy is a rare condition presenting with muscle weakness and atrophy in the distribution of the trigeminal nerve without sensory changes. We present a challenging case with clinical features that mimic progressive hemifacial atrophy (PHA), a disease characterized by slowly progressive, unilateral facial atrophy that can be accompanied by inflammation and sclerosis as early features.

A 55-year-old man presented with right-sided ptosis and progressive right-sided facial atrophy of 4 years’ duration. A clinical diagnosis of PHA was made by the rheumatology department, and the patient was referred to the dermatology department for further evaluation. Examination at presentation revealed right-sided subcutaneous atrophy of the cheek, temple, and forehead extending to the scalp with absence of sclerosis, pigmentary alteration, or typical linear morphea lesions (Figures 1 and 2). The patient had no sensory changes in the affected area.

Workup by the dermatology department included magnetic resonance imaging (MRI) of the face and scalp, which demonstrated denervation muscle atrophy exclusively in the distribution of the third branch of the right trigeminal nerve, including severe atrophy of the right temporalis and masseter muscles and moderate atrophy of the pterygoid muscles. No signs of inflammation, fibrosis, or atrophy of the skin or subcutaneous fat were found, ruling out a diagnosis of PHA.

The patient was referred to the neurology department where he was found to have a normal neurologic examination with the exception of right-sided ptosis and temporalis and masseter muscle atrophy. Notably, the patient had normal sensation in the distribution of the trigeminal nerve and normal strength of the masseter and temporalis muscles.

An extensive workup by the neurology department was completed, including magnetic resonance angiography, eyeblink testing, and testing for causes of neuropathies (eg, infectious, autoimmune, vitamin deficiencies, toxin related). Of note, magnetic resonance angiography showed no abnormalities within the cavernous sinus or trigeminal cave but showed potential vascular compression of the trigeminal nerve, which was believed to be an incidental finding. The remainder of the workup was unremarkable. Based on muscle denervation atrophy in the distribution of the third branch of the trigeminal nerve in the absence of sensory symptoms or deficits, the patient’s presentation was consistent with trigeminal motor neuropathy.

In reported cases, the pathogenesis of trigeminal motor neuropathy is attributed to tumors, trauma, stroke, viral infection, and autoimmune reaction.^1-6 In other reported cases the cause is unknown,^6-8 as was the case in our patient. Magnetic resonance angiography revealed potential vascular compression of the trigeminal nerve, which has been previously reported to cause trigeminal neuropathy.⁹ However, patients with trigeminal neuropathy presented with sensory changes in the distribution of the trigeminal nerve as opposed to motor symptoms and muscle atrophy.

We present a case of trigeminal motor neuropathy presenting as PHA. Progressive hemifacial atrophy is a rare, slowly progressive disease characterized by unilateral atrophy of the skin, subcutis, muscle, and bony structures of the face. Onset usually is during childhood, though later onset has been reported.¹⁰ The pathogenesis of PHA is not well understood, though trauma, infection, immune-mediated causes, sympathetic dysfunction, and metabolic dysfunction have been proposed.¹¹ Diagnosis of PHA typically is based on clinical presentation, but histology and imaging are useful. In contrast to trigeminal motor neuropathy, MRI findings in PHA demonstrate involvement of the skin.¹²

Differentiation between PHA and trigeminal motor neuropathy is important because treatment differs. Treatment of trigeminal motor neuropathy depends on the etiology and may include removal of underlying neoplasms, while treatment of PHA depends on disease activity. The initial goal when treating PHA is to improve symptoms and slow disease progression; immunosuppressants may be considered. Facial reconstruction is an option when PHA is stable.

In this case, the features differentiating trigeminal motor neuropathy from PHA include age of onset and MRI as well as clinical findings of muscle atrophy limited to the distribution of the third branch of the trigeminal nerve. Although PHA is a rare disorder, this case demonstrates the importance of including trigeminal motor neuropathy in the differential diagnosis.

LAS VEGAS – Crohn’s patients with a history of smoking and/or elevated C-reactive protein (CRP) level at initiation of vedolizumab were less likely respond to the drug, a small, single-center study showed.

“Right now there are a variety of medications to treat Crohn’s disease, but there isn’t a set criteria [for] what [drug] works for which kind of patient,” Adam A. Dhedhi, MD, said in an interview at the Crohn’s & Colitis Congress, a partnership of the Crohn’s & Colitis Foundation and the American Gastroenterological Association. “We’re trying to figure out if we can find a predictor of response to vedolizumab.” Manufactured by Millennium Pharmaceuticals, vedolizumab is a gut-selective monoclonal antibody to alpha4beta7 integrin that prevents transportation of leukocytes into gastrointestinal mucosa.

*This story was updated on 3/26.

[email protected]

SOURCE: Dhedhi AA et al. Crohn’s & Colitis Congress, Poster 207.

LAS VEGAS – Crohn’s patients with a history of smoking and/or elevated C-reactive protein (CRP) level at initiation of vedolizumab were less likely respond to the drug, a small, single-center study showed.

“Right now there are a variety of medications to treat Crohn’s disease, but there isn’t a set criteria [for] what [drug] works for which kind of patient,” Adam A. Dhedhi, MD, said in an interview at the Crohn’s & Colitis Congress, a partnership of the Crohn’s & Colitis Foundation and the American Gastroenterological Association. “We’re trying to figure out if we can find a predictor of response to vedolizumab.” Manufactured by Millennium Pharmaceuticals, vedolizumab is a gut-selective monoclonal antibody to alpha4beta7 integrin that prevents transportation of leukocytes into gastrointestinal mucosa.

*This story was updated on 3/26.

[email protected]

SOURCE: Dhedhi AA et al. Crohn’s & Colitis Congress, Poster 207.

LAS VEGAS – Crohn’s patients with a history of smoking and/or elevated C-reactive protein (CRP) level at initiation of vedolizumab were less likely respond to the drug, a small, single-center study showed.

“Right now there are a variety of medications to treat Crohn’s disease, but there isn’t a set criteria [for] what [drug] works for which kind of patient,” Adam A. Dhedhi, MD, said in an interview at the Crohn’s & Colitis Congress, a partnership of the Crohn’s & Colitis Foundation and the American Gastroenterological Association. “We’re trying to figure out if we can find a predictor of response to vedolizumab.” Manufactured by Millennium Pharmaceuticals, vedolizumab is a gut-selective monoclonal antibody to alpha4beta7 integrin that prevents transportation of leukocytes into gastrointestinal mucosa.

*This story was updated on 3/26.

[email protected]

SOURCE: Dhedhi AA et al. Crohn’s & Colitis Congress, Poster 207.

“She will eat when she is hungry.” That in so many words is the mantra of grandparents blessed with experience and common sense and of most pediatricians when consulting parents challenged with a picky eater. From birth, children understand the simple equation that to survive they must eat. With rare exception, the motivating power of hunger can be leveraged for success even with infants who have spent their first months relying on enteral feedings. I have written an entire book based solely on the premise that if you present a young child food she will eat it ... eventually (“Coping With a Picky Eater: A Guide for the Perplexed Parent” New York: Simon and Schuster, 1998).

But if we reverse the words to read, “When she is eating, she is hungry,” do we have an equally valid observation? I think we have ample evidence that it is not.

Wavebreakmedia/Thinkstock

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Email him at [email protected].

“She will eat when she is hungry.” That in so many words is the mantra of grandparents blessed with experience and common sense and of most pediatricians when consulting parents challenged with a picky eater. From birth, children understand the simple equation that to survive they must eat. With rare exception, the motivating power of hunger can be leveraged for success even with infants who have spent their first months relying on enteral feedings. I have written an entire book based solely on the premise that if you present a young child food she will eat it ... eventually (“Coping With a Picky Eater: A Guide for the Perplexed Parent” New York: Simon and Schuster, 1998).

But if we reverse the words to read, “When she is eating, she is hungry,” do we have an equally valid observation? I think we have ample evidence that it is not.

Wavebreakmedia/Thinkstock

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Email him at [email protected].

“She will eat when she is hungry.” That in so many words is the mantra of grandparents blessed with experience and common sense and of most pediatricians when consulting parents challenged with a picky eater. From birth, children understand the simple equation that to survive they must eat. With rare exception, the motivating power of hunger can be leveraged for success even with infants who have spent their first months relying on enteral feedings. I have written an entire book based solely on the premise that if you present a young child food she will eat it ... eventually (“Coping With a Picky Eater: A Guide for the Perplexed Parent” New York: Simon and Schuster, 1998).

But if we reverse the words to read, “When she is eating, she is hungry,” do we have an equally valid observation? I think we have ample evidence that it is not.

Wavebreakmedia/Thinkstock

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Email him at [email protected].

A 70-year-old man with chronic obstructive pulmonary disease (COPD) is admitted with increased shortness of breath. His O₂ saturation levels are usually 90%, but they’re now running 84%-88%. He has had increasing symptoms for the past 3 days.

copyright designer491/Thinkstock

What would be your next step?

A) Begin a 5-day course of corticosteroids.

B) Begin a 14-day course of corticosteroids.

C) Begin azithromycin.

D) Start BiPAP.

E) Obtain D-dimer.

This is a situation we face frequently. COPD exacerbations are a clinical diagnosis that is often jumped to as the diagnosis in patients with COPD who have increasing dyspnea. This diagnosis is frequently correct – but not always.

Patients with COPD also may be at risk for or have heart failure, which can present with identical symptoms, including widespread wheezing. We are currently in a severe influenza epidemic, and influenza can mimic a COPD exacerbation or be the trigger.

About 20 years ago, I was out of the country when one of my patients with COPD was admitted to the hospital with a COPD exacerbation. I saw him in follow-up a week after his hospitalization. He was very dyspneic and had a room air oxygen saturation of 75%. He told me his dyspnea started a few days after he had injured his leg on a wood pile in his yard.

On exam, his right leg had 3+ edema; left leg, no edema. He reported to me that he was treated for 5 days with steroids and nebulizers, with minimal change in his dyspnea. I reviewed the chart, and five physicians had seen him while he was in the hospital. Starting with the emergency department, the diagnosis was COPD exacerbation, with no differential diagnosis in any note.

The patient had multiple pulmonary emboli, and he eventually improved with anticoagulation.

In 2009, Jacques Rizkallah, MD, and his colleagues published a systematic review and meta-analysis of articles looking at the prevalence of pulmonary emboli (PE) in patients diagnosed/treated for a COPD exacerbation.¹ They found five articles comprising a total of 550 patients who met inclusion criteria. The prevalence was 19.9% (P = .014). The prevalence was much higher (24.7%) for hospitalized patients than it was for outpatients (3.3%). A very important finding in this study: There was no difference in symptoms between patients who did and did not have a pulmonary embolus.

Evrim Eylem Akpinar, MD, and colleagues studied all admissions for acute exacerbations of COPD at one hospital in Turkey over a 2-year period.² A total of 172 patients admitted for COPD exacerbations were studied. The prevalence of pulmonary embolus was 29%.

In this study, patients who were obese or immobile were more likely to have pulmonary emboli. Pleuritic chest pain and lower-limb asymmetry were signs and symptoms more commonly found in patients who had PE. Obesity was the highest independent predictor (odds ratio, 4.97) for pulmonary embolus.

Floor Aleva, MD, and colleagues recently completed a systematic review and meta-analysis on prevalence and localization of pulmonary embolus in patients with acute exacerbations of COPD.³ They found similar numbers to the previous meta-analysis (16.1%) in a total of 880 patients. They also looked at location in the lungs of the emboli and found that two-thirds of the patients had pulmonary emboli in locations that had clear indication for anticoagulation treatment.

This is important, because criticisms of earlier studies were that clinically insignificant pulmonary emboli might be being found in the studies and that they had little to do with the patients’ symptoms.

In the case presented, I think that getting a D-dimer test would be the next best step. Acute exacerbation of COPD still is the most likely diagnosis, but PE is a plausible diagnosis that should be evaluated. If the D-dimer is normal, workup for PE would be complete. If elevated, then given the 20% prevalence of PE, a CT angiography would be warranted.

Key pearl: Among patients hospitalized for COPD exacerbations, 16%-24% have pulmonary embolism.

Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and he serves as third-year medical student clerkship director at the University of Washington. Contact Dr. Paauw at [email protected].

References

1. Chest. 2009 Mar;135(3):786-93.

2. J Bras Pneumol. 2014 Jan-Feb;40(1):38-45.

3. Chest. 2017 Mar;151(3):544-54.


 

A 70-year-old man with chronic obstructive pulmonary disease (COPD) is admitted with increased shortness of breath. His O₂ saturation levels are usually 90%, but they’re now running 84%-88%. He has had increasing symptoms for the past 3 days.

copyright designer491/Thinkstock

What would be your next step?

A) Begin a 5-day course of corticosteroids.

B) Begin a 14-day course of corticosteroids.

C) Begin azithromycin.

D) Start BiPAP.

E) Obtain D-dimer.

This is a situation we face frequently. COPD exacerbations are a clinical diagnosis that is often jumped to as the diagnosis in patients with COPD who have increasing dyspnea. This diagnosis is frequently correct – but not always.

Patients with COPD also may be at risk for or have heart failure, which can present with identical symptoms, including widespread wheezing. We are currently in a severe influenza epidemic, and influenza can mimic a COPD exacerbation or be the trigger.

About 20 years ago, I was out of the country when one of my patients with COPD was admitted to the hospital with a COPD exacerbation. I saw him in follow-up a week after his hospitalization. He was very dyspneic and had a room air oxygen saturation of 75%. He told me his dyspnea started a few days after he had injured his leg on a wood pile in his yard.

On exam, his right leg had 3+ edema; left leg, no edema. He reported to me that he was treated for 5 days with steroids and nebulizers, with minimal change in his dyspnea. I reviewed the chart, and five physicians had seen him while he was in the hospital. Starting with the emergency department, the diagnosis was COPD exacerbation, with no differential diagnosis in any note.

The patient had multiple pulmonary emboli, and he eventually improved with anticoagulation.

In 2009, Jacques Rizkallah, MD, and his colleagues published a systematic review and meta-analysis of articles looking at the prevalence of pulmonary emboli (PE) in patients diagnosed/treated for a COPD exacerbation.¹ They found five articles comprising a total of 550 patients who met inclusion criteria. The prevalence was 19.9% (P = .014). The prevalence was much higher (24.7%) for hospitalized patients than it was for outpatients (3.3%). A very important finding in this study: There was no difference in symptoms between patients who did and did not have a pulmonary embolus.

Evrim Eylem Akpinar, MD, and colleagues studied all admissions for acute exacerbations of COPD at one hospital in Turkey over a 2-year period.² A total of 172 patients admitted for COPD exacerbations were studied. The prevalence of pulmonary embolus was 29%.

In this study, patients who were obese or immobile were more likely to have pulmonary emboli. Pleuritic chest pain and lower-limb asymmetry were signs and symptoms more commonly found in patients who had PE. Obesity was the highest independent predictor (odds ratio, 4.97) for pulmonary embolus.

Floor Aleva, MD, and colleagues recently completed a systematic review and meta-analysis on prevalence and localization of pulmonary embolus in patients with acute exacerbations of COPD.³ They found similar numbers to the previous meta-analysis (16.1%) in a total of 880 patients. They also looked at location in the lungs of the emboli and found that two-thirds of the patients had pulmonary emboli in locations that had clear indication for anticoagulation treatment.

This is important, because criticisms of earlier studies were that clinically insignificant pulmonary emboli might be being found in the studies and that they had little to do with the patients’ symptoms.

In the case presented, I think that getting a D-dimer test would be the next best step. Acute exacerbation of COPD still is the most likely diagnosis, but PE is a plausible diagnosis that should be evaluated. If the D-dimer is normal, workup for PE would be complete. If elevated, then given the 20% prevalence of PE, a CT angiography would be warranted.

Key pearl: Among patients hospitalized for COPD exacerbations, 16%-24% have pulmonary embolism.

Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and he serves as third-year medical student clerkship director at the University of Washington. Contact Dr. Paauw at [email protected].

References

1. Chest. 2009 Mar;135(3):786-93.

2. J Bras Pneumol. 2014 Jan-Feb;40(1):38-45.

3. Chest. 2017 Mar;151(3):544-54.


 

A 70-year-old man with chronic obstructive pulmonary disease (COPD) is admitted with increased shortness of breath. His O₂ saturation levels are usually 90%, but they’re now running 84%-88%. He has had increasing symptoms for the past 3 days.

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What would be your next step?

A) Begin a 5-day course of corticosteroids.

B) Begin a 14-day course of corticosteroids.

C) Begin azithromycin.

D) Start BiPAP.

E) Obtain D-dimer.

This is a situation we face frequently. COPD exacerbations are a clinical diagnosis that is often jumped to as the diagnosis in patients with COPD who have increasing dyspnea. This diagnosis is frequently correct – but not always.

Patients with COPD also may be at risk for or have heart failure, which can present with identical symptoms, including widespread wheezing. We are currently in a severe influenza epidemic, and influenza can mimic a COPD exacerbation or be the trigger.

About 20 years ago, I was out of the country when one of my patients with COPD was admitted to the hospital with a COPD exacerbation. I saw him in follow-up a week after his hospitalization. He was very dyspneic and had a room air oxygen saturation of 75%. He told me his dyspnea started a few days after he had injured his leg on a wood pile in his yard.

On exam, his right leg had 3+ edema; left leg, no edema. He reported to me that he was treated for 5 days with steroids and nebulizers, with minimal change in his dyspnea. I reviewed the chart, and five physicians had seen him while he was in the hospital. Starting with the emergency department, the diagnosis was COPD exacerbation, with no differential diagnosis in any note.

The patient had multiple pulmonary emboli, and he eventually improved with anticoagulation.

In 2009, Jacques Rizkallah, MD, and his colleagues published a systematic review and meta-analysis of articles looking at the prevalence of pulmonary emboli (PE) in patients diagnosed/treated for a COPD exacerbation.¹ They found five articles comprising a total of 550 patients who met inclusion criteria. The prevalence was 19.9% (P = .014). The prevalence was much higher (24.7%) for hospitalized patients than it was for outpatients (3.3%). A very important finding in this study: There was no difference in symptoms between patients who did and did not have a pulmonary embolus.

Evrim Eylem Akpinar, MD, and colleagues studied all admissions for acute exacerbations of COPD at one hospital in Turkey over a 2-year period.² A total of 172 patients admitted for COPD exacerbations were studied. The prevalence of pulmonary embolus was 29%.

In this study, patients who were obese or immobile were more likely to have pulmonary emboli. Pleuritic chest pain and lower-limb asymmetry were signs and symptoms more commonly found in patients who had PE. Obesity was the highest independent predictor (odds ratio, 4.97) for pulmonary embolus.

Floor Aleva, MD, and colleagues recently completed a systematic review and meta-analysis on prevalence and localization of pulmonary embolus in patients with acute exacerbations of COPD.³ They found similar numbers to the previous meta-analysis (16.1%) in a total of 880 patients. They also looked at location in the lungs of the emboli and found that two-thirds of the patients had pulmonary emboli in locations that had clear indication for anticoagulation treatment.

This is important, because criticisms of earlier studies were that clinically insignificant pulmonary emboli might be being found in the studies and that they had little to do with the patients’ symptoms.

In the case presented, I think that getting a D-dimer test would be the next best step. Acute exacerbation of COPD still is the most likely diagnosis, but PE is a plausible diagnosis that should be evaluated. If the D-dimer is normal, workup for PE would be complete. If elevated, then given the 20% prevalence of PE, a CT angiography would be warranted.

Key pearl: Among patients hospitalized for COPD exacerbations, 16%-24% have pulmonary embolism.

Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and he serves as third-year medical student clerkship director at the University of Washington. Contact Dr. Paauw at [email protected].

References

1. Chest. 2009 Mar;135(3):786-93.

2. J Bras Pneumol. 2014 Jan-Feb;40(1):38-45.

3. Chest. 2017 Mar;151(3):544-54.


 

Cesarean deliveries may reduce a woman’s risk for urinary incontinence and pelvic organ prolapse but may raise her risk of complications with future pregnancies, based on data from a literature review including nearly 30,000,000 women.

Rates of cesarean delivery in 2016, often without medical indication, were approximately 25%, 32%, and 41% in Western Europe, North America, and South America, respectively, wrote Oonagh E. Keag, MD, of the Royal Infirmary of Edinburgh and colleagues in a study published in PLOS Medicine.

Martin Valigursky/Thinkstock

SOURCE: Keag OE et al. PLoS Med. 2018 Jan 23. 15(1):e1002494.

Cesarean deliveries may reduce a woman’s risk for urinary incontinence and pelvic organ prolapse but may raise her risk of complications with future pregnancies, based on data from a literature review including nearly 30,000,000 women.

Rates of cesarean delivery in 2016, often without medical indication, were approximately 25%, 32%, and 41% in Western Europe, North America, and South America, respectively, wrote Oonagh E. Keag, MD, of the Royal Infirmary of Edinburgh and colleagues in a study published in PLOS Medicine.

Martin Valigursky/Thinkstock

SOURCE: Keag OE et al. PLoS Med. 2018 Jan 23. 15(1):e1002494.

Cesarean deliveries may reduce a woman’s risk for urinary incontinence and pelvic organ prolapse but may raise her risk of complications with future pregnancies, based on data from a literature review including nearly 30,000,000 women.

Rates of cesarean delivery in 2016, often without medical indication, were approximately 25%, 32%, and 41% in Western Europe, North America, and South America, respectively, wrote Oonagh E. Keag, MD, of the Royal Infirmary of Edinburgh and colleagues in a study published in PLOS Medicine.

Martin Valigursky/Thinkstock

SOURCE: Keag OE et al. PLoS Med. 2018 Jan 23. 15(1):e1002494.