The Journal of Family Practice

This patient had erythroderma, which involves widespread erythema and scaling of the majority of the skin. Erythroderma can be caused by severe variants of several skin disorders, including atopic dermatitis, contact dermatitis, and psoriasis. In this case, a punch biopsy from the forearm was most consistent with erythrodermic psoriasis.

Erythrodermic psoriasis is a rare subtype of psoriasis and most often develops as an exacerbation of preexisting plaque psoriasis and is defined by erythema, scale, and desquamation covering 75% to 90% of the body surface.¹ The alteration in the skin negatively affects heat exchange and hemodynamics and can be life threatening. Many cases develop as a rebound reaction in patients with preexisting psoriasis treated with systemic steroids that are discontinued. Patients with dehydration, poor urinary output, hypotension, or significant weakness may benefit from supportive inpatient care while treatment is initiated.¹

Initial treatment options for patients with erythrodermic psoriasis include biologics and steroid-sparing immunosuppressants, such as cyclosporine and acitretin. While a patient awaits the initiation of a definitive therapy, topical triamcinolone 0.1% may be applied over the entire skin surface twice daily and covered with 2 layers of scrubs or pajamas. The pair closest to the skin should be slightly damp and the outer pair should be dry to help retain heat. These are referred to as wet wraps or wet pajama wraps.

The patient described here was hemodynamically stable and was allowed to initiate wet pajama wrap therapy at home while awaiting initiation of adalimumab as an outpatient. He has improved dramatically with adalimumab given subcutaneously every 2 weeks.

‌

Photos and text for Photo Rounds Friday courtesy of Jonathan Karnes, MD (copyright retained). Dr. Karnes is the medical director of MDFMR Dermatology Services, Augusta, ME.

This patient had erythroderma, which involves widespread erythema and scaling of the majority of the skin. Erythroderma can be caused by severe variants of several skin disorders, including atopic dermatitis, contact dermatitis, and psoriasis. In this case, a punch biopsy from the forearm was most consistent with erythrodermic psoriasis.

Erythrodermic psoriasis is a rare subtype of psoriasis and most often develops as an exacerbation of preexisting plaque psoriasis and is defined by erythema, scale, and desquamation covering 75% to 90% of the body surface.¹ The alteration in the skin negatively affects heat exchange and hemodynamics and can be life threatening. Many cases develop as a rebound reaction in patients with preexisting psoriasis treated with systemic steroids that are discontinued. Patients with dehydration, poor urinary output, hypotension, or significant weakness may benefit from supportive inpatient care while treatment is initiated.¹

Initial treatment options for patients with erythrodermic psoriasis include biologics and steroid-sparing immunosuppressants, such as cyclosporine and acitretin. While a patient awaits the initiation of a definitive therapy, topical triamcinolone 0.1% may be applied over the entire skin surface twice daily and covered with 2 layers of scrubs or pajamas. The pair closest to the skin should be slightly damp and the outer pair should be dry to help retain heat. These are referred to as wet wraps or wet pajama wraps.

The patient described here was hemodynamically stable and was allowed to initiate wet pajama wrap therapy at home while awaiting initiation of adalimumab as an outpatient. He has improved dramatically with adalimumab given subcutaneously every 2 weeks.

‌

Photos and text for Photo Rounds Friday courtesy of Jonathan Karnes, MD (copyright retained). Dr. Karnes is the medical director of MDFMR Dermatology Services, Augusta, ME.

This patient had erythroderma, which involves widespread erythema and scaling of the majority of the skin. Erythroderma can be caused by severe variants of several skin disorders, including atopic dermatitis, contact dermatitis, and psoriasis. In this case, a punch biopsy from the forearm was most consistent with erythrodermic psoriasis.

Erythrodermic psoriasis is a rare subtype of psoriasis and most often develops as an exacerbation of preexisting plaque psoriasis and is defined by erythema, scale, and desquamation covering 75% to 90% of the body surface.¹ The alteration in the skin negatively affects heat exchange and hemodynamics and can be life threatening. Many cases develop as a rebound reaction in patients with preexisting psoriasis treated with systemic steroids that are discontinued. Patients with dehydration, poor urinary output, hypotension, or significant weakness may benefit from supportive inpatient care while treatment is initiated.¹

Initial treatment options for patients with erythrodermic psoriasis include biologics and steroid-sparing immunosuppressants, such as cyclosporine and acitretin. While a patient awaits the initiation of a definitive therapy, topical triamcinolone 0.1% may be applied over the entire skin surface twice daily and covered with 2 layers of scrubs or pajamas. The pair closest to the skin should be slightly damp and the outer pair should be dry to help retain heat. These are referred to as wet wraps or wet pajama wraps.

The patient described here was hemodynamically stable and was allowed to initiate wet pajama wrap therapy at home while awaiting initiation of adalimumab as an outpatient. He has improved dramatically with adalimumab given subcutaneously every 2 weeks.

‌

Photos and text for Photo Rounds Friday courtesy of Jonathan Karnes, MD (copyright retained). Dr. Karnes is the medical director of MDFMR Dermatology Services, Augusta, ME.

A scoop shave biopsy was performed, including at least a 1-mm margin of normal-looking skin. Pathology was consistent with melanoma in situ.

Melanoma in situ, also called Stage 0 melanoma, is defined by atypical melanocytes that have not begun to invade the dermis and, therefore, have a Breslow thickness of 0 mm. While invasive melanoma is responsible for the largest number of skin cancer deaths in the United States (estimated to be 7990 in 2023), melanoma in situ maintains a very high cure rate when treated appropriately.¹

Dermoscopy can help differentiate melanoma from benign nevi or other benign skin lesions. In this case, dermoscopy revealed a fine pigment network at the periphery that indicated this lesion was made up of melanocytes. There were also atypical vascular markings (the milky red color) in the center. Taken together, these findings were strongly indicative of melanoma.

Standard of care for melanoma in situ is a wide local excision with a margin of 5 to 10 mm. Melanoma in situ does not require sentinel lymph node biopsy. However, a lymph node biopsy would have been necessary if the melanoma had been ≥ 1 mm in thickness or if it had been ≥ 0.8 mm in thickness with higher-risk features, such as an increased number of mitoses per high-power field on pathology. Mohs micrographic surgery (MMS) is emerging as an alternative method to wide local excision to treat melanoma in situ. However, it can only be done in specialized centers that can do rapid immunohistochemical staining on frozen sections. MMS is especially useful in cosmetically sensitive areas of the body and in areas where the true size of the melanoma in situ is unclear.

This patient subsequently underwent a wide local excision in the office with a margin of 6 mm. A sentinel lymph node biopsy was not performed. The patient will continue with skin surveillance consisting of full skin exams 3 to 4 times in the first year of diagnosis, then twice annually for Years 2 to 5. He will then come in for annual skin exams after that.

‌

Photos and text for Photo Rounds Friday courtesy of Jonathan Karnes, MD (copyright retained). Dr. Karnes is the medical director of MDFMR Dermatology Services, Augusta, ME.

A scoop shave biopsy was performed, including at least a 1-mm margin of normal-looking skin. Pathology was consistent with melanoma in situ.

Melanoma in situ, also called Stage 0 melanoma, is defined by atypical melanocytes that have not begun to invade the dermis and, therefore, have a Breslow thickness of 0 mm. While invasive melanoma is responsible for the largest number of skin cancer deaths in the United States (estimated to be 7990 in 2023), melanoma in situ maintains a very high cure rate when treated appropriately.¹

Dermoscopy can help differentiate melanoma from benign nevi or other benign skin lesions. In this case, dermoscopy revealed a fine pigment network at the periphery that indicated this lesion was made up of melanocytes. There were also atypical vascular markings (the milky red color) in the center. Taken together, these findings were strongly indicative of melanoma.

Standard of care for melanoma in situ is a wide local excision with a margin of 5 to 10 mm. Melanoma in situ does not require sentinel lymph node biopsy. However, a lymph node biopsy would have been necessary if the melanoma had been ≥ 1 mm in thickness or if it had been ≥ 0.8 mm in thickness with higher-risk features, such as an increased number of mitoses per high-power field on pathology. Mohs micrographic surgery (MMS) is emerging as an alternative method to wide local excision to treat melanoma in situ. However, it can only be done in specialized centers that can do rapid immunohistochemical staining on frozen sections. MMS is especially useful in cosmetically sensitive areas of the body and in areas where the true size of the melanoma in situ is unclear.

This patient subsequently underwent a wide local excision in the office with a margin of 6 mm. A sentinel lymph node biopsy was not performed. The patient will continue with skin surveillance consisting of full skin exams 3 to 4 times in the first year of diagnosis, then twice annually for Years 2 to 5. He will then come in for annual skin exams after that.

‌

Photos and text for Photo Rounds Friday courtesy of Jonathan Karnes, MD (copyright retained). Dr. Karnes is the medical director of MDFMR Dermatology Services, Augusta, ME.

A scoop shave biopsy was performed, including at least a 1-mm margin of normal-looking skin. Pathology was consistent with melanoma in situ.

Melanoma in situ, also called Stage 0 melanoma, is defined by atypical melanocytes that have not begun to invade the dermis and, therefore, have a Breslow thickness of 0 mm. While invasive melanoma is responsible for the largest number of skin cancer deaths in the United States (estimated to be 7990 in 2023), melanoma in situ maintains a very high cure rate when treated appropriately.¹

Dermoscopy can help differentiate melanoma from benign nevi or other benign skin lesions. In this case, dermoscopy revealed a fine pigment network at the periphery that indicated this lesion was made up of melanocytes. There were also atypical vascular markings (the milky red color) in the center. Taken together, these findings were strongly indicative of melanoma.

Standard of care for melanoma in situ is a wide local excision with a margin of 5 to 10 mm. Melanoma in situ does not require sentinel lymph node biopsy. However, a lymph node biopsy would have been necessary if the melanoma had been ≥ 1 mm in thickness or if it had been ≥ 0.8 mm in thickness with higher-risk features, such as an increased number of mitoses per high-power field on pathology. Mohs micrographic surgery (MMS) is emerging as an alternative method to wide local excision to treat melanoma in situ. However, it can only be done in specialized centers that can do rapid immunohistochemical staining on frozen sections. MMS is especially useful in cosmetically sensitive areas of the body and in areas where the true size of the melanoma in situ is unclear.

This patient subsequently underwent a wide local excision in the office with a margin of 6 mm. A sentinel lymph node biopsy was not performed. The patient will continue with skin surveillance consisting of full skin exams 3 to 4 times in the first year of diagnosis, then twice annually for Years 2 to 5. He will then come in for annual skin exams after that.

‌

Photos and text for Photo Rounds Friday courtesy of Jonathan Karnes, MD (copyright retained). Dr. Karnes is the medical director of MDFMR Dermatology Services, Augusta, ME.

In January 2023, the American College of Physicians (ACP) published updated recommendations on the treatment of adults with major depressive disorder (MDD).¹ The ACP guidelines address initial treatment of patients in the acute phase of mild and moderate-to-severe MDD. Here’s what the ACP recommends, as well as 6 important takeaways.

Recommendations for initial treatment of those with mild or moderate-to-severe MDD center around cognitive behavioral therapy (CBT) and second-generation antidepressants (SGA). For patients in the acute phase of mild MDD, the recommendation is for monotherapy with CBT. However, if CBT is not an option due to cost and/or availability of services, the use of an SGA is acceptable.

For patients in the acute phase of moderate-to-severe MDD, either CBT, an SGA, or a combination of both is recommended.

If initial treatment does not work … Up to 70% of patients with moderate-to-severe MDD will not respond to the initial therapy chosen. If a patient does not respond to initial treatment with an SGA, consider 1 of the following:

• Switching to CBT
• Adding on CBT while continuing the SGA
• Changing to a different SGA
• Adding a second pharmacologic agent.

6 key takeaways. The full guideline should be read for a more complete discussion of the many clinical considerations of these treatment options. However, the most important points include:

• Employ shared clinical decision-making and consider the individual characteristics of each patient when making treatment decisions.

• Consider generic options when using an SGA; generic options appear to be as effective as more expensive brand-name products.

• Start with a low-dose SGA and increase gradually to an approved maximum dose before determining there has been no response.

• Monitor frequently for medication adverse effects.

• Monitor the patient for thoughts about self-harm for the first 2 months.

• Continue treatment for 4 to 9 months once remission is achieved.

A word about strength of evidence. While these recommendations are based on an extensive review of the best available evidence, most are based on low-certainty evidence—illustrating the amount of clinical research still needed on this topic. The exceptions are monotherapy with either CBT or SGA for initial treatment of moderate-to-severe MDD, both of which are based on moderate-strength evidence and received a strong recommendation. The panel felt there was insufficient evidence to assess complementary and alternative interventions including exercise and omega-3 fatty acids.

In January 2023, the American College of Physicians (ACP) published updated recommendations on the treatment of adults with major depressive disorder (MDD).¹ The ACP guidelines address initial treatment of patients in the acute phase of mild and moderate-to-severe MDD. Here’s what the ACP recommends, as well as 6 important takeaways.

Recommendations for initial treatment of those with mild or moderate-to-severe MDD center around cognitive behavioral therapy (CBT) and second-generation antidepressants (SGA). For patients in the acute phase of mild MDD, the recommendation is for monotherapy with CBT. However, if CBT is not an option due to cost and/or availability of services, the use of an SGA is acceptable.

For patients in the acute phase of moderate-to-severe MDD, either CBT, an SGA, or a combination of both is recommended.

If initial treatment does not work … Up to 70% of patients with moderate-to-severe MDD will not respond to the initial therapy chosen. If a patient does not respond to initial treatment with an SGA, consider 1 of the following:

• Switching to CBT
• Adding on CBT while continuing the SGA
• Changing to a different SGA
• Adding a second pharmacologic agent.

6 key takeaways. The full guideline should be read for a more complete discussion of the many clinical considerations of these treatment options. However, the most important points include:

• Employ shared clinical decision-making and consider the individual characteristics of each patient when making treatment decisions.

• Consider generic options when using an SGA; generic options appear to be as effective as more expensive brand-name products.

• Start with a low-dose SGA and increase gradually to an approved maximum dose before determining there has been no response.

• Monitor frequently for medication adverse effects.

• Monitor the patient for thoughts about self-harm for the first 2 months.

• Continue treatment for 4 to 9 months once remission is achieved.

A word about strength of evidence. While these recommendations are based on an extensive review of the best available evidence, most are based on low-certainty evidence—illustrating the amount of clinical research still needed on this topic. The exceptions are monotherapy with either CBT or SGA for initial treatment of moderate-to-severe MDD, both of which are based on moderate-strength evidence and received a strong recommendation. The panel felt there was insufficient evidence to assess complementary and alternative interventions including exercise and omega-3 fatty acids.

In January 2023, the American College of Physicians (ACP) published updated recommendations on the treatment of adults with major depressive disorder (MDD).¹ The ACP guidelines address initial treatment of patients in the acute phase of mild and moderate-to-severe MDD. Here’s what the ACP recommends, as well as 6 important takeaways.

Recommendations for initial treatment of those with mild or moderate-to-severe MDD center around cognitive behavioral therapy (CBT) and second-generation antidepressants (SGA). For patients in the acute phase of mild MDD, the recommendation is for monotherapy with CBT. However, if CBT is not an option due to cost and/or availability of services, the use of an SGA is acceptable.

For patients in the acute phase of moderate-to-severe MDD, either CBT, an SGA, or a combination of both is recommended.

If initial treatment does not work … Up to 70% of patients with moderate-to-severe MDD will not respond to the initial therapy chosen. If a patient does not respond to initial treatment with an SGA, consider 1 of the following:

• Switching to CBT
• Adding on CBT while continuing the SGA
• Changing to a different SGA
• Adding a second pharmacologic agent.

6 key takeaways. The full guideline should be read for a more complete discussion of the many clinical considerations of these treatment options. However, the most important points include:

• Employ shared clinical decision-making and consider the individual characteristics of each patient when making treatment decisions.

• Consider generic options when using an SGA; generic options appear to be as effective as more expensive brand-name products.

• Start with a low-dose SGA and increase gradually to an approved maximum dose before determining there has been no response.

• Monitor frequently for medication adverse effects.

• Monitor the patient for thoughts about self-harm for the first 2 months.

• Continue treatment for 4 to 9 months once remission is achieved.

A word about strength of evidence. While these recommendations are based on an extensive review of the best available evidence, most are based on low-certainty evidence—illustrating the amount of clinical research still needed on this topic. The exceptions are monotherapy with either CBT or SGA for initial treatment of moderate-to-severe MDD, both of which are based on moderate-strength evidence and received a strong recommendation. The panel felt there was insufficient evidence to assess complementary and alternative interventions including exercise and omega-3 fatty acids.

Clustered erythematous macular to papular lesions, especially those that stop at clothing lines, are a frequent manifestation of insect bites. In this case, the lesions lacked a central punctum that is common in many insect bites, so the most likely culprit was bed bugs. It is likely that this patient’s friend inadvertently brought the bed bugs into the home in her luggage or packed belongings. Over time, they spread around the home, causing the patient’s bites and inflammation. When questioned, the patient noted that she could actually see bugs around the couch in her home.

The scientific name for bed bugs is Cimex lectularis. Bed bugs require a blood meal from a host to survive, but they do not remain attached to the human body. Instead, they live in nearby fabrics. Bed bugs are visible to the naked eye when they are in the open, although they usually remain along the seams of fabric, edges of bedding, or in cracks and crevices. Often the feces of bed bugs will collect and be seen as dark spots or streaks on bedding.¹

Treatment hinges on the eradication of the bed bugs. The erythematous itching lesions will resolve spontaneously over 1 to 2 weeks. Topical corticosteroids, including hydrocortisone, can be used as necessary to control the itching. Oral antihistamines can also help with itching.

Eradication of all the bed bugs in the home can be difficult and warrant professional extermination services. Washing clothing in hot water of at least 140 °F will kill the insects. Freezing items below –4 °F for at least 2 hours is also effective but may not be possible with home freezers.

It’s worth noting that resistance to insecticides has developed, making chemical eradication difficult. An alternative extermination protocol involves heating an entire home to the required temperatures to eradicate the infestation.¹

This patient noted that she had already thrown away the couch, clothes, and bedding where she had seen the insects and had sprayed her apartment with insecticide. She was counseled to contact a professional exterminator to further evaluate the home for any additional areas of infestation and treat if any bed bugs were still in the home. She was also counseled to use loratadine 10 mg/d orally and topical 1% hydrocortisone ointment, as needed, for the itching and inflammation.

‌

Photo and text courtesy of Daniel Stulberg, MD, FAAFP, Professor and Chair, Department of Family and Community Medicine, Western Michigan University Homer Stryker, MD School of Medicine, Kalamazoo.

Clustered erythematous macular to papular lesions, especially those that stop at clothing lines, are a frequent manifestation of insect bites. In this case, the lesions lacked a central punctum that is common in many insect bites, so the most likely culprit was bed bugs. It is likely that this patient’s friend inadvertently brought the bed bugs into the home in her luggage or packed belongings. Over time, they spread around the home, causing the patient’s bites and inflammation. When questioned, the patient noted that she could actually see bugs around the couch in her home.

The scientific name for bed bugs is Cimex lectularis. Bed bugs require a blood meal from a host to survive, but they do not remain attached to the human body. Instead, they live in nearby fabrics. Bed bugs are visible to the naked eye when they are in the open, although they usually remain along the seams of fabric, edges of bedding, or in cracks and crevices. Often the feces of bed bugs will collect and be seen as dark spots or streaks on bedding.¹

Treatment hinges on the eradication of the bed bugs. The erythematous itching lesions will resolve spontaneously over 1 to 2 weeks. Topical corticosteroids, including hydrocortisone, can be used as necessary to control the itching. Oral antihistamines can also help with itching.

Eradication of all the bed bugs in the home can be difficult and warrant professional extermination services. Washing clothing in hot water of at least 140 °F will kill the insects. Freezing items below –4 °F for at least 2 hours is also effective but may not be possible with home freezers.

It’s worth noting that resistance to insecticides has developed, making chemical eradication difficult. An alternative extermination protocol involves heating an entire home to the required temperatures to eradicate the infestation.¹

This patient noted that she had already thrown away the couch, clothes, and bedding where she had seen the insects and had sprayed her apartment with insecticide. She was counseled to contact a professional exterminator to further evaluate the home for any additional areas of infestation and treat if any bed bugs were still in the home. She was also counseled to use loratadine 10 mg/d orally and topical 1% hydrocortisone ointment, as needed, for the itching and inflammation.

‌

Photo and text courtesy of Daniel Stulberg, MD, FAAFP, Professor and Chair, Department of Family and Community Medicine, Western Michigan University Homer Stryker, MD School of Medicine, Kalamazoo.

Clustered erythematous macular to papular lesions, especially those that stop at clothing lines, are a frequent manifestation of insect bites. In this case, the lesions lacked a central punctum that is common in many insect bites, so the most likely culprit was bed bugs. It is likely that this patient’s friend inadvertently brought the bed bugs into the home in her luggage or packed belongings. Over time, they spread around the home, causing the patient’s bites and inflammation. When questioned, the patient noted that she could actually see bugs around the couch in her home.

The scientific name for bed bugs is Cimex lectularis. Bed bugs require a blood meal from a host to survive, but they do not remain attached to the human body. Instead, they live in nearby fabrics. Bed bugs are visible to the naked eye when they are in the open, although they usually remain along the seams of fabric, edges of bedding, or in cracks and crevices. Often the feces of bed bugs will collect and be seen as dark spots or streaks on bedding.¹

Treatment hinges on the eradication of the bed bugs. The erythematous itching lesions will resolve spontaneously over 1 to 2 weeks. Topical corticosteroids, including hydrocortisone, can be used as necessary to control the itching. Oral antihistamines can also help with itching.

Eradication of all the bed bugs in the home can be difficult and warrant professional extermination services. Washing clothing in hot water of at least 140 °F will kill the insects. Freezing items below –4 °F for at least 2 hours is also effective but may not be possible with home freezers.

It’s worth noting that resistance to insecticides has developed, making chemical eradication difficult. An alternative extermination protocol involves heating an entire home to the required temperatures to eradicate the infestation.¹

This patient noted that she had already thrown away the couch, clothes, and bedding where she had seen the insects and had sprayed her apartment with insecticide. She was counseled to contact a professional exterminator to further evaluate the home for any additional areas of infestation and treat if any bed bugs were still in the home. She was also counseled to use loratadine 10 mg/d orally and topical 1% hydrocortisone ointment, as needed, for the itching and inflammation.

‌

Photo and text courtesy of Daniel Stulberg, MD, FAAFP, Professor and Chair, Department of Family and Community Medicine, Western Michigan University Homer Stryker, MD School of Medicine, Kalamazoo.

This linear pattern of hyper-pigmented, often verrucous tissue oriented along Blaschko skin lines is typical for linear epidermal nevi (LEN). In some cases, lesions are not in a linear pattern and are actually in more of a localized or whorled pattern (called epidermal nevi).

LEN are usually present at birth, as in this individual. They are frequently seen on the head and neck region and are often asymptomatic. LEN are considered a birthmark that develops because of a genetic abnormality that typically affects keratinocytes. This genetic mutation only affects a portion of the body (mosaicism) without affecting the overall genetics of the individual. This is important to note because LEN do not typically have a hereditary component or implications for offspring. While usually asymptomatic and localized, LEN can be associated with extracutaneous and neurologic difficulties. In these situations, it is called epidermal nevus syndrome, and is more common if the LEN occur on the face or head.¹

Since LEN are usually asymptomatic, treatment is not required unless the lesions affect the function of adjacent structures, such as the eyes, lips, or nose. Due to their frequent presence on the face or other visible areas, some patients may choose to get these lesions treated for cosmetic purposes. In the past, full-thickness excision was recommended. Topical medications are ineffective, and superficial shave excision usually leads to recurrence. More recently, destructive laser treatments have been used, with success, to reduce the appearance of the lesions.²

This patient was not concerned about the appearance of the asymptomatic lesions and chose not to have any treatment.

‌

Photo and text courtesy of Daniel Stulberg, MD, FAAFP, Professor and Chair, Department of Family and Community Medicine, Western Michigan University Homer Stryker, MD School of Medicine, Kalamazoo.

This linear pattern of hyper-pigmented, often verrucous tissue oriented along Blaschko skin lines is typical for linear epidermal nevi (LEN). In some cases, lesions are not in a linear pattern and are actually in more of a localized or whorled pattern (called epidermal nevi).

LEN are usually present at birth, as in this individual. They are frequently seen on the head and neck region and are often asymptomatic. LEN are considered a birthmark that develops because of a genetic abnormality that typically affects keratinocytes. This genetic mutation only affects a portion of the body (mosaicism) without affecting the overall genetics of the individual. This is important to note because LEN do not typically have a hereditary component or implications for offspring. While usually asymptomatic and localized, LEN can be associated with extracutaneous and neurologic difficulties. In these situations, it is called epidermal nevus syndrome, and is more common if the LEN occur on the face or head.¹

Since LEN are usually asymptomatic, treatment is not required unless the lesions affect the function of adjacent structures, such as the eyes, lips, or nose. Due to their frequent presence on the face or other visible areas, some patients may choose to get these lesions treated for cosmetic purposes. In the past, full-thickness excision was recommended. Topical medications are ineffective, and superficial shave excision usually leads to recurrence. More recently, destructive laser treatments have been used, with success, to reduce the appearance of the lesions.²

This patient was not concerned about the appearance of the asymptomatic lesions and chose not to have any treatment.

‌

Photo and text courtesy of Daniel Stulberg, MD, FAAFP, Professor and Chair, Department of Family and Community Medicine, Western Michigan University Homer Stryker, MD School of Medicine, Kalamazoo.

This linear pattern of hyper-pigmented, often verrucous tissue oriented along Blaschko skin lines is typical for linear epidermal nevi (LEN). In some cases, lesions are not in a linear pattern and are actually in more of a localized or whorled pattern (called epidermal nevi).

LEN are usually present at birth, as in this individual. They are frequently seen on the head and neck region and are often asymptomatic. LEN are considered a birthmark that develops because of a genetic abnormality that typically affects keratinocytes. This genetic mutation only affects a portion of the body (mosaicism) without affecting the overall genetics of the individual. This is important to note because LEN do not typically have a hereditary component or implications for offspring. While usually asymptomatic and localized, LEN can be associated with extracutaneous and neurologic difficulties. In these situations, it is called epidermal nevus syndrome, and is more common if the LEN occur on the face or head.¹

Since LEN are usually asymptomatic, treatment is not required unless the lesions affect the function of adjacent structures, such as the eyes, lips, or nose. Due to their frequent presence on the face or other visible areas, some patients may choose to get these lesions treated for cosmetic purposes. In the past, full-thickness excision was recommended. Topical medications are ineffective, and superficial shave excision usually leads to recurrence. More recently, destructive laser treatments have been used, with success, to reduce the appearance of the lesions.²

This patient was not concerned about the appearance of the asymptomatic lesions and chose not to have any treatment.

‌

Photo and text courtesy of Daniel Stulberg, MD, FAAFP, Professor and Chair, Department of Family and Community Medicine, Western Michigan University Homer Stryker, MD School of Medicine, Kalamazoo.

The Centers for Disease Control and Prevention (CDC) recently published updated guidelines on prescribing opioids for pain that stress the need for a flexible and individual approach to pain management.¹ New recommendations emphasize the use of nonopioid therapies whenever appropriate, support consideration of opioid therapy for patients with acute pain when the benefits are expected to outweigh the risks, and urge clinicians to work with patients receiving opioid therapy to determine whether it should be continued or tapered.

This revision to the agency’s 2016 guidelines is aimed at primary care clinicians who prescribe opioids to adult outpatients for treatment of pain. The recommendations are not meant for patients with sickle-cell disease or cancer-related pain, or those receiving palliative and end-of-life care.

Why an update was needed. In 2021, more than 107,000 Americans died of a drug overdose.² Although prescription opioids caused only about 16% of these deaths, they account for a population death rate of 4:100,000—which, despite national efforts, has not changed much since 2013.^3,4

Following publication of the CDC’s 2016 guidelines on prescribing opioids for chronic pain,⁵ there was a decline in opioid prescribing but not in related deaths. Furthermore, there appeared to have been some negative effects of reduced prescribing, including untreated and undertreated pain, and rapid tapering or sudden discontinuation of opioids in chronic users, causing withdrawal symptoms and psychological distress in these patients. To address these issues, the CDC published the new guideline in 2022.¹

Categories of pain. The guideline panel classified pain into 3 categories: acute pain (duration of < 1 month), subacute pain (duration of 1-3 months), and chronic pain (duration of > 3 months).

When to prescribe opioids. The guidelines recommend a new approach to deciding whether to prescribe opioid therapy. In most cases, nonopioid options—such as nonsteroidal anti-inflammatory drugs (NSAIDs) and exercise—should be tried first, since they are as effective as opioids for many types of acute, subacute, and chronic pain. Opioids should be considered if these options fail and the potential benefits outweigh the risks. In moderate-to-severe acute pain, opioids are an option if NSAIDs are unlikely to be effective or are contraindicated.¹

How to prescribe opioids. Before prescribing opioids, clinicians should discuss with the patient the known risks and benefits and offer an accompanying prescription for naloxone. Opioids should be prescribed at the lowest effective dose and for a time period limited to the expected duration of the pain. When starting opioids, immediate-release opioids should be prescribed instead of extended-release or long-acting opioids.¹

Precautionary measures. Clinicians should review the patient’s history of controlled substance prescriptions via their state’s prescription drug monitoring program and consider the use of toxicology testing to determine whether the patient is receiving high-risk opioid dosages or combinations. Clinicians should be especially cautious about prescribing opioids and benzodiazepines concurrently.¹

Continue or stop opioid treatment? A new recommendation advises clinicians to individually assess the benefits and risks of continuing therapy for patients who have been receiving opioids chronically. Whenever the decision is made to stop or reduce treatment, remember that opioid therapy should not be stopped abruptly or reduced quickly. The guideline panel suggests tapering by 10% per month.¹

Finally, patients with opioid use disorder should be offered or referred for treatment with medications. Detoxification alone, without medication, is not recommended.¹

The Centers for Disease Control and Prevention (CDC) recently published updated guidelines on prescribing opioids for pain that stress the need for a flexible and individual approach to pain management.¹ New recommendations emphasize the use of nonopioid therapies whenever appropriate, support consideration of opioid therapy for patients with acute pain when the benefits are expected to outweigh the risks, and urge clinicians to work with patients receiving opioid therapy to determine whether it should be continued or tapered.

This revision to the agency’s 2016 guidelines is aimed at primary care clinicians who prescribe opioids to adult outpatients for treatment of pain. The recommendations are not meant for patients with sickle-cell disease or cancer-related pain, or those receiving palliative and end-of-life care.

Why an update was needed. In 2021, more than 107,000 Americans died of a drug overdose.² Although prescription opioids caused only about 16% of these deaths, they account for a population death rate of 4:100,000—which, despite national efforts, has not changed much since 2013.^3,4

Following publication of the CDC’s 2016 guidelines on prescribing opioids for chronic pain,⁵ there was a decline in opioid prescribing but not in related deaths. Furthermore, there appeared to have been some negative effects of reduced prescribing, including untreated and undertreated pain, and rapid tapering or sudden discontinuation of opioids in chronic users, causing withdrawal symptoms and psychological distress in these patients. To address these issues, the CDC published the new guideline in 2022.¹

Categories of pain. The guideline panel classified pain into 3 categories: acute pain (duration of < 1 month), subacute pain (duration of 1-3 months), and chronic pain (duration of > 3 months).

When to prescribe opioids. The guidelines recommend a new approach to deciding whether to prescribe opioid therapy. In most cases, nonopioid options—such as nonsteroidal anti-inflammatory drugs (NSAIDs) and exercise—should be tried first, since they are as effective as opioids for many types of acute, subacute, and chronic pain. Opioids should be considered if these options fail and the potential benefits outweigh the risks. In moderate-to-severe acute pain, opioids are an option if NSAIDs are unlikely to be effective or are contraindicated.¹

How to prescribe opioids. Before prescribing opioids, clinicians should discuss with the patient the known risks and benefits and offer an accompanying prescription for naloxone. Opioids should be prescribed at the lowest effective dose and for a time period limited to the expected duration of the pain. When starting opioids, immediate-release opioids should be prescribed instead of extended-release or long-acting opioids.¹

Precautionary measures. Clinicians should review the patient’s history of controlled substance prescriptions via their state’s prescription drug monitoring program and consider the use of toxicology testing to determine whether the patient is receiving high-risk opioid dosages or combinations. Clinicians should be especially cautious about prescribing opioids and benzodiazepines concurrently.¹

Continue or stop opioid treatment? A new recommendation advises clinicians to individually assess the benefits and risks of continuing therapy for patients who have been receiving opioids chronically. Whenever the decision is made to stop or reduce treatment, remember that opioid therapy should not be stopped abruptly or reduced quickly. The guideline panel suggests tapering by 10% per month.¹

Finally, patients with opioid use disorder should be offered or referred for treatment with medications. Detoxification alone, without medication, is not recommended.¹

The Centers for Disease Control and Prevention (CDC) recently published updated guidelines on prescribing opioids for pain that stress the need for a flexible and individual approach to pain management.¹ New recommendations emphasize the use of nonopioid therapies whenever appropriate, support consideration of opioid therapy for patients with acute pain when the benefits are expected to outweigh the risks, and urge clinicians to work with patients receiving opioid therapy to determine whether it should be continued or tapered.

This revision to the agency’s 2016 guidelines is aimed at primary care clinicians who prescribe opioids to adult outpatients for treatment of pain. The recommendations are not meant for patients with sickle-cell disease or cancer-related pain, or those receiving palliative and end-of-life care.

Why an update was needed. In 2021, more than 107,000 Americans died of a drug overdose.² Although prescription opioids caused only about 16% of these deaths, they account for a population death rate of 4:100,000—which, despite national efforts, has not changed much since 2013.^3,4

Following publication of the CDC’s 2016 guidelines on prescribing opioids for chronic pain,⁵ there was a decline in opioid prescribing but not in related deaths. Furthermore, there appeared to have been some negative effects of reduced prescribing, including untreated and undertreated pain, and rapid tapering or sudden discontinuation of opioids in chronic users, causing withdrawal symptoms and psychological distress in these patients. To address these issues, the CDC published the new guideline in 2022.¹

Categories of pain. The guideline panel classified pain into 3 categories: acute pain (duration of < 1 month), subacute pain (duration of 1-3 months), and chronic pain (duration of > 3 months).

When to prescribe opioids. The guidelines recommend a new approach to deciding whether to prescribe opioid therapy. In most cases, nonopioid options—such as nonsteroidal anti-inflammatory drugs (NSAIDs) and exercise—should be tried first, since they are as effective as opioids for many types of acute, subacute, and chronic pain. Opioids should be considered if these options fail and the potential benefits outweigh the risks. In moderate-to-severe acute pain, opioids are an option if NSAIDs are unlikely to be effective or are contraindicated.¹

How to prescribe opioids. Before prescribing opioids, clinicians should discuss with the patient the known risks and benefits and offer an accompanying prescription for naloxone. Opioids should be prescribed at the lowest effective dose and for a time period limited to the expected duration of the pain. When starting opioids, immediate-release opioids should be prescribed instead of extended-release or long-acting opioids.¹

Precautionary measures. Clinicians should review the patient’s history of controlled substance prescriptions via their state’s prescription drug monitoring program and consider the use of toxicology testing to determine whether the patient is receiving high-risk opioid dosages or combinations. Clinicians should be especially cautious about prescribing opioids and benzodiazepines concurrently.¹

Continue or stop opioid treatment? A new recommendation advises clinicians to individually assess the benefits and risks of continuing therapy for patients who have been receiving opioids chronically. Whenever the decision is made to stop or reduce treatment, remember that opioid therapy should not be stopped abruptly or reduced quickly. The guideline panel suggests tapering by 10% per month.¹

Finally, patients with opioid use disorder should be offered or referred for treatment with medications. Detoxification alone, without medication, is not recommended.¹

The gyrate or cerebriform pattern of inflammatory, often pus-filled, subcutaneous tracts of the scalp pointed to a diagnosis of dissecting cellulitis. This patient did not have the fluctuant tracts frequently seen in more active disease but did have the scarring and alopecia common with this disorder.

Dissecting cellulitis is similar to acne and hidradenitis suppurativa in that it starts with follicular plugging. This plugging leads to inflammation, dilation and rupture of the follicle, and purulent sinus tract formation. The sinus tracts of the scalp can be extensive. Dissecting cellulitis is most common in 18- to 40-year-olds and more common in Black individuals.¹ When it occurs in conjunction with cystic acne and hidradenitis suppurativa, it is known as the follicular occlusion triad syndrome.

While oral antibiotics are an option for the treatment of dissecting cellulitis, oral isotretinoin is the first-line approach. Tumor necrosis factor alfa inhibitors have also been used with success, according to case reports.¹

Given that this patient had a small area of current inflammation, he was started on oral doxycycline 100 mg twice daily for 2 months. He was scheduled for a follow-up appointment in 3 months to reassess his progress and to explore treatment with isotretinoin if the condition worsened or did not improve.

‌

Photo and text courtesy of Daniel Stulberg, MD, FAAFP, Professor and Chair, Department of Family and Community Medicine, Western Michigan University Homer Stryker, MD School of Medicine, Kalamazoo.

The gyrate or cerebriform pattern of inflammatory, often pus-filled, subcutaneous tracts of the scalp pointed to a diagnosis of dissecting cellulitis. This patient did not have the fluctuant tracts frequently seen in more active disease but did have the scarring and alopecia common with this disorder.

Dissecting cellulitis is similar to acne and hidradenitis suppurativa in that it starts with follicular plugging. This plugging leads to inflammation, dilation and rupture of the follicle, and purulent sinus tract formation. The sinus tracts of the scalp can be extensive. Dissecting cellulitis is most common in 18- to 40-year-olds and more common in Black individuals.¹ When it occurs in conjunction with cystic acne and hidradenitis suppurativa, it is known as the follicular occlusion triad syndrome.

While oral antibiotics are an option for the treatment of dissecting cellulitis, oral isotretinoin is the first-line approach. Tumor necrosis factor alfa inhibitors have also been used with success, according to case reports.¹

Given that this patient had a small area of current inflammation, he was started on oral doxycycline 100 mg twice daily for 2 months. He was scheduled for a follow-up appointment in 3 months to reassess his progress and to explore treatment with isotretinoin if the condition worsened or did not improve.

‌

Photo and text courtesy of Daniel Stulberg, MD, FAAFP, Professor and Chair, Department of Family and Community Medicine, Western Michigan University Homer Stryker, MD School of Medicine, Kalamazoo.

The gyrate or cerebriform pattern of inflammatory, often pus-filled, subcutaneous tracts of the scalp pointed to a diagnosis of dissecting cellulitis. This patient did not have the fluctuant tracts frequently seen in more active disease but did have the scarring and alopecia common with this disorder.

Dissecting cellulitis is similar to acne and hidradenitis suppurativa in that it starts with follicular plugging. This plugging leads to inflammation, dilation and rupture of the follicle, and purulent sinus tract formation. The sinus tracts of the scalp can be extensive. Dissecting cellulitis is most common in 18- to 40-year-olds and more common in Black individuals.¹ When it occurs in conjunction with cystic acne and hidradenitis suppurativa, it is known as the follicular occlusion triad syndrome.

While oral antibiotics are an option for the treatment of dissecting cellulitis, oral isotretinoin is the first-line approach. Tumor necrosis factor alfa inhibitors have also been used with success, according to case reports.¹

Given that this patient had a small area of current inflammation, he was started on oral doxycycline 100 mg twice daily for 2 months. He was scheduled for a follow-up appointment in 3 months to reassess his progress and to explore treatment with isotretinoin if the condition worsened or did not improve.

‌

Photo and text courtesy of Daniel Stulberg, MD, FAAFP, Professor and Chair, Department of Family and Community Medicine, Western Michigan University Homer Stryker, MD School of Medicine, Kalamazoo.

This patient’s targetoid and tingling skin lesions, in association with herpes simplex virus (HSV) infection, are a classic presentation of erythema multiforme (EM).

EM is an acute, self-limited, immune-mediated process that most commonly arises in a symmetrical pattern on acral surfaces. These lesions may be accompanied by eruptions on oral, anogenital, or ocular mucosa. EM is classified into 2 subtypes: major and minor. EM major refers to EM with significant mucosal involvement on at least 2 mucosal sites; it may also manifest with a prodrome of fevers, arthralgias, and malaise. EM minor is used to classify EM with minimal mucosal involvement.¹

The term “multiforme” denotes the varied dermatologic changes, including macules, papules, and targetoid lesions with 3 identifiable zones, which are pathognomonic for EM. The classic 3 zones consist of an inner dusky, vesicular, or necrotic center; a middle elevated edematous surrounding ring; and an outer ring of macular erythema. Patients may also present with an atypical macular target lesion, characterized by fewer than 3 zones with an ill-defined border between the zones. The lesions may be asymptomatic, or patients may describe an itchy or burning sensation.

The differential diagnosis of EM includes urticaria, fixed drug eruption, subacute lupus erythematosus, Kawasaki disease, erythema annulare centrifugum, vasculitis, and Stevens-Johnson syndrome.

Infections with HSV types 1 or 2 are the leading cause of EM and are thought to involve a cell-mediated immune process directed against viral antigens in skin.² Other infectious causes include cytomegalovirus, Epstein-Barr virus, influenza virus, and—rarely—newer strains of coronavirus.³ Pharmacologic reactions are the cause in a small percentage of patients, and may involve nonsteroidal anti-inflammatory drugs, antibiotics, sulfonamides, antiepileptics, and tumor necrosis factor-alpha inhibitors. Studies also link the development of EM to primary malignancy, autoimmune disease, and immunizations.¹

The treatment of EM is dependent on the clinical course and severity of the disease. If a causative agent is identified, it should be discontinued (if a drug) or treated (if an infection). Topical antiseptic mouthwashes, antihistamines, and topical corticosteroids can be used to relieve cutaneous discomfort. Biologics and immunosuppressants can be used with patients who have severe symptoms or functional impairment. Patients who have recurrences associated with HSV should be given antiviral prophylaxis for 6 months consisting of oral acyclovir 10 mg/kg/d, valacyclovir 500 to 1000 mg/d, or famciclovir 250 mg twice daily.¹

Given the recurrent nature of this patient’s disease, and its association with HSV outbreaks, he was prescribed prophylactic valacyclovir 1000 mg/d orally for 6 months to reduce HSV outbreaks and hopefully prevent future EM episodes.

‌

Photo courtesy of Cyrelle F. Finan, MD. Text courtesy of Lynn Midani, BS, University of New Mexico School of Medicine, and Cyrelle F. Finan, MD, Department of Dermatology, and Daniel Stulberg, MD, FAAFP, Department of Family and Community Medicine, Western Michigan University Homer Stryker, MD School of Medicine, Kalamazoo.

This patient’s targetoid and tingling skin lesions, in association with herpes simplex virus (HSV) infection, are a classic presentation of erythema multiforme (EM).

EM is an acute, self-limited, immune-mediated process that most commonly arises in a symmetrical pattern on acral surfaces. These lesions may be accompanied by eruptions on oral, anogenital, or ocular mucosa. EM is classified into 2 subtypes: major and minor. EM major refers to EM with significant mucosal involvement on at least 2 mucosal sites; it may also manifest with a prodrome of fevers, arthralgias, and malaise. EM minor is used to classify EM with minimal mucosal involvement.¹

The term “multiforme” denotes the varied dermatologic changes, including macules, papules, and targetoid lesions with 3 identifiable zones, which are pathognomonic for EM. The classic 3 zones consist of an inner dusky, vesicular, or necrotic center; a middle elevated edematous surrounding ring; and an outer ring of macular erythema. Patients may also present with an atypical macular target lesion, characterized by fewer than 3 zones with an ill-defined border between the zones. The lesions may be asymptomatic, or patients may describe an itchy or burning sensation.

The differential diagnosis of EM includes urticaria, fixed drug eruption, subacute lupus erythematosus, Kawasaki disease, erythema annulare centrifugum, vasculitis, and Stevens-Johnson syndrome.

Infections with HSV types 1 or 2 are the leading cause of EM and are thought to involve a cell-mediated immune process directed against viral antigens in skin.² Other infectious causes include cytomegalovirus, Epstein-Barr virus, influenza virus, and—rarely—newer strains of coronavirus.³ Pharmacologic reactions are the cause in a small percentage of patients, and may involve nonsteroidal anti-inflammatory drugs, antibiotics, sulfonamides, antiepileptics, and tumor necrosis factor-alpha inhibitors. Studies also link the development of EM to primary malignancy, autoimmune disease, and immunizations.¹

The treatment of EM is dependent on the clinical course and severity of the disease. If a causative agent is identified, it should be discontinued (if a drug) or treated (if an infection). Topical antiseptic mouthwashes, antihistamines, and topical corticosteroids can be used to relieve cutaneous discomfort. Biologics and immunosuppressants can be used with patients who have severe symptoms or functional impairment. Patients who have recurrences associated with HSV should be given antiviral prophylaxis for 6 months consisting of oral acyclovir 10 mg/kg/d, valacyclovir 500 to 1000 mg/d, or famciclovir 250 mg twice daily.¹

Given the recurrent nature of this patient’s disease, and its association with HSV outbreaks, he was prescribed prophylactic valacyclovir 1000 mg/d orally for 6 months to reduce HSV outbreaks and hopefully prevent future EM episodes.

‌

Photo courtesy of Cyrelle F. Finan, MD. Text courtesy of Lynn Midani, BS, University of New Mexico School of Medicine, and Cyrelle F. Finan, MD, Department of Dermatology, and Daniel Stulberg, MD, FAAFP, Department of Family and Community Medicine, Western Michigan University Homer Stryker, MD School of Medicine, Kalamazoo.

This patient’s targetoid and tingling skin lesions, in association with herpes simplex virus (HSV) infection, are a classic presentation of erythema multiforme (EM).

EM is an acute, self-limited, immune-mediated process that most commonly arises in a symmetrical pattern on acral surfaces. These lesions may be accompanied by eruptions on oral, anogenital, or ocular mucosa. EM is classified into 2 subtypes: major and minor. EM major refers to EM with significant mucosal involvement on at least 2 mucosal sites; it may also manifest with a prodrome of fevers, arthralgias, and malaise. EM minor is used to classify EM with minimal mucosal involvement.¹

The term “multiforme” denotes the varied dermatologic changes, including macules, papules, and targetoid lesions with 3 identifiable zones, which are pathognomonic for EM. The classic 3 zones consist of an inner dusky, vesicular, or necrotic center; a middle elevated edematous surrounding ring; and an outer ring of macular erythema. Patients may also present with an atypical macular target lesion, characterized by fewer than 3 zones with an ill-defined border between the zones. The lesions may be asymptomatic, or patients may describe an itchy or burning sensation.

The differential diagnosis of EM includes urticaria, fixed drug eruption, subacute lupus erythematosus, Kawasaki disease, erythema annulare centrifugum, vasculitis, and Stevens-Johnson syndrome.

Infections with HSV types 1 or 2 are the leading cause of EM and are thought to involve a cell-mediated immune process directed against viral antigens in skin.² Other infectious causes include cytomegalovirus, Epstein-Barr virus, influenza virus, and—rarely—newer strains of coronavirus.³ Pharmacologic reactions are the cause in a small percentage of patients, and may involve nonsteroidal anti-inflammatory drugs, antibiotics, sulfonamides, antiepileptics, and tumor necrosis factor-alpha inhibitors. Studies also link the development of EM to primary malignancy, autoimmune disease, and immunizations.¹

The treatment of EM is dependent on the clinical course and severity of the disease. If a causative agent is identified, it should be discontinued (if a drug) or treated (if an infection). Topical antiseptic mouthwashes, antihistamines, and topical corticosteroids can be used to relieve cutaneous discomfort. Biologics and immunosuppressants can be used with patients who have severe symptoms or functional impairment. Patients who have recurrences associated with HSV should be given antiviral prophylaxis for 6 months consisting of oral acyclovir 10 mg/kg/d, valacyclovir 500 to 1000 mg/d, or famciclovir 250 mg twice daily.¹

Given the recurrent nature of this patient’s disease, and its association with HSV outbreaks, he was prescribed prophylactic valacyclovir 1000 mg/d orally for 6 months to reduce HSV outbreaks and hopefully prevent future EM episodes.

‌

Photo courtesy of Cyrelle F. Finan, MD. Text courtesy of Lynn Midani, BS, University of New Mexico School of Medicine, and Cyrelle F. Finan, MD, Department of Dermatology, and Daniel Stulberg, MD, FAAFP, Department of Family and Community Medicine, Western Michigan University Homer Stryker, MD School of Medicine, Kalamazoo.

THE CASE

A 14-year-old boy sought care at our clinic for persistent chest pain after being hit in the chest with a teammate’s shoulder during a basketball game 3 weeks earlier. He had aching midsternal chest pain that worsened with direct pressure and when he sneezed, twisted, or bent forward. There was no bruising or swelling.

On examination, the patient demonstrated normal perfusion and normal work of breathing. He had focal tenderness with palpation at the manubrium with no noticeable step-off, and mild tenderness at the adjacent costochondral junctions and over his pectoral muscles. His sternal pain along the proximal sternum was reproducible with a weighted wall push-up. Although the patient maintained full range of motion in his upper extremities, he did have sternal pain with flexion, abduction, and external rotation of the bilateral upper extremities against resistance. Anteroposterior (AP) and lateral chest radiographs were unremarkable.

THE DIAGNOSIS

The unremarkable chest radiographs prompted further investigation with a diagnostic ultrasound, which revealed a small cortical defect with overlying anechoic fluid collection in the area of focal tenderness. T2-weighted magnetic resonance imaging (MRI) of the chest was performed; it revealed a transverse, nondisplaced fracture of the superior body of the sternum with surrounding bone marrow edema (FIGURE).

DISCUSSION

Fractures of the sternum comprise < 1% of traumatic fractures and have a low mortality rate (0.7%).^1,2 The rarity of these fractures is attributed to the ribs’ elastic recoil, which protects the chest wall from anterior ­forces.^1,3 These fractures are even more unusual in children due to the increased elasticity of their chest walls.^4-6 Thus, it takes a significant amount of force for a child’s sternum to fracture.

While isolated sternum fractures can occur, two-thirds of sternum fractures are nonisolated and are associated with injuries to surrounding structures (including the heart, lungs, and vasculature) or fractures of the ribs and spine.^2,3 Most often, these injuries are caused by significant blunt trauma to the anterior chest, rapid deceleration, or flexion-­compression injury.^2,3 They are typically transverse and localized, with 70% of fractures occurring in the mid-body and 17.6% at the manubriosternal joint.^1,3,6

Athletes with a sternal fracture typically present as our patient did, with a history of blunt force trauma to the chest and with pain and tenderness over the anterior midline of the chest that increases with respiration or movement.¹ A physical examination that includes chest palpation and auscultation of the heart and lungs must be performed to rule out damage to intrathoracic structures and assess the patient’s cardiac and pulmonary stability. An electrocardiogram should be performed to confirm that there are no cardiovascular complications.^3,4

Initial imaging should include AP and lateral chest radiographs because any displacement will occur in the sagittal plane.^1,2,4-6 If the radiograph shows no clear pathology, follow up with computed tomography, ultrasound, MRI, or technetium bone scans to gain additional information.¹ Diagnosis of sternal fractures is especially difficult in children due to the presence of ossification centers for bone growth, which may be misinterpreted as a sternal fracture in the absence of a proper understanding of sternal development.^5,6 On ultrasound, sternal fractures appear as a sharp step-off in the cortex, whereas in the absence of fracture, there is no cortical step-off and the cartilaginous plate between ossification centers appears in line with the cortex.⁷

Continue to: A self-limiting injury that requires proper pain control

Isolated sternal fractures are typically self-limiting with a good prognosis.² These injuries are managed supportively with rest, ice, and analgesics¹; proper pain control is crucial to prevent respiratory compromise.⁸

Complete recovery for most patients occurs in 10 to 12 weeks.⁹ Recovery periods longer than 12 weeks are associated with nonisolated sternal fractures that are complicated by soft-tissue injury, injuries to the chest wall (such as sternoclavicular joint dislocation, usually from a fall on the shoulder), or fracture nonunion.^1,2,5

Although sternum fractures are rare in pediatric patients, twothirds of these fractures are associated with injuries to surrounding structures.

Anterior sternoclavicular joint dislocations and stable posterior dislocations are managed with closed reduction and immobilization in a figure-of-eight brace.¹ Operative management is reserved for patients with displaced fractures, sternal deformity, chest wall instability, respiratory insufficiency, uncontrolled pain, or fracture nonunion.^1,3,8

A return-to-play protocol can begin once the patient is asymptomatic.¹ The timeframe for a full return to play can vary from 6 weeks to 6 months, depending on the severity of the fracture.¹ This process is guided by how quickly the symptoms resolve and by radiographic stability.⁹

Our patient was followed every 3 to 4 weeks and started physical therapy 6 weeks after his injury occurred. He was held from play for 10 weeks and gradually returned to play; he returned to full-contact activity after tolerating a practice without pain.

THE TAKEAWAY

Children typically have greater chest wall elasticity, and thus, it is unusual for them to sustain a sternal fracture. Diagnosis in children is complicated by the presence of ossification centers for bone growth on imaging. In this case, the fracture was first noticed on ultrasound and confirmed with MRI. Since these fractures can be associated with damage to surrounding structures, additional injuries should be considered when evaluating a patient with a sternum fracture.

CORRESPONDENCE
Catherine Romaine, East Carolina University, Brody School of Medicine, 600 Moye Boulevard, Greenville, NC 27834; [email protected]

THE CASE

A 14-year-old boy sought care at our clinic for persistent chest pain after being hit in the chest with a teammate’s shoulder during a basketball game 3 weeks earlier. He had aching midsternal chest pain that worsened with direct pressure and when he sneezed, twisted, or bent forward. There was no bruising or swelling.

On examination, the patient demonstrated normal perfusion and normal work of breathing. He had focal tenderness with palpation at the manubrium with no noticeable step-off, and mild tenderness at the adjacent costochondral junctions and over his pectoral muscles. His sternal pain along the proximal sternum was reproducible with a weighted wall push-up. Although the patient maintained full range of motion in his upper extremities, he did have sternal pain with flexion, abduction, and external rotation of the bilateral upper extremities against resistance. Anteroposterior (AP) and lateral chest radiographs were unremarkable.

THE DIAGNOSIS

The unremarkable chest radiographs prompted further investigation with a diagnostic ultrasound, which revealed a small cortical defect with overlying anechoic fluid collection in the area of focal tenderness. T2-weighted magnetic resonance imaging (MRI) of the chest was performed; it revealed a transverse, nondisplaced fracture of the superior body of the sternum with surrounding bone marrow edema (FIGURE).

DISCUSSION

Fractures of the sternum comprise < 1% of traumatic fractures and have a low mortality rate (0.7%).^1,2 The rarity of these fractures is attributed to the ribs’ elastic recoil, which protects the chest wall from anterior ­forces.^1,3 These fractures are even more unusual in children due to the increased elasticity of their chest walls.^4-6 Thus, it takes a significant amount of force for a child’s sternum to fracture.

While isolated sternum fractures can occur, two-thirds of sternum fractures are nonisolated and are associated with injuries to surrounding structures (including the heart, lungs, and vasculature) or fractures of the ribs and spine.^2,3 Most often, these injuries are caused by significant blunt trauma to the anterior chest, rapid deceleration, or flexion-­compression injury.^2,3 They are typically transverse and localized, with 70% of fractures occurring in the mid-body and 17.6% at the manubriosternal joint.^1,3,6

Athletes with a sternal fracture typically present as our patient did, with a history of blunt force trauma to the chest and with pain and tenderness over the anterior midline of the chest that increases with respiration or movement.¹ A physical examination that includes chest palpation and auscultation of the heart and lungs must be performed to rule out damage to intrathoracic structures and assess the patient’s cardiac and pulmonary stability. An electrocardiogram should be performed to confirm that there are no cardiovascular complications.^3,4

Initial imaging should include AP and lateral chest radiographs because any displacement will occur in the sagittal plane.^1,2,4-6 If the radiograph shows no clear pathology, follow up with computed tomography, ultrasound, MRI, or technetium bone scans to gain additional information.¹ Diagnosis of sternal fractures is especially difficult in children due to the presence of ossification centers for bone growth, which may be misinterpreted as a sternal fracture in the absence of a proper understanding of sternal development.^5,6 On ultrasound, sternal fractures appear as a sharp step-off in the cortex, whereas in the absence of fracture, there is no cortical step-off and the cartilaginous plate between ossification centers appears in line with the cortex.⁷

Continue to: A self-limiting injury that requires proper pain control

Isolated sternal fractures are typically self-limiting with a good prognosis.² These injuries are managed supportively with rest, ice, and analgesics¹; proper pain control is crucial to prevent respiratory compromise.⁸

Complete recovery for most patients occurs in 10 to 12 weeks.⁹ Recovery periods longer than 12 weeks are associated with nonisolated sternal fractures that are complicated by soft-tissue injury, injuries to the chest wall (such as sternoclavicular joint dislocation, usually from a fall on the shoulder), or fracture nonunion.^1,2,5

Although sternum fractures are rare in pediatric patients, twothirds of these fractures are associated with injuries to surrounding structures.

Anterior sternoclavicular joint dislocations and stable posterior dislocations are managed with closed reduction and immobilization in a figure-of-eight brace.¹ Operative management is reserved for patients with displaced fractures, sternal deformity, chest wall instability, respiratory insufficiency, uncontrolled pain, or fracture nonunion.^1,3,8

A return-to-play protocol can begin once the patient is asymptomatic.¹ The timeframe for a full return to play can vary from 6 weeks to 6 months, depending on the severity of the fracture.¹ This process is guided by how quickly the symptoms resolve and by radiographic stability.⁹

Our patient was followed every 3 to 4 weeks and started physical therapy 6 weeks after his injury occurred. He was held from play for 10 weeks and gradually returned to play; he returned to full-contact activity after tolerating a practice without pain.

THE TAKEAWAY

Children typically have greater chest wall elasticity, and thus, it is unusual for them to sustain a sternal fracture. Diagnosis in children is complicated by the presence of ossification centers for bone growth on imaging. In this case, the fracture was first noticed on ultrasound and confirmed with MRI. Since these fractures can be associated with damage to surrounding structures, additional injuries should be considered when evaluating a patient with a sternum fracture.

CORRESPONDENCE
Catherine Romaine, East Carolina University, Brody School of Medicine, 600 Moye Boulevard, Greenville, NC 27834; [email protected]

THE CASE

A 14-year-old boy sought care at our clinic for persistent chest pain after being hit in the chest with a teammate’s shoulder during a basketball game 3 weeks earlier. He had aching midsternal chest pain that worsened with direct pressure and when he sneezed, twisted, or bent forward. There was no bruising or swelling.

On examination, the patient demonstrated normal perfusion and normal work of breathing. He had focal tenderness with palpation at the manubrium with no noticeable step-off, and mild tenderness at the adjacent costochondral junctions and over his pectoral muscles. His sternal pain along the proximal sternum was reproducible with a weighted wall push-up. Although the patient maintained full range of motion in his upper extremities, he did have sternal pain with flexion, abduction, and external rotation of the bilateral upper extremities against resistance. Anteroposterior (AP) and lateral chest radiographs were unremarkable.

THE DIAGNOSIS

The unremarkable chest radiographs prompted further investigation with a diagnostic ultrasound, which revealed a small cortical defect with overlying anechoic fluid collection in the area of focal tenderness. T2-weighted magnetic resonance imaging (MRI) of the chest was performed; it revealed a transverse, nondisplaced fracture of the superior body of the sternum with surrounding bone marrow edema (FIGURE).

DISCUSSION

Fractures of the sternum comprise < 1% of traumatic fractures and have a low mortality rate (0.7%).^1,2 The rarity of these fractures is attributed to the ribs’ elastic recoil, which protects the chest wall from anterior ­forces.^1,3 These fractures are even more unusual in children due to the increased elasticity of their chest walls.^4-6 Thus, it takes a significant amount of force for a child’s sternum to fracture.

While isolated sternum fractures can occur, two-thirds of sternum fractures are nonisolated and are associated with injuries to surrounding structures (including the heart, lungs, and vasculature) or fractures of the ribs and spine.^2,3 Most often, these injuries are caused by significant blunt trauma to the anterior chest, rapid deceleration, or flexion-­compression injury.^2,3 They are typically transverse and localized, with 70% of fractures occurring in the mid-body and 17.6% at the manubriosternal joint.^1,3,6

Athletes with a sternal fracture typically present as our patient did, with a history of blunt force trauma to the chest and with pain and tenderness over the anterior midline of the chest that increases with respiration or movement.¹ A physical examination that includes chest palpation and auscultation of the heart and lungs must be performed to rule out damage to intrathoracic structures and assess the patient’s cardiac and pulmonary stability. An electrocardiogram should be performed to confirm that there are no cardiovascular complications.^3,4

Initial imaging should include AP and lateral chest radiographs because any displacement will occur in the sagittal plane.^1,2,4-6 If the radiograph shows no clear pathology, follow up with computed tomography, ultrasound, MRI, or technetium bone scans to gain additional information.¹ Diagnosis of sternal fractures is especially difficult in children due to the presence of ossification centers for bone growth, which may be misinterpreted as a sternal fracture in the absence of a proper understanding of sternal development.^5,6 On ultrasound, sternal fractures appear as a sharp step-off in the cortex, whereas in the absence of fracture, there is no cortical step-off and the cartilaginous plate between ossification centers appears in line with the cortex.⁷

Continue to: A self-limiting injury that requires proper pain control

Isolated sternal fractures are typically self-limiting with a good prognosis.² These injuries are managed supportively with rest, ice, and analgesics¹; proper pain control is crucial to prevent respiratory compromise.⁸

Complete recovery for most patients occurs in 10 to 12 weeks.⁹ Recovery periods longer than 12 weeks are associated with nonisolated sternal fractures that are complicated by soft-tissue injury, injuries to the chest wall (such as sternoclavicular joint dislocation, usually from a fall on the shoulder), or fracture nonunion.^1,2,5

Although sternum fractures are rare in pediatric patients, twothirds of these fractures are associated with injuries to surrounding structures.

Anterior sternoclavicular joint dislocations and stable posterior dislocations are managed with closed reduction and immobilization in a figure-of-eight brace.¹ Operative management is reserved for patients with displaced fractures, sternal deformity, chest wall instability, respiratory insufficiency, uncontrolled pain, or fracture nonunion.^1,3,8

A return-to-play protocol can begin once the patient is asymptomatic.¹ The timeframe for a full return to play can vary from 6 weeks to 6 months, depending on the severity of the fracture.¹ This process is guided by how quickly the symptoms resolve and by radiographic stability.⁹

Our patient was followed every 3 to 4 weeks and started physical therapy 6 weeks after his injury occurred. He was held from play for 10 weeks and gradually returned to play; he returned to full-contact activity after tolerating a practice without pain.

THE TAKEAWAY

Children typically have greater chest wall elasticity, and thus, it is unusual for them to sustain a sternal fracture. Diagnosis in children is complicated by the presence of ossification centers for bone growth on imaging. In this case, the fracture was first noticed on ultrasound and confirmed with MRI. Since these fractures can be associated with damage to surrounding structures, additional injuries should be considered when evaluating a patient with a sternum fracture.

CORRESPONDENCE
Catherine Romaine, East Carolina University, Brody School of Medicine, 600 Moye Boulevard, Greenville, NC 27834; [email protected]