MDedge Dermatology

To the Editor:

Etanercept is an immune-modulating drug used for the treatment of a variety of diseases including psoriasis, rheumatoid arthritis, and ankylosing spondylitis. It is an anti–tumor necrosis factor (TNF) fusion protein consisting of an extracellular domain of the p75 TNF receptor and the Fc portion of human IgG.¹ Etanercept is well known for its immunosuppressive side effects. A handful of case reports have provided evidence of squamous cell cancers in the setting of etanercept therapy. The most comprehensive description was a case series by Brewer et al² describing 4 patients with squamous cell carcinoma (SCC) that developed 1 to 17 months after the initiation of etanercept therapy. We present a case of a patient diagnosed with psoriasis and concomitant porokeratosis who developed multiple SCCs and squamous proliferations after initiation of etanercept therapy.

A 66-year-old man was referred to our clinic for treatment of psoriasis, as noted on a biopsy of the right ankle diagnosed several years prior. He was being treated with etanercept 50 mg twice weekly. Other treatments included calcipotriene–betamethasone dipropionate, salicylic acid gel, intralesional triamcinolone, clobetasol, and urea 40%. Physical examination revealed multiple erythematous tender nodules with hyperkeratotic scale distributed on the right arm and leg (Figure 1) that were concerning for SCC. Biopsies from 6 lesions revealed multiple SCC/keratoacanthomas (KAs) with verrucous features (Figure 2). Primers for human papillomavirus (HPV) 6, 11, 16, 18, 31, 33, and 51 were all negative. At that time, etanercept was discontinued. The patient was referred for Mohs micrographic surgery and underwent excision of several SCC lesions including an approximately 7-cm SCC on the right ankle (Figure 1B). Positron emission tomography/computed tomography found hypermetabolic lymphadenopathy. A follow-up biopsy of the inguinal nodes identified no malignant cells. Given their multiplicity, the patient was initiated on a prolonged course of a retinoid with acitretin 35 mg daily. The clearance of the large 7-cm lesion with a single stage of Mohs micrographic surgery directed suspicion to a pseudoepitheliomatous or HPV-induced cause for the lesions. Rereview of the original 6 biopsies indicated 1 definitive SCC on the right wrist, 2 KAs, and 3 that were most consistent with verruca vulgaris. At 1-year follow-up, most of the hyperkeratotic lesions had resolved with continued acitretin. Baseline porokeratosis lesions that were abundantly present on the arms and legs resolved by 1-year follow-up (Figure 3A).

The link between classic porokeratosis and the development of squamous cell proliferations is well established. Ninomiya et al³ noted a possible mechanism of p53 overexpression in the epidermis of porokeratotic lesions that may make the lesions particularly susceptible to the development of immunosuppression-induced SCC. Etanercept is an immune-modulating drug with well-known immunosuppressive side effects including reactivation of HPV as well as the development of SCCs.

Our patient initially was diagnosed with psoriasis and etanercept was initiated. The presence of coexistent porokeratosis likely predisposed him to etanercept-induced squamous proliferations including 2 SCCs and verrucous lesions, with histologic features suggesting SCC/KA. Histopathology revealed a cornoid lamella in SCC (Figure 3B), suggesting development of malignancy within epithelial clones, as noted by Lee et al.⁴

Targeted systemic therapies may lead to the formation of SCCs. The association between epidermal growth factor receptor (EGFR) kinase inhibitors and SCC formation is well known. For instance, sorafenib—a multikinase inhibitor that is downstream in the EGFR pathway—has been noted to induce epidermal growths including KAs and SCCs.⁵ There has been no definitive causal relationship identified between the development of SCC and TNF-α inhibitors. It has been suggested that perhaps there is an unmasking effect, as subclinical SCC manifests after TNF-α inhibition that leads to SCC development. Discontinuation of etanercept and resolution of lesions highlights a potential role of TNF-α inhibition and tumorigenesis of SCCs, especially in the background of porokeratosis. Vigilance for development of immunosuppression-induced malignancy, especially squamous cell proliferations, has become exceedingly important with exponentially increasing use of biologic therapies in medicine.

To the Editor:

Etanercept is an immune-modulating drug used for the treatment of a variety of diseases including psoriasis, rheumatoid arthritis, and ankylosing spondylitis. It is an anti–tumor necrosis factor (TNF) fusion protein consisting of an extracellular domain of the p75 TNF receptor and the Fc portion of human IgG.¹ Etanercept is well known for its immunosuppressive side effects. A handful of case reports have provided evidence of squamous cell cancers in the setting of etanercept therapy. The most comprehensive description was a case series by Brewer et al² describing 4 patients with squamous cell carcinoma (SCC) that developed 1 to 17 months after the initiation of etanercept therapy. We present a case of a patient diagnosed with psoriasis and concomitant porokeratosis who developed multiple SCCs and squamous proliferations after initiation of etanercept therapy.

A 66-year-old man was referred to our clinic for treatment of psoriasis, as noted on a biopsy of the right ankle diagnosed several years prior. He was being treated with etanercept 50 mg twice weekly. Other treatments included calcipotriene–betamethasone dipropionate, salicylic acid gel, intralesional triamcinolone, clobetasol, and urea 40%. Physical examination revealed multiple erythematous tender nodules with hyperkeratotic scale distributed on the right arm and leg (Figure 1) that were concerning for SCC. Biopsies from 6 lesions revealed multiple SCC/keratoacanthomas (KAs) with verrucous features (Figure 2). Primers for human papillomavirus (HPV) 6, 11, 16, 18, 31, 33, and 51 were all negative. At that time, etanercept was discontinued. The patient was referred for Mohs micrographic surgery and underwent excision of several SCC lesions including an approximately 7-cm SCC on the right ankle (Figure 1B). Positron emission tomography/computed tomography found hypermetabolic lymphadenopathy. A follow-up biopsy of the inguinal nodes identified no malignant cells. Given their multiplicity, the patient was initiated on a prolonged course of a retinoid with acitretin 35 mg daily. The clearance of the large 7-cm lesion with a single stage of Mohs micrographic surgery directed suspicion to a pseudoepitheliomatous or HPV-induced cause for the lesions. Rereview of the original 6 biopsies indicated 1 definitive SCC on the right wrist, 2 KAs, and 3 that were most consistent with verruca vulgaris. At 1-year follow-up, most of the hyperkeratotic lesions had resolved with continued acitretin. Baseline porokeratosis lesions that were abundantly present on the arms and legs resolved by 1-year follow-up (Figure 3A).

The link between classic porokeratosis and the development of squamous cell proliferations is well established. Ninomiya et al³ noted a possible mechanism of p53 overexpression in the epidermis of porokeratotic lesions that may make the lesions particularly susceptible to the development of immunosuppression-induced SCC. Etanercept is an immune-modulating drug with well-known immunosuppressive side effects including reactivation of HPV as well as the development of SCCs.

Our patient initially was diagnosed with psoriasis and etanercept was initiated. The presence of coexistent porokeratosis likely predisposed him to etanercept-induced squamous proliferations including 2 SCCs and verrucous lesions, with histologic features suggesting SCC/KA. Histopathology revealed a cornoid lamella in SCC (Figure 3B), suggesting development of malignancy within epithelial clones, as noted by Lee et al.⁴

Targeted systemic therapies may lead to the formation of SCCs. The association between epidermal growth factor receptor (EGFR) kinase inhibitors and SCC formation is well known. For instance, sorafenib—a multikinase inhibitor that is downstream in the EGFR pathway—has been noted to induce epidermal growths including KAs and SCCs.⁵ There has been no definitive causal relationship identified between the development of SCC and TNF-α inhibitors. It has been suggested that perhaps there is an unmasking effect, as subclinical SCC manifests after TNF-α inhibition that leads to SCC development. Discontinuation of etanercept and resolution of lesions highlights a potential role of TNF-α inhibition and tumorigenesis of SCCs, especially in the background of porokeratosis. Vigilance for development of immunosuppression-induced malignancy, especially squamous cell proliferations, has become exceedingly important with exponentially increasing use of biologic therapies in medicine.

To the Editor:

Etanercept is an immune-modulating drug used for the treatment of a variety of diseases including psoriasis, rheumatoid arthritis, and ankylosing spondylitis. It is an anti–tumor necrosis factor (TNF) fusion protein consisting of an extracellular domain of the p75 TNF receptor and the Fc portion of human IgG.¹ Etanercept is well known for its immunosuppressive side effects. A handful of case reports have provided evidence of squamous cell cancers in the setting of etanercept therapy. The most comprehensive description was a case series by Brewer et al² describing 4 patients with squamous cell carcinoma (SCC) that developed 1 to 17 months after the initiation of etanercept therapy. We present a case of a patient diagnosed with psoriasis and concomitant porokeratosis who developed multiple SCCs and squamous proliferations after initiation of etanercept therapy.

A 66-year-old man was referred to our clinic for treatment of psoriasis, as noted on a biopsy of the right ankle diagnosed several years prior. He was being treated with etanercept 50 mg twice weekly. Other treatments included calcipotriene–betamethasone dipropionate, salicylic acid gel, intralesional triamcinolone, clobetasol, and urea 40%. Physical examination revealed multiple erythematous tender nodules with hyperkeratotic scale distributed on the right arm and leg (Figure 1) that were concerning for SCC. Biopsies from 6 lesions revealed multiple SCC/keratoacanthomas (KAs) with verrucous features (Figure 2). Primers for human papillomavirus (HPV) 6, 11, 16, 18, 31, 33, and 51 were all negative. At that time, etanercept was discontinued. The patient was referred for Mohs micrographic surgery and underwent excision of several SCC lesions including an approximately 7-cm SCC on the right ankle (Figure 1B). Positron emission tomography/computed tomography found hypermetabolic lymphadenopathy. A follow-up biopsy of the inguinal nodes identified no malignant cells. Given their multiplicity, the patient was initiated on a prolonged course of a retinoid with acitretin 35 mg daily. The clearance of the large 7-cm lesion with a single stage of Mohs micrographic surgery directed suspicion to a pseudoepitheliomatous or HPV-induced cause for the lesions. Rereview of the original 6 biopsies indicated 1 definitive SCC on the right wrist, 2 KAs, and 3 that were most consistent with verruca vulgaris. At 1-year follow-up, most of the hyperkeratotic lesions had resolved with continued acitretin. Baseline porokeratosis lesions that were abundantly present on the arms and legs resolved by 1-year follow-up (Figure 3A).

The link between classic porokeratosis and the development of squamous cell proliferations is well established. Ninomiya et al³ noted a possible mechanism of p53 overexpression in the epidermis of porokeratotic lesions that may make the lesions particularly susceptible to the development of immunosuppression-induced SCC. Etanercept is an immune-modulating drug with well-known immunosuppressive side effects including reactivation of HPV as well as the development of SCCs.

Our patient initially was diagnosed with psoriasis and etanercept was initiated. The presence of coexistent porokeratosis likely predisposed him to etanercept-induced squamous proliferations including 2 SCCs and verrucous lesions, with histologic features suggesting SCC/KA. Histopathology revealed a cornoid lamella in SCC (Figure 3B), suggesting development of malignancy within epithelial clones, as noted by Lee et al.⁴

Targeted systemic therapies may lead to the formation of SCCs. The association between epidermal growth factor receptor (EGFR) kinase inhibitors and SCC formation is well known. For instance, sorafenib—a multikinase inhibitor that is downstream in the EGFR pathway—has been noted to induce epidermal growths including KAs and SCCs.⁵ There has been no definitive causal relationship identified between the development of SCC and TNF-α inhibitors. It has been suggested that perhaps there is an unmasking effect, as subclinical SCC manifests after TNF-α inhibition that leads to SCC development. Discontinuation of etanercept and resolution of lesions highlights a potential role of TNF-α inhibition and tumorigenesis of SCCs, especially in the background of porokeratosis. Vigilance for development of immunosuppression-induced malignancy, especially squamous cell proliferations, has become exceedingly important with exponentially increasing use of biologic therapies in medicine.

Obesity, atopic dermatitis, psychiatric disease, and arthritis are the most common comorbidities among infants, children, and adolescents with psoriasis, while predictors of moderate to severe disease include morphology, non-White race, and culture-confirmed infection.

Those are among the key findings from a retrospective analysis of pediatric psoriasis patients who were seen at the University of California, San Francisco, over a 24-year period.

“Overall, our data support prior findings of age- and sex-based differences in location and morphology and presents new information demonstrating associations with severity,” presenting study author Carmel Aghdasi said during the annual meeting of the Society for Pediatric Dermatology. “We provide evidence of the increased use of systemic and biologic therapies over time, an important step in ensuring pediatric patients are adequately treated.”

To characterize the demographics, clinical features, comorbidities, and treatments, and to determine predictors of severity and changes in treatment patterns over 2 decades in a large cohort of pediatric psoriasis patients, Ms. Aghdasi, a 4th-year medical student at the University of California, San Francisco, and colleagues retrospectively evaluated the records of 754 pediatric patients up to 18 years of age who were seen at UCSF for psoriasis from 1997 to 2021. They collected demographic, clinical, familial, comorbidity, and treatment data and divided the cohort into two groups by date of last visit.

Group 1 consisted of 332 patients whose last visit was between 2001 and 2011, while the second group included 422 patients whose last visit was between 2012 and 2021. The researchers also divided the cohort into three age groups: infants (0-2 years of age), children (3-12 years of age), and adolescents (13-18 years of age).

Slightly more than half of the patients (55%) were female and 67% presented between ages 3 and 12. (Seventy-four patients were in the youngest category, 0-2 years, when they presented.) The average age of disease onset was 7 years, the average age at presentation to pediatric dermatology was 8.8 years, and 37% of the total cohort were overweight or obese. The top four comorbidities were being overweight or obese (37%), followed by atopic dermatitis (19%), psychiatric disease (7%), and arthritis (4%).

Plaque was the most common morphology (56%), while the most common sites of involvement were the head and neck (69%), extremities (61%), and trunk (44%). About half of the cohort (51%) had mild disease, 15% had culture-confirmed infections (9% had Streptococcal infections), and 66% of patients reported itch as a symptom.

The researchers observed that inverse psoriasis was significantly more common in infants and decreased with age. Anogenital involvement was more common in males and in those aged 0-2, while head and neck involvement was more common in females. Nail involvement was more common in childhood.

Topical therapy was the most common treatment overall and by far the most common among those in the 0-2 age category. “Overall, phototherapy was used in childhood and adolescents but almost never in infancy,” Ms. Aghdasi said. “Looking at changes in systemic treatment over time, conventional systemic use increased in infants and children and decreased in adolescents. Biologic use increased in all ages, most notably in children aged 3-12 years old.”

Multivariate regression analyses revealed that the following independent variables predicted moderate to severe psoriasis: adolescent age (adjusted odds ratio, 1.9; P = .03), guttate morphology (aOR, 2.2; P = .006), plaque and guttate morphology (aOR, 7.6; P less than .001), pustular or erythrodermic morphology (aOR, 5; P = .003), culture-confirmed infection (aOR, 2; P = .007), Black race (aOR, 3.3; P = .007), Asian race (aOR, 1.8; P = .04, and Hispanic race (aOR, 1.9; P = .03).

“Further analysis is needed to elucidate the influence of race on severity and of the clinical utility of infection as a marker of severity,” Ms. Aghdasi said. “Interestingly, we did not find that obesity was a marker of severity in our cohort.”

In an interview, senior study author Kelly M. Cordoro, MD, professor of dermatology and pediatrics at UCSF, noted that this finding conflicts with prior studies showing an association between obesity and severe psoriasis in children.

[email protected]

Obesity, atopic dermatitis, psychiatric disease, and arthritis are the most common comorbidities among infants, children, and adolescents with psoriasis, while predictors of moderate to severe disease include morphology, non-White race, and culture-confirmed infection.

Those are among the key findings from a retrospective analysis of pediatric psoriasis patients who were seen at the University of California, San Francisco, over a 24-year period.

“Overall, our data support prior findings of age- and sex-based differences in location and morphology and presents new information demonstrating associations with severity,” presenting study author Carmel Aghdasi said during the annual meeting of the Society for Pediatric Dermatology. “We provide evidence of the increased use of systemic and biologic therapies over time, an important step in ensuring pediatric patients are adequately treated.”

To characterize the demographics, clinical features, comorbidities, and treatments, and to determine predictors of severity and changes in treatment patterns over 2 decades in a large cohort of pediatric psoriasis patients, Ms. Aghdasi, a 4th-year medical student at the University of California, San Francisco, and colleagues retrospectively evaluated the records of 754 pediatric patients up to 18 years of age who were seen at UCSF for psoriasis from 1997 to 2021. They collected demographic, clinical, familial, comorbidity, and treatment data and divided the cohort into two groups by date of last visit.

Group 1 consisted of 332 patients whose last visit was between 2001 and 2011, while the second group included 422 patients whose last visit was between 2012 and 2021. The researchers also divided the cohort into three age groups: infants (0-2 years of age), children (3-12 years of age), and adolescents (13-18 years of age).

Slightly more than half of the patients (55%) were female and 67% presented between ages 3 and 12. (Seventy-four patients were in the youngest category, 0-2 years, when they presented.) The average age of disease onset was 7 years, the average age at presentation to pediatric dermatology was 8.8 years, and 37% of the total cohort were overweight or obese. The top four comorbidities were being overweight or obese (37%), followed by atopic dermatitis (19%), psychiatric disease (7%), and arthritis (4%).

Plaque was the most common morphology (56%), while the most common sites of involvement were the head and neck (69%), extremities (61%), and trunk (44%). About half of the cohort (51%) had mild disease, 15% had culture-confirmed infections (9% had Streptococcal infections), and 66% of patients reported itch as a symptom.

The researchers observed that inverse psoriasis was significantly more common in infants and decreased with age. Anogenital involvement was more common in males and in those aged 0-2, while head and neck involvement was more common in females. Nail involvement was more common in childhood.

Topical therapy was the most common treatment overall and by far the most common among those in the 0-2 age category. “Overall, phototherapy was used in childhood and adolescents but almost never in infancy,” Ms. Aghdasi said. “Looking at changes in systemic treatment over time, conventional systemic use increased in infants and children and decreased in adolescents. Biologic use increased in all ages, most notably in children aged 3-12 years old.”

Multivariate regression analyses revealed that the following independent variables predicted moderate to severe psoriasis: adolescent age (adjusted odds ratio, 1.9; P = .03), guttate morphology (aOR, 2.2; P = .006), plaque and guttate morphology (aOR, 7.6; P less than .001), pustular or erythrodermic morphology (aOR, 5; P = .003), culture-confirmed infection (aOR, 2; P = .007), Black race (aOR, 3.3; P = .007), Asian race (aOR, 1.8; P = .04, and Hispanic race (aOR, 1.9; P = .03).

“Further analysis is needed to elucidate the influence of race on severity and of the clinical utility of infection as a marker of severity,” Ms. Aghdasi said. “Interestingly, we did not find that obesity was a marker of severity in our cohort.”

In an interview, senior study author Kelly M. Cordoro, MD, professor of dermatology and pediatrics at UCSF, noted that this finding conflicts with prior studies showing an association between obesity and severe psoriasis in children.

[email protected]

Obesity, atopic dermatitis, psychiatric disease, and arthritis are the most common comorbidities among infants, children, and adolescents with psoriasis, while predictors of moderate to severe disease include morphology, non-White race, and culture-confirmed infection.

Those are among the key findings from a retrospective analysis of pediatric psoriasis patients who were seen at the University of California, San Francisco, over a 24-year period.

“Overall, our data support prior findings of age- and sex-based differences in location and morphology and presents new information demonstrating associations with severity,” presenting study author Carmel Aghdasi said during the annual meeting of the Society for Pediatric Dermatology. “We provide evidence of the increased use of systemic and biologic therapies over time, an important step in ensuring pediatric patients are adequately treated.”

To characterize the demographics, clinical features, comorbidities, and treatments, and to determine predictors of severity and changes in treatment patterns over 2 decades in a large cohort of pediatric psoriasis patients, Ms. Aghdasi, a 4th-year medical student at the University of California, San Francisco, and colleagues retrospectively evaluated the records of 754 pediatric patients up to 18 years of age who were seen at UCSF for psoriasis from 1997 to 2021. They collected demographic, clinical, familial, comorbidity, and treatment data and divided the cohort into two groups by date of last visit.

Group 1 consisted of 332 patients whose last visit was between 2001 and 2011, while the second group included 422 patients whose last visit was between 2012 and 2021. The researchers also divided the cohort into three age groups: infants (0-2 years of age), children (3-12 years of age), and adolescents (13-18 years of age).

Slightly more than half of the patients (55%) were female and 67% presented between ages 3 and 12. (Seventy-four patients were in the youngest category, 0-2 years, when they presented.) The average age of disease onset was 7 years, the average age at presentation to pediatric dermatology was 8.8 years, and 37% of the total cohort were overweight or obese. The top four comorbidities were being overweight or obese (37%), followed by atopic dermatitis (19%), psychiatric disease (7%), and arthritis (4%).

Plaque was the most common morphology (56%), while the most common sites of involvement were the head and neck (69%), extremities (61%), and trunk (44%). About half of the cohort (51%) had mild disease, 15% had culture-confirmed infections (9% had Streptococcal infections), and 66% of patients reported itch as a symptom.

The researchers observed that inverse psoriasis was significantly more common in infants and decreased with age. Anogenital involvement was more common in males and in those aged 0-2, while head and neck involvement was more common in females. Nail involvement was more common in childhood.

Topical therapy was the most common treatment overall and by far the most common among those in the 0-2 age category. “Overall, phototherapy was used in childhood and adolescents but almost never in infancy,” Ms. Aghdasi said. “Looking at changes in systemic treatment over time, conventional systemic use increased in infants and children and decreased in adolescents. Biologic use increased in all ages, most notably in children aged 3-12 years old.”

Multivariate regression analyses revealed that the following independent variables predicted moderate to severe psoriasis: adolescent age (adjusted odds ratio, 1.9; P = .03), guttate morphology (aOR, 2.2; P = .006), plaque and guttate morphology (aOR, 7.6; P less than .001), pustular or erythrodermic morphology (aOR, 5; P = .003), culture-confirmed infection (aOR, 2; P = .007), Black race (aOR, 3.3; P = .007), Asian race (aOR, 1.8; P = .04, and Hispanic race (aOR, 1.9; P = .03).

“Further analysis is needed to elucidate the influence of race on severity and of the clinical utility of infection as a marker of severity,” Ms. Aghdasi said. “Interestingly, we did not find that obesity was a marker of severity in our cohort.”

In an interview, senior study author Kelly M. Cordoro, MD, professor of dermatology and pediatrics at UCSF, noted that this finding conflicts with prior studies showing an association between obesity and severe psoriasis in children.

[email protected]

To the Editor:

A 56-year-old man with a history of stage IV metastatic penile squamous cell carcinoma treated with penectomy and chemotherapy with 5-fluorouracil and cisplatin presented with several painful ulcerations in the groin, abdomen, and thighs. The lesions initially appeared in the groin and were treated as bacterial abscesses with antibiotics. Over the next few weeks, new lesions appeared on the abdomen and thighs. An additional cycle of chemotherapy led to a reduction in number; however, they again increased within a few weeks. Medications included enoxaparin followed by 3 weeks of warfarin use due to a right leg deep vein thrombosis.

Physical examination revealed multiple 1- to 4-cm, firm, ulcerated nodules on the bilateral inguinal folds, abdomen, and upper thighs, as well as areas of livedo racemosa and noninflammatory retiform purpura with central ulceration (Figures 1 and 2). This retiform purpura was both perilesional and in areas without ulcerations. Laboratory values included the following: sodium, 127 mmol/L (reference range, 136–145 mmol/L); prothrombin time, 16.1 seconds (reference range, 11–15 seconds); white blood cell count, 20.69×10⁹/L (reference range, 4.5–11.0×10⁹/L) with 87% neutrophils (reference range, 54%–62%); hemoglobin, 6.1 g/dL (reference range, 13.5–17.5 g/dL); hematocrit, 18.8% (reference range, 41%–53%); platelets, 474×10⁹/L (reference range, 150–400×10⁹/L); D-dimer, 0.77 mg/L (reference range, ≤0.50 mg/L); fibrinogen, 489 mg/dL (reference range, 150–400 mg/dL); prior urine culture positive for Pseudomonas aeruginosa. He was negative for hepatitis B and hepatitis C viruses as well as HIV, and the lesions were not clinically consistent with herpes simplex virus, as they were not scalloped or circinate. Punch biopsies were obtained from a nodule on the left leg and a purpuric patch on the right leg.

Ischemic cutaneous lesions less commonly occur in the setting of malignancy and can be the result of both direct and indirect systemic effects from the cancer. Malignancies are known to directly trigger vasculopathies in other organs, most commonly the lungs, through 2 primary mechanisms. First, in carcinomatous arteriopathy, metastatic cells promote fibrocellular intimal proliferation of small pulmonary arteries and arterioles leading to stenosis, thrombosis, and obliteration. This mechanism has been described in pulmonary thrombotic microangiopathy secondary to lung carcinoma.⁴ This pathophysiology likely is also what underlies paraneoplastic acral vascular syndromes, which culminate in digital ischemia. Hypothesized mechanisms for this ischemia also range from vasospasm to thromboembolism.⁵ Secondly, in vasculitis carcinomatosa, metastatic tumor cells damage or block vessel walls, resulting in end-organ ischemia. Vasculitis carcinomatosa is a well-known phenomenon in angiocentric and intravascular lymphoid malignancies (typically of B-T or natural killer/T-cell origin) but also has been reported in a case of gastric adenocarcinoma with arterial invasion.⁶ This process is different than carcinoma telangiectoides where malignant cells may be present in the vasculature on histopathology but not trigger thrombosis and ischemic skin necrosis.

Systemic coagulopathies such as disseminated intravascular coagulation (DIC), thrombotic thrombocytopenia purpura, and catastrophic antiphospholipid antibody syndrome can occur in the setting of malignancies.⁷ Clinically, all may present with livedo racemosa, noninflammatory retiform purpura, and widespread skin necrosis. In adult patients, purpura fulminans most often is seen in the setting of sepsis and DIC, with accompanying evidence of microangiopathy.⁸ Catastrophic antiphospholipid antibody syndrome can be triggered by malignancy and is characterized by central nervous system, renal, pulmonary, and gastrointestinal complications. Skin involvement such as ulcers, livedo reticularis, and gangrene have been reported.⁹ Other causes of thrombotic vasculopathy include warfarin necrosis, heparin-induced thrombotic thrombocytopenia, calciphylaxis, and angioinvasive infections.⁸ Warfarin necrosis and heparin-induced thrombotic thrombocytopenia typically present days after initiating therapy with the respective medication. Calciphylaxis typically occurs in patients on dialysis, though it may occur in nonuremic patients including those with malignancy.⁸ Patients with malignancies on chemotherapy can become neutropenic and are at risk for ecthyma gangrenosum due to P aeruginosa and other gram-negative rods, Staphylococcus aureus, and angioinvasive fungi.¹⁰

Based on clinical, histopathological, and laboratory data, we favored a diagnosis of cutaneous carcinomatous arteriopathy. Vasculitis carcinomatosa was a possibility despite the lack of vasculotropism on histopathology, which may have been due to biopsy site selection. Systemic coagulopathies such as DIC, thrombotic thrombocytopenia purpura, and catastrophic antiphospholipid antibody syndrome were unlikely, as the ischemic skin lesions and livedo racemosa were limited to areas adjacent to cutaneous metastases, and the patient lacked other common multiorgan manifestations or laboratory findings. Although our patient was on warfarin, he was on a stable dose for weeks and histopathologic features of subcutaneous thrombosis were not seen. The biopsy also was not consistent with calciphylaxis. Ecthyma gangrenosum was unlikely given the lack of organisms on histopathology and negative skin and blood cultures. Although additional laboratory testing in this patient may have included cryoglobulins and cryofibrinogens, both entities were unlikely due to a lack of ischemic acral lesions.

In conclusion, we present a case of localized thrombotic vasculopathy that likely was secondary to cutaneous carcinomatous arteriopathy in the setting of cutaneous metastatic penile squamous cell carcinoma. The differential diagnosis of retiform purpura, livedo racemosa, and other signs of cutaneous ischemia in patients with metastatic cancer is broad and can be the result of both direct and indirect systemic effects from the cancer. Appropriate workup in these cases should include skin biopsies for histopathology and culture, medication review, and laboratory evaluation for systemic coagulopathies.

To the Editor:

A 56-year-old man with a history of stage IV metastatic penile squamous cell carcinoma treated with penectomy and chemotherapy with 5-fluorouracil and cisplatin presented with several painful ulcerations in the groin, abdomen, and thighs. The lesions initially appeared in the groin and were treated as bacterial abscesses with antibiotics. Over the next few weeks, new lesions appeared on the abdomen and thighs. An additional cycle of chemotherapy led to a reduction in number; however, they again increased within a few weeks. Medications included enoxaparin followed by 3 weeks of warfarin use due to a right leg deep vein thrombosis.

Physical examination revealed multiple 1- to 4-cm, firm, ulcerated nodules on the bilateral inguinal folds, abdomen, and upper thighs, as well as areas of livedo racemosa and noninflammatory retiform purpura with central ulceration (Figures 1 and 2). This retiform purpura was both perilesional and in areas without ulcerations. Laboratory values included the following: sodium, 127 mmol/L (reference range, 136–145 mmol/L); prothrombin time, 16.1 seconds (reference range, 11–15 seconds); white blood cell count, 20.69×10⁹/L (reference range, 4.5–11.0×10⁹/L) with 87% neutrophils (reference range, 54%–62%); hemoglobin, 6.1 g/dL (reference range, 13.5–17.5 g/dL); hematocrit, 18.8% (reference range, 41%–53%); platelets, 474×10⁹/L (reference range, 150–400×10⁹/L); D-dimer, 0.77 mg/L (reference range, ≤0.50 mg/L); fibrinogen, 489 mg/dL (reference range, 150–400 mg/dL); prior urine culture positive for Pseudomonas aeruginosa. He was negative for hepatitis B and hepatitis C viruses as well as HIV, and the lesions were not clinically consistent with herpes simplex virus, as they were not scalloped or circinate. Punch biopsies were obtained from a nodule on the left leg and a purpuric patch on the right leg.

Ischemic cutaneous lesions less commonly occur in the setting of malignancy and can be the result of both direct and indirect systemic effects from the cancer. Malignancies are known to directly trigger vasculopathies in other organs, most commonly the lungs, through 2 primary mechanisms. First, in carcinomatous arteriopathy, metastatic cells promote fibrocellular intimal proliferation of small pulmonary arteries and arterioles leading to stenosis, thrombosis, and obliteration. This mechanism has been described in pulmonary thrombotic microangiopathy secondary to lung carcinoma.⁴ This pathophysiology likely is also what underlies paraneoplastic acral vascular syndromes, which culminate in digital ischemia. Hypothesized mechanisms for this ischemia also range from vasospasm to thromboembolism.⁵ Secondly, in vasculitis carcinomatosa, metastatic tumor cells damage or block vessel walls, resulting in end-organ ischemia. Vasculitis carcinomatosa is a well-known phenomenon in angiocentric and intravascular lymphoid malignancies (typically of B-T or natural killer/T-cell origin) but also has been reported in a case of gastric adenocarcinoma with arterial invasion.⁶ This process is different than carcinoma telangiectoides where malignant cells may be present in the vasculature on histopathology but not trigger thrombosis and ischemic skin necrosis.

Systemic coagulopathies such as disseminated intravascular coagulation (DIC), thrombotic thrombocytopenia purpura, and catastrophic antiphospholipid antibody syndrome can occur in the setting of malignancies.⁷ Clinically, all may present with livedo racemosa, noninflammatory retiform purpura, and widespread skin necrosis. In adult patients, purpura fulminans most often is seen in the setting of sepsis and DIC, with accompanying evidence of microangiopathy.⁸ Catastrophic antiphospholipid antibody syndrome can be triggered by malignancy and is characterized by central nervous system, renal, pulmonary, and gastrointestinal complications. Skin involvement such as ulcers, livedo reticularis, and gangrene have been reported.⁹ Other causes of thrombotic vasculopathy include warfarin necrosis, heparin-induced thrombotic thrombocytopenia, calciphylaxis, and angioinvasive infections.⁸ Warfarin necrosis and heparin-induced thrombotic thrombocytopenia typically present days after initiating therapy with the respective medication. Calciphylaxis typically occurs in patients on dialysis, though it may occur in nonuremic patients including those with malignancy.⁸ Patients with malignancies on chemotherapy can become neutropenic and are at risk for ecthyma gangrenosum due to P aeruginosa and other gram-negative rods, Staphylococcus aureus, and angioinvasive fungi.¹⁰

Based on clinical, histopathological, and laboratory data, we favored a diagnosis of cutaneous carcinomatous arteriopathy. Vasculitis carcinomatosa was a possibility despite the lack of vasculotropism on histopathology, which may have been due to biopsy site selection. Systemic coagulopathies such as DIC, thrombotic thrombocytopenia purpura, and catastrophic antiphospholipid antibody syndrome were unlikely, as the ischemic skin lesions and livedo racemosa were limited to areas adjacent to cutaneous metastases, and the patient lacked other common multiorgan manifestations or laboratory findings. Although our patient was on warfarin, he was on a stable dose for weeks and histopathologic features of subcutaneous thrombosis were not seen. The biopsy also was not consistent with calciphylaxis. Ecthyma gangrenosum was unlikely given the lack of organisms on histopathology and negative skin and blood cultures. Although additional laboratory testing in this patient may have included cryoglobulins and cryofibrinogens, both entities were unlikely due to a lack of ischemic acral lesions.

In conclusion, we present a case of localized thrombotic vasculopathy that likely was secondary to cutaneous carcinomatous arteriopathy in the setting of cutaneous metastatic penile squamous cell carcinoma. The differential diagnosis of retiform purpura, livedo racemosa, and other signs of cutaneous ischemia in patients with metastatic cancer is broad and can be the result of both direct and indirect systemic effects from the cancer. Appropriate workup in these cases should include skin biopsies for histopathology and culture, medication review, and laboratory evaluation for systemic coagulopathies.

To the Editor:

A 56-year-old man with a history of stage IV metastatic penile squamous cell carcinoma treated with penectomy and chemotherapy with 5-fluorouracil and cisplatin presented with several painful ulcerations in the groin, abdomen, and thighs. The lesions initially appeared in the groin and were treated as bacterial abscesses with antibiotics. Over the next few weeks, new lesions appeared on the abdomen and thighs. An additional cycle of chemotherapy led to a reduction in number; however, they again increased within a few weeks. Medications included enoxaparin followed by 3 weeks of warfarin use due to a right leg deep vein thrombosis.

Physical examination revealed multiple 1- to 4-cm, firm, ulcerated nodules on the bilateral inguinal folds, abdomen, and upper thighs, as well as areas of livedo racemosa and noninflammatory retiform purpura with central ulceration (Figures 1 and 2). This retiform purpura was both perilesional and in areas without ulcerations. Laboratory values included the following: sodium, 127 mmol/L (reference range, 136–145 mmol/L); prothrombin time, 16.1 seconds (reference range, 11–15 seconds); white blood cell count, 20.69×10⁹/L (reference range, 4.5–11.0×10⁹/L) with 87% neutrophils (reference range, 54%–62%); hemoglobin, 6.1 g/dL (reference range, 13.5–17.5 g/dL); hematocrit, 18.8% (reference range, 41%–53%); platelets, 474×10⁹/L (reference range, 150–400×10⁹/L); D-dimer, 0.77 mg/L (reference range, ≤0.50 mg/L); fibrinogen, 489 mg/dL (reference range, 150–400 mg/dL); prior urine culture positive for Pseudomonas aeruginosa. He was negative for hepatitis B and hepatitis C viruses as well as HIV, and the lesions were not clinically consistent with herpes simplex virus, as they were not scalloped or circinate. Punch biopsies were obtained from a nodule on the left leg and a purpuric patch on the right leg.

Ischemic cutaneous lesions less commonly occur in the setting of malignancy and can be the result of both direct and indirect systemic effects from the cancer. Malignancies are known to directly trigger vasculopathies in other organs, most commonly the lungs, through 2 primary mechanisms. First, in carcinomatous arteriopathy, metastatic cells promote fibrocellular intimal proliferation of small pulmonary arteries and arterioles leading to stenosis, thrombosis, and obliteration. This mechanism has been described in pulmonary thrombotic microangiopathy secondary to lung carcinoma.⁴ This pathophysiology likely is also what underlies paraneoplastic acral vascular syndromes, which culminate in digital ischemia. Hypothesized mechanisms for this ischemia also range from vasospasm to thromboembolism.⁵ Secondly, in vasculitis carcinomatosa, metastatic tumor cells damage or block vessel walls, resulting in end-organ ischemia. Vasculitis carcinomatosa is a well-known phenomenon in angiocentric and intravascular lymphoid malignancies (typically of B-T or natural killer/T-cell origin) but also has been reported in a case of gastric adenocarcinoma with arterial invasion.⁶ This process is different than carcinoma telangiectoides where malignant cells may be present in the vasculature on histopathology but not trigger thrombosis and ischemic skin necrosis.

Systemic coagulopathies such as disseminated intravascular coagulation (DIC), thrombotic thrombocytopenia purpura, and catastrophic antiphospholipid antibody syndrome can occur in the setting of malignancies.⁷ Clinically, all may present with livedo racemosa, noninflammatory retiform purpura, and widespread skin necrosis. In adult patients, purpura fulminans most often is seen in the setting of sepsis and DIC, with accompanying evidence of microangiopathy.⁸ Catastrophic antiphospholipid antibody syndrome can be triggered by malignancy and is characterized by central nervous system, renal, pulmonary, and gastrointestinal complications. Skin involvement such as ulcers, livedo reticularis, and gangrene have been reported.⁹ Other causes of thrombotic vasculopathy include warfarin necrosis, heparin-induced thrombotic thrombocytopenia, calciphylaxis, and angioinvasive infections.⁸ Warfarin necrosis and heparin-induced thrombotic thrombocytopenia typically present days after initiating therapy with the respective medication. Calciphylaxis typically occurs in patients on dialysis, though it may occur in nonuremic patients including those with malignancy.⁸ Patients with malignancies on chemotherapy can become neutropenic and are at risk for ecthyma gangrenosum due to P aeruginosa and other gram-negative rods, Staphylococcus aureus, and angioinvasive fungi.¹⁰

Based on clinical, histopathological, and laboratory data, we favored a diagnosis of cutaneous carcinomatous arteriopathy. Vasculitis carcinomatosa was a possibility despite the lack of vasculotropism on histopathology, which may have been due to biopsy site selection. Systemic coagulopathies such as DIC, thrombotic thrombocytopenia purpura, and catastrophic antiphospholipid antibody syndrome were unlikely, as the ischemic skin lesions and livedo racemosa were limited to areas adjacent to cutaneous metastases, and the patient lacked other common multiorgan manifestations or laboratory findings. Although our patient was on warfarin, he was on a stable dose for weeks and histopathologic features of subcutaneous thrombosis were not seen. The biopsy also was not consistent with calciphylaxis. Ecthyma gangrenosum was unlikely given the lack of organisms on histopathology and negative skin and blood cultures. Although additional laboratory testing in this patient may have included cryoglobulins and cryofibrinogens, both entities were unlikely due to a lack of ischemic acral lesions.

In conclusion, we present a case of localized thrombotic vasculopathy that likely was secondary to cutaneous carcinomatous arteriopathy in the setting of cutaneous metastatic penile squamous cell carcinoma. The differential diagnosis of retiform purpura, livedo racemosa, and other signs of cutaneous ischemia in patients with metastatic cancer is broad and can be the result of both direct and indirect systemic effects from the cancer. Appropriate workup in these cases should include skin biopsies for histopathology and culture, medication review, and laboratory evaluation for systemic coagulopathies.

Intraosseous (IO) access can afford a lifesaving means of vascular access in emergency settings, as it allows for the administration of large volumes of fluids, blood products, and medications at high flow rates directly into the highly vascularized osseous medullary cavity.¹ Fortunately, the complication rate with this resuscitative effort is low, with many reports demonstrating complication rates of less than 1%.² The most commonly reported complications include fluid extravasation, osteomyelitis, traumatic bone fracture, and epiphyseal plate damage.^1-3 Although compartment syndrome and skin necrosis have been reported,^4,5 there is no comprehensive list of sequelae resulting from fluid extravasation in the literature, and there are no known studies examining the incidence and types of cutaneous complications. In this study, we sought to evaluate the dermatologic impacts of this procedure.

Methods

We performed a retrospective chart review approved by the institutional review board at a large metropolitan level I trauma center in the Midwestern United States spanning 18 consecutive months to identify all patients who underwent IO line placement, either en route to or upon arrival at the trauma center. The electronic medical records of 113 patients (age range, 10 days–94 years) were identified using either an automated natural language look-up program with keywords including intraosseous access and IO or a Current Procedural Terminology code 36680. Data including patient age, reason for IO insertion, anatomic location of the IO, and complications secondary to IO line placement were recorded.

Results

We identified an overall complication rate of 2.7% (3/113), with only 1 patient showing isolated cutaneous complications from IO line placement. The complications in the first 2 patients included compartment syndrome following IO line placement in the right tibia and needle breakage during IO line placement. The third patient, a 30-year-old heart transplant recipient, developed tense bullae on the left leg 5 days after a resuscitative effort required IO access through the bilateral tibiae. The patient had received vasopressors as well as 750 mL of normal saline through these access points. Two days after resuscitation, she developed an enlarging ecchymosis around the left IO access point. On day 5, cutaneous findings included 2 large firm bullae on a purpuric base overlying the left proximal tibia and patella (Figure 1). After an ultrasound revealed no connection to the underlying joint space, the bullae were incised and drained for patient comfort, as she reported pain and undue pressure at the knee joint on initial dermatologic consultation. These symptoms abated after the procedure. Cultures of bullous fluid were negative for infection. Histopathologic examination revealed a subepidermal split with underlying minimal mixed inflammation, favoring the diagnosis of traumatic bullae.

At a scheduled 7-month dermatology follow-up, the wound bed appeared to be healing well with surrounding scarring with no residual bleeding or drainage (Figure 2) despite the patient reporting a protracted course of wound healing requiring debridement due to eschar formation and multiple follow-up appointments with the wound care service.

Comment

The most commonly reported complications with IO line placement result from fluid infiltration of the subcutaneous tissue secondary to catheter misplacement.^1,3 Extravasated fluid may lead to tissue damage, compartment syndrome, and even tissue necrosis in some cases.^1,4,5 Localized cellulitis and the formation of subcutaneous abscesses also have been reported, albeit rarely.^3,5

In our retrospective cohort review, we identified an additional potential complication of IO line placement that has not been widely reported—development of large traumatic bullae. It is most likely that this patient’s IO catheter became dislodged, resulting in extravasation of fluids into the dermal and subcutaneous tissues.

Our findings support the previously noted complication rate of less than 1% following IO line placement, with an overall complication rate of 2.7% that included only 1 patient with a cutaneous complication.² Given this low incidence, providers may not be used to recognizing such complications, leading to delayed or incorrect diagnosis of these entities. While there are certain conditions in which IO insertion is contraindicated, including severe bone diseases (eg, osteogenesis imperfecta, osteomyelitis), overlying cellulitis, and bone fracture, these conditions are rare and can be avoided in most cases by use of an alternative site for needle insertion.² Due to the widespread utility of this tool and its few contraindications, its use in hospitalized patients is rapidly increasing, necessitating a need for quick recognition of potential complications.

From previous data on the incidence of traumatic blisters with underlying bone fractures, there are several identifiable risk factors that could be extended to patients at high risk for developing cutaneous IO complications secondary to the trauma associated with needle insertion,⁶ including wound-healing impairments in patients with fragile lymphatics, peripheral vascular disease, diabetes, or collagen vascular diseases (eg, lupus, rheumatoid arthritis, Sjögren syndrome). Patients with these conditions should be closely monitored for the development of bullae.⁶ While the patient we highlighted in our study did not have a history of such conditions, her history of cardiac disease, recent resuscitation attempts, and immunosuppression certainly could have contributed to suboptimal tissue agility and repair after IO line placement.

Conclusion

Intraosseous access is a safe, effective, and reliable option for vascular access in both pediatric and adult populations that is widely used in both prehospital (ie, paramedic administered) and hospital settings, including intensive care units, emergency departments, and any acute situation where rapid vascular access is necessary. This retrospective chart review examining the incidence and types of cutaneous complications associated with IO line placement at a level I trauma center revealed a total complication rate similar to those reported in previous studies and also highlighted a unique postprocedural cutaneous finding of traumatic bullae. Although no unified management recommendations currently exist, providers should consider this complication in the differential for hospitalized patients with large, atypical, asymmetric bullae in the absence of an alternative explanation for such skin findings.

Intraosseous (IO) access can afford a lifesaving means of vascular access in emergency settings, as it allows for the administration of large volumes of fluids, blood products, and medications at high flow rates directly into the highly vascularized osseous medullary cavity.¹ Fortunately, the complication rate with this resuscitative effort is low, with many reports demonstrating complication rates of less than 1%.² The most commonly reported complications include fluid extravasation, osteomyelitis, traumatic bone fracture, and epiphyseal plate damage.^1-3 Although compartment syndrome and skin necrosis have been reported,^4,5 there is no comprehensive list of sequelae resulting from fluid extravasation in the literature, and there are no known studies examining the incidence and types of cutaneous complications. In this study, we sought to evaluate the dermatologic impacts of this procedure.

Methods

We performed a retrospective chart review approved by the institutional review board at a large metropolitan level I trauma center in the Midwestern United States spanning 18 consecutive months to identify all patients who underwent IO line placement, either en route to or upon arrival at the trauma center. The electronic medical records of 113 patients (age range, 10 days–94 years) were identified using either an automated natural language look-up program with keywords including intraosseous access and IO or a Current Procedural Terminology code 36680. Data including patient age, reason for IO insertion, anatomic location of the IO, and complications secondary to IO line placement were recorded.

Results

We identified an overall complication rate of 2.7% (3/113), with only 1 patient showing isolated cutaneous complications from IO line placement. The complications in the first 2 patients included compartment syndrome following IO line placement in the right tibia and needle breakage during IO line placement. The third patient, a 30-year-old heart transplant recipient, developed tense bullae on the left leg 5 days after a resuscitative effort required IO access through the bilateral tibiae. The patient had received vasopressors as well as 750 mL of normal saline through these access points. Two days after resuscitation, she developed an enlarging ecchymosis around the left IO access point. On day 5, cutaneous findings included 2 large firm bullae on a purpuric base overlying the left proximal tibia and patella (Figure 1). After an ultrasound revealed no connection to the underlying joint space, the bullae were incised and drained for patient comfort, as she reported pain and undue pressure at the knee joint on initial dermatologic consultation. These symptoms abated after the procedure. Cultures of bullous fluid were negative for infection. Histopathologic examination revealed a subepidermal split with underlying minimal mixed inflammation, favoring the diagnosis of traumatic bullae.

At a scheduled 7-month dermatology follow-up, the wound bed appeared to be healing well with surrounding scarring with no residual bleeding or drainage (Figure 2) despite the patient reporting a protracted course of wound healing requiring debridement due to eschar formation and multiple follow-up appointments with the wound care service.

Comment

The most commonly reported complications with IO line placement result from fluid infiltration of the subcutaneous tissue secondary to catheter misplacement.^1,3 Extravasated fluid may lead to tissue damage, compartment syndrome, and even tissue necrosis in some cases.^1,4,5 Localized cellulitis and the formation of subcutaneous abscesses also have been reported, albeit rarely.^3,5

In our retrospective cohort review, we identified an additional potential complication of IO line placement that has not been widely reported—development of large traumatic bullae. It is most likely that this patient’s IO catheter became dislodged, resulting in extravasation of fluids into the dermal and subcutaneous tissues.

Our findings support the previously noted complication rate of less than 1% following IO line placement, with an overall complication rate of 2.7% that included only 1 patient with a cutaneous complication.² Given this low incidence, providers may not be used to recognizing such complications, leading to delayed or incorrect diagnosis of these entities. While there are certain conditions in which IO insertion is contraindicated, including severe bone diseases (eg, osteogenesis imperfecta, osteomyelitis), overlying cellulitis, and bone fracture, these conditions are rare and can be avoided in most cases by use of an alternative site for needle insertion.² Due to the widespread utility of this tool and its few contraindications, its use in hospitalized patients is rapidly increasing, necessitating a need for quick recognition of potential complications.

From previous data on the incidence of traumatic blisters with underlying bone fractures, there are several identifiable risk factors that could be extended to patients at high risk for developing cutaneous IO complications secondary to the trauma associated with needle insertion,⁶ including wound-healing impairments in patients with fragile lymphatics, peripheral vascular disease, diabetes, or collagen vascular diseases (eg, lupus, rheumatoid arthritis, Sjögren syndrome). Patients with these conditions should be closely monitored for the development of bullae.⁶ While the patient we highlighted in our study did not have a history of such conditions, her history of cardiac disease, recent resuscitation attempts, and immunosuppression certainly could have contributed to suboptimal tissue agility and repair after IO line placement.

Conclusion

Intraosseous access is a safe, effective, and reliable option for vascular access in both pediatric and adult populations that is widely used in both prehospital (ie, paramedic administered) and hospital settings, including intensive care units, emergency departments, and any acute situation where rapid vascular access is necessary. This retrospective chart review examining the incidence and types of cutaneous complications associated with IO line placement at a level I trauma center revealed a total complication rate similar to those reported in previous studies and also highlighted a unique postprocedural cutaneous finding of traumatic bullae. Although no unified management recommendations currently exist, providers should consider this complication in the differential for hospitalized patients with large, atypical, asymmetric bullae in the absence of an alternative explanation for such skin findings.

Intraosseous (IO) access can afford a lifesaving means of vascular access in emergency settings, as it allows for the administration of large volumes of fluids, blood products, and medications at high flow rates directly into the highly vascularized osseous medullary cavity.¹ Fortunately, the complication rate with this resuscitative effort is low, with many reports demonstrating complication rates of less than 1%.² The most commonly reported complications include fluid extravasation, osteomyelitis, traumatic bone fracture, and epiphyseal plate damage.^1-3 Although compartment syndrome and skin necrosis have been reported,^4,5 there is no comprehensive list of sequelae resulting from fluid extravasation in the literature, and there are no known studies examining the incidence and types of cutaneous complications. In this study, we sought to evaluate the dermatologic impacts of this procedure.

Methods

We performed a retrospective chart review approved by the institutional review board at a large metropolitan level I trauma center in the Midwestern United States spanning 18 consecutive months to identify all patients who underwent IO line placement, either en route to or upon arrival at the trauma center. The electronic medical records of 113 patients (age range, 10 days–94 years) were identified using either an automated natural language look-up program with keywords including intraosseous access and IO or a Current Procedural Terminology code 36680. Data including patient age, reason for IO insertion, anatomic location of the IO, and complications secondary to IO line placement were recorded.

Results

We identified an overall complication rate of 2.7% (3/113), with only 1 patient showing isolated cutaneous complications from IO line placement. The complications in the first 2 patients included compartment syndrome following IO line placement in the right tibia and needle breakage during IO line placement. The third patient, a 30-year-old heart transplant recipient, developed tense bullae on the left leg 5 days after a resuscitative effort required IO access through the bilateral tibiae. The patient had received vasopressors as well as 750 mL of normal saline through these access points. Two days after resuscitation, she developed an enlarging ecchymosis around the left IO access point. On day 5, cutaneous findings included 2 large firm bullae on a purpuric base overlying the left proximal tibia and patella (Figure 1). After an ultrasound revealed no connection to the underlying joint space, the bullae were incised and drained for patient comfort, as she reported pain and undue pressure at the knee joint on initial dermatologic consultation. These symptoms abated after the procedure. Cultures of bullous fluid were negative for infection. Histopathologic examination revealed a subepidermal split with underlying minimal mixed inflammation, favoring the diagnosis of traumatic bullae.

At a scheduled 7-month dermatology follow-up, the wound bed appeared to be healing well with surrounding scarring with no residual bleeding or drainage (Figure 2) despite the patient reporting a protracted course of wound healing requiring debridement due to eschar formation and multiple follow-up appointments with the wound care service.

Comment

The most commonly reported complications with IO line placement result from fluid infiltration of the subcutaneous tissue secondary to catheter misplacement.^1,3 Extravasated fluid may lead to tissue damage, compartment syndrome, and even tissue necrosis in some cases.^1,4,5 Localized cellulitis and the formation of subcutaneous abscesses also have been reported, albeit rarely.^3,5

In our retrospective cohort review, we identified an additional potential complication of IO line placement that has not been widely reported—development of large traumatic bullae. It is most likely that this patient’s IO catheter became dislodged, resulting in extravasation of fluids into the dermal and subcutaneous tissues.

Our findings support the previously noted complication rate of less than 1% following IO line placement, with an overall complication rate of 2.7% that included only 1 patient with a cutaneous complication.² Given this low incidence, providers may not be used to recognizing such complications, leading to delayed or incorrect diagnosis of these entities. While there are certain conditions in which IO insertion is contraindicated, including severe bone diseases (eg, osteogenesis imperfecta, osteomyelitis), overlying cellulitis, and bone fracture, these conditions are rare and can be avoided in most cases by use of an alternative site for needle insertion.² Due to the widespread utility of this tool and its few contraindications, its use in hospitalized patients is rapidly increasing, necessitating a need for quick recognition of potential complications.

From previous data on the incidence of traumatic blisters with underlying bone fractures, there are several identifiable risk factors that could be extended to patients at high risk for developing cutaneous IO complications secondary to the trauma associated with needle insertion,⁶ including wound-healing impairments in patients with fragile lymphatics, peripheral vascular disease, diabetes, or collagen vascular diseases (eg, lupus, rheumatoid arthritis, Sjögren syndrome). Patients with these conditions should be closely monitored for the development of bullae.⁶ While the patient we highlighted in our study did not have a history of such conditions, her history of cardiac disease, recent resuscitation attempts, and immunosuppression certainly could have contributed to suboptimal tissue agility and repair after IO line placement.

Conclusion

Intraosseous access is a safe, effective, and reliable option for vascular access in both pediatric and adult populations that is widely used in both prehospital (ie, paramedic administered) and hospital settings, including intensive care units, emergency departments, and any acute situation where rapid vascular access is necessary. This retrospective chart review examining the incidence and types of cutaneous complications associated with IO line placement at a level I trauma center revealed a total complication rate similar to those reported in previous studies and also highlighted a unique postprocedural cutaneous finding of traumatic bullae. Although no unified management recommendations currently exist, providers should consider this complication in the differential for hospitalized patients with large, atypical, asymmetric bullae in the absence of an alternative explanation for such skin findings.

Insert clove A into nostril B

Just when you start wondering what crazy and potentially dangerous thing people can do to themselves next, comes a crazy and potentially dangerous new trend. The good folks at TikTok have provided patients a new treatment for stuffed up sinuses.

Dangerous? Well, that’s what doctors say, anyway.

“We typically do not recommend putting anything into the nostril for the obvious fact that it could get dislodged or lodged up into the nasal cavity,” Anthony Del Signore, MD, of Mount Sinai Union Square, New York, told TODAY.

“Not only does it have the potential to rot or cause a nasal obstruction, it can induce an episode of sinusitis,” Omid Mehdizadeh, MD, of Providence Saint John’s Health Center, Santa Monica, Calif., explained to Shape.

But who doesn't want to breathe easier and keep blood-sucking vampires at bay?

Max Pixel

Seeing faces in random places?

Ever look up at the clouds, at a fast-moving train, or into your morning bowl of cereal and see two eyes, a nose, and a mouth looking back at you? You may shake it off and think you’re imagining something, but it's actually your brain doing what it’s built to do and researchers know why.

The phenomenon is called face pareidolia, and it’s technically an error function of the human brain. Evolution has molded our brains to rapidly identify faces, according to David Alais, PhD, of the University of Sydney, Australia, lead author of the study.

“But the system plays ‘fast and loose’ by applying a crude template of two eyes over a nose and mouth. Lots of things can satisfy that template and thus trigger a face detection response,” he said in a separate statement. But not only are we seeing faces, our brains go one step further and seemingly give those faces feelings.

University of Sydney

Corporate dream manipulation

Advertisements are quite literally everywhere. On billboards, in commercials, in videos, in movies; the list goes on and on. Still, at least you can shut your eyes and be mercifully free of corporate interference inside your own head, right? Right?

Early in 2021, Coors launched an ad campaign that seemed to be a b bit of a gimmick, if not a joke. Coors claimed that if people watched an ad before bed, and played an 8-hour soundscape while sleeping, their dreams would be filled with crisp mountains and cold, thirst-quenching beverages. While, the Coors campaign didn’t go viral, someone was paying attention. A group of 35 leading researchers published an open letter on the subject of corporate dream manipulation, in the journal Dream Engineering.

"Multiple marketing studies are openly testing new ways to alter and motivate purchasing behavior through dream and sleep hacking. The commercial, for-profit use of dream incubation is rapidly becoming a reality," wrote the investigators. "As sleep and dream researchers, we are deeply concerned about marketing plans aimed at generating profits at the cost of interfering with our natural nocturnal memory processing."

People have tried to manipulate their dreams for countless years, but only in recent years have scientists attempted to target or manipulate behavior through dreams. In a 2014 study, smokers exposed to tobacco smoke and rotten egg smell while sleeping reduced their cigarette consumption by 30%.

Free-Photos/Pixabay

Got breast milk?

As we know, breast milk has endless benefits for newbords and babies, but many things can stand in the way of a mother’s ability to breastfeed. Baby formula has served as a good enough substitute. But now, there might be something that’s even better.

A start-up company called BIOMILQ created a product that could be groundbreaking. Using “breakthrough mammary biotechnology,” BIOMILQ created cell-cultured breast milk.

Focus_on_Nature/Getty Images

Insert clove A into nostril B

Just when you start wondering what crazy and potentially dangerous thing people can do to themselves next, comes a crazy and potentially dangerous new trend. The good folks at TikTok have provided patients a new treatment for stuffed up sinuses.

Dangerous? Well, that’s what doctors say, anyway.

“We typically do not recommend putting anything into the nostril for the obvious fact that it could get dislodged or lodged up into the nasal cavity,” Anthony Del Signore, MD, of Mount Sinai Union Square, New York, told TODAY.

“Not only does it have the potential to rot or cause a nasal obstruction, it can induce an episode of sinusitis,” Omid Mehdizadeh, MD, of Providence Saint John’s Health Center, Santa Monica, Calif., explained to Shape.

But who doesn't want to breathe easier and keep blood-sucking vampires at bay?

Max Pixel

Seeing faces in random places?

Ever look up at the clouds, at a fast-moving train, or into your morning bowl of cereal and see two eyes, a nose, and a mouth looking back at you? You may shake it off and think you’re imagining something, but it's actually your brain doing what it’s built to do and researchers know why.

The phenomenon is called face pareidolia, and it’s technically an error function of the human brain. Evolution has molded our brains to rapidly identify faces, according to David Alais, PhD, of the University of Sydney, Australia, lead author of the study.

“But the system plays ‘fast and loose’ by applying a crude template of two eyes over a nose and mouth. Lots of things can satisfy that template and thus trigger a face detection response,” he said in a separate statement. But not only are we seeing faces, our brains go one step further and seemingly give those faces feelings.

University of Sydney

Corporate dream manipulation

Advertisements are quite literally everywhere. On billboards, in commercials, in videos, in movies; the list goes on and on. Still, at least you can shut your eyes and be mercifully free of corporate interference inside your own head, right? Right?

Early in 2021, Coors launched an ad campaign that seemed to be a b bit of a gimmick, if not a joke. Coors claimed that if people watched an ad before bed, and played an 8-hour soundscape while sleeping, their dreams would be filled with crisp mountains and cold, thirst-quenching beverages. While, the Coors campaign didn’t go viral, someone was paying attention. A group of 35 leading researchers published an open letter on the subject of corporate dream manipulation, in the journal Dream Engineering.

"Multiple marketing studies are openly testing new ways to alter and motivate purchasing behavior through dream and sleep hacking. The commercial, for-profit use of dream incubation is rapidly becoming a reality," wrote the investigators. "As sleep and dream researchers, we are deeply concerned about marketing plans aimed at generating profits at the cost of interfering with our natural nocturnal memory processing."

People have tried to manipulate their dreams for countless years, but only in recent years have scientists attempted to target or manipulate behavior through dreams. In a 2014 study, smokers exposed to tobacco smoke and rotten egg smell while sleeping reduced their cigarette consumption by 30%.

Free-Photos/Pixabay

Got breast milk?

As we know, breast milk has endless benefits for newbords and babies, but many things can stand in the way of a mother’s ability to breastfeed. Baby formula has served as a good enough substitute. But now, there might be something that’s even better.

A start-up company called BIOMILQ created a product that could be groundbreaking. Using “breakthrough mammary biotechnology,” BIOMILQ created cell-cultured breast milk.

Focus_on_Nature/Getty Images

Insert clove A into nostril B

Just when you start wondering what crazy and potentially dangerous thing people can do to themselves next, comes a crazy and potentially dangerous new trend. The good folks at TikTok have provided patients a new treatment for stuffed up sinuses.

Dangerous? Well, that’s what doctors say, anyway.

“We typically do not recommend putting anything into the nostril for the obvious fact that it could get dislodged or lodged up into the nasal cavity,” Anthony Del Signore, MD, of Mount Sinai Union Square, New York, told TODAY.

“Not only does it have the potential to rot or cause a nasal obstruction, it can induce an episode of sinusitis,” Omid Mehdizadeh, MD, of Providence Saint John’s Health Center, Santa Monica, Calif., explained to Shape.

But who doesn't want to breathe easier and keep blood-sucking vampires at bay?

Max Pixel

Seeing faces in random places?

Ever look up at the clouds, at a fast-moving train, or into your morning bowl of cereal and see two eyes, a nose, and a mouth looking back at you? You may shake it off and think you’re imagining something, but it's actually your brain doing what it’s built to do and researchers know why.

The phenomenon is called face pareidolia, and it’s technically an error function of the human brain. Evolution has molded our brains to rapidly identify faces, according to David Alais, PhD, of the University of Sydney, Australia, lead author of the study.

“But the system plays ‘fast and loose’ by applying a crude template of two eyes over a nose and mouth. Lots of things can satisfy that template and thus trigger a face detection response,” he said in a separate statement. But not only are we seeing faces, our brains go one step further and seemingly give those faces feelings.

University of Sydney

Corporate dream manipulation

Advertisements are quite literally everywhere. On billboards, in commercials, in videos, in movies; the list goes on and on. Still, at least you can shut your eyes and be mercifully free of corporate interference inside your own head, right? Right?

Early in 2021, Coors launched an ad campaign that seemed to be a b bit of a gimmick, if not a joke. Coors claimed that if people watched an ad before bed, and played an 8-hour soundscape while sleeping, their dreams would be filled with crisp mountains and cold, thirst-quenching beverages. While, the Coors campaign didn’t go viral, someone was paying attention. A group of 35 leading researchers published an open letter on the subject of corporate dream manipulation, in the journal Dream Engineering.

"Multiple marketing studies are openly testing new ways to alter and motivate purchasing behavior through dream and sleep hacking. The commercial, for-profit use of dream incubation is rapidly becoming a reality," wrote the investigators. "As sleep and dream researchers, we are deeply concerned about marketing plans aimed at generating profits at the cost of interfering with our natural nocturnal memory processing."

People have tried to manipulate their dreams for countless years, but only in recent years have scientists attempted to target or manipulate behavior through dreams. In a 2014 study, smokers exposed to tobacco smoke and rotten egg smell while sleeping reduced their cigarette consumption by 30%.

Free-Photos/Pixabay

Got breast milk?

As we know, breast milk has endless benefits for newbords and babies, but many things can stand in the way of a mother’s ability to breastfeed. Baby formula has served as a good enough substitute. But now, there might be something that’s even better.

A start-up company called BIOMILQ created a product that could be groundbreaking. Using “breakthrough mammary biotechnology,” BIOMILQ created cell-cultured breast milk.

Focus_on_Nature/Getty Images

The contagious Delta variant has become the dominant form of the coronavirus in the United States, now accounting for more than 51% of COVID-19 cases in the country, according to new CDC data to updated on July 6.

The variant, also known as B.1.617.2 and first detected in India, makes up more than 80% of new cases in some Midwestern states, including Iowa, Kansas, and Missouri. Delta also accounts for 74% of cases in Western states such as Colorado and Utah and 59% of cases in Southern states such as Louisiana and Texas.

Communities with low vaccination rates are bearing the brunt of new Delta cases. Public health experts are urging those who are unvaccinated to get a shot to protect themselves and their communities against future surges.

“Right now we have two Americas: the vaccinated and the unvaccinated,” Paul Offit, MD, an infectious disease specialist at Children’s Hospital of Philadelphia, told NPR.

“We’re feeling pretty good right now because it’s the summer,” he said. “But come winter, if we still have a significant percentage of the population that is unvaccinated, we’re going to see this virus surge again.”

So far, COVID-19 vaccines appear to protect people against the Delta variant. But health officials are watching other variants that could evade vaccine protection and lead to major outbreaks this year.

For instance, certain mutations in the Epsilon variant may allow it to evade the immunity from past infections and current COVID-19 vaccines, according to a new study published July 1 in the Science. The variant, also known as B.1.427/B.1.429 and first identified in California, has now been reported in 34 countries and could become widespread in the United States.

Researchers from the University of Washington and clinics in Switzerland tested the variant in blood samples from vaccinated people, as well as those who were previously infected with COVID-19. They found that the neutralizing power was reduced by about 2 to 3½ times.

The research team also visualized the variant and found that three mutations on Epsilon’s spike protein allow the virus to escape certain antibodies and lower the strength of vaccines.

Epsilon “relies on an indirect and unusual neutralization-escape strategy,” they wrote, saying that understanding these escape routes could help scientists track new variants, curb the pandemic, and create booster shots.

In Australia, for instance, public health officials have detected the Lambda variant, which could be more infectious than the Delta variant and resistant to vaccines, according to Sky News.

A hotel quarantine program in New South Wales identified the variant in someone who had returned from travel, the news outlet reported. Also known as C.37, Lambda was named a “variant of interest” by the World Health Organization in June.

Lambda was first identified in Peru in December and now accounts for more than 80% of the country’s cases, according to the Financial Times. It has since been found in 27 countries, including the U.S., U.K., and Germany.

The variant has seven mutations on the spike protein that allow the virus to infect human cells, the news outlet reported. One mutation is like another mutation on the Delta variant, which could make it more contagious.

In a preprint study published July 1, researchers at the University of Chile at Santiago found that Lambda is better able to escape antibodies created by the CoronaVac vaccine made by Sinovac in China. In the paper, which hasn’t yet been peer-reviewed, researchers tested blood samples from local health care workers in Santiago who had received two doses of the vaccine.

“Our data revealed that the spike protein ... carries mutations conferring increased infectivity and the ability to escape from neutralizing antibodies,” they wrote.

The research team urged countries to continue testing for contagious variants, even in areas with high vaccination rates, so scientists can identify mutations quickly and analyze whether new variants can escape vaccines.

“The world has to get its act together,” Saad Omer, PhD, director of the Yale Institute for Global Health, told NPR. “Otherwise yet another, potentially more dangerous, variant could emerge.”

A version of this article first appeared on WebMD.com.

The contagious Delta variant has become the dominant form of the coronavirus in the United States, now accounting for more than 51% of COVID-19 cases in the country, according to new CDC data to updated on July 6.

The variant, also known as B.1.617.2 and first detected in India, makes up more than 80% of new cases in some Midwestern states, including Iowa, Kansas, and Missouri. Delta also accounts for 74% of cases in Western states such as Colorado and Utah and 59% of cases in Southern states such as Louisiana and Texas.

Communities with low vaccination rates are bearing the brunt of new Delta cases. Public health experts are urging those who are unvaccinated to get a shot to protect themselves and their communities against future surges.

“Right now we have two Americas: the vaccinated and the unvaccinated,” Paul Offit, MD, an infectious disease specialist at Children’s Hospital of Philadelphia, told NPR.

“We’re feeling pretty good right now because it’s the summer,” he said. “But come winter, if we still have a significant percentage of the population that is unvaccinated, we’re going to see this virus surge again.”

So far, COVID-19 vaccines appear to protect people against the Delta variant. But health officials are watching other variants that could evade vaccine protection and lead to major outbreaks this year.

For instance, certain mutations in the Epsilon variant may allow it to evade the immunity from past infections and current COVID-19 vaccines, according to a new study published July 1 in the Science. The variant, also known as B.1.427/B.1.429 and first identified in California, has now been reported in 34 countries and could become widespread in the United States.

Researchers from the University of Washington and clinics in Switzerland tested the variant in blood samples from vaccinated people, as well as those who were previously infected with COVID-19. They found that the neutralizing power was reduced by about 2 to 3½ times.

The research team also visualized the variant and found that three mutations on Epsilon’s spike protein allow the virus to escape certain antibodies and lower the strength of vaccines.

Epsilon “relies on an indirect and unusual neutralization-escape strategy,” they wrote, saying that understanding these escape routes could help scientists track new variants, curb the pandemic, and create booster shots.

In Australia, for instance, public health officials have detected the Lambda variant, which could be more infectious than the Delta variant and resistant to vaccines, according to Sky News.

A hotel quarantine program in New South Wales identified the variant in someone who had returned from travel, the news outlet reported. Also known as C.37, Lambda was named a “variant of interest” by the World Health Organization in June.

Lambda was first identified in Peru in December and now accounts for more than 80% of the country’s cases, according to the Financial Times. It has since been found in 27 countries, including the U.S., U.K., and Germany.

The variant has seven mutations on the spike protein that allow the virus to infect human cells, the news outlet reported. One mutation is like another mutation on the Delta variant, which could make it more contagious.

In a preprint study published July 1, researchers at the University of Chile at Santiago found that Lambda is better able to escape antibodies created by the CoronaVac vaccine made by Sinovac in China. In the paper, which hasn’t yet been peer-reviewed, researchers tested blood samples from local health care workers in Santiago who had received two doses of the vaccine.

“Our data revealed that the spike protein ... carries mutations conferring increased infectivity and the ability to escape from neutralizing antibodies,” they wrote.

The research team urged countries to continue testing for contagious variants, even in areas with high vaccination rates, so scientists can identify mutations quickly and analyze whether new variants can escape vaccines.

“The world has to get its act together,” Saad Omer, PhD, director of the Yale Institute for Global Health, told NPR. “Otherwise yet another, potentially more dangerous, variant could emerge.”

A version of this article first appeared on WebMD.com.

The contagious Delta variant has become the dominant form of the coronavirus in the United States, now accounting for more than 51% of COVID-19 cases in the country, according to new CDC data to updated on July 6.

The variant, also known as B.1.617.2 and first detected in India, makes up more than 80% of new cases in some Midwestern states, including Iowa, Kansas, and Missouri. Delta also accounts for 74% of cases in Western states such as Colorado and Utah and 59% of cases in Southern states such as Louisiana and Texas.

Communities with low vaccination rates are bearing the brunt of new Delta cases. Public health experts are urging those who are unvaccinated to get a shot to protect themselves and their communities against future surges.

“Right now we have two Americas: the vaccinated and the unvaccinated,” Paul Offit, MD, an infectious disease specialist at Children’s Hospital of Philadelphia, told NPR.

“We’re feeling pretty good right now because it’s the summer,” he said. “But come winter, if we still have a significant percentage of the population that is unvaccinated, we’re going to see this virus surge again.”

So far, COVID-19 vaccines appear to protect people against the Delta variant. But health officials are watching other variants that could evade vaccine protection and lead to major outbreaks this year.

For instance, certain mutations in the Epsilon variant may allow it to evade the immunity from past infections and current COVID-19 vaccines, according to a new study published July 1 in the Science. The variant, also known as B.1.427/B.1.429 and first identified in California, has now been reported in 34 countries and could become widespread in the United States.

Researchers from the University of Washington and clinics in Switzerland tested the variant in blood samples from vaccinated people, as well as those who were previously infected with COVID-19. They found that the neutralizing power was reduced by about 2 to 3½ times.

The research team also visualized the variant and found that three mutations on Epsilon’s spike protein allow the virus to escape certain antibodies and lower the strength of vaccines.

Epsilon “relies on an indirect and unusual neutralization-escape strategy,” they wrote, saying that understanding these escape routes could help scientists track new variants, curb the pandemic, and create booster shots.

In Australia, for instance, public health officials have detected the Lambda variant, which could be more infectious than the Delta variant and resistant to vaccines, according to Sky News.

A hotel quarantine program in New South Wales identified the variant in someone who had returned from travel, the news outlet reported. Also known as C.37, Lambda was named a “variant of interest” by the World Health Organization in June.

Lambda was first identified in Peru in December and now accounts for more than 80% of the country’s cases, according to the Financial Times. It has since been found in 27 countries, including the U.S., U.K., and Germany.

The variant has seven mutations on the spike protein that allow the virus to infect human cells, the news outlet reported. One mutation is like another mutation on the Delta variant, which could make it more contagious.

In a preprint study published July 1, researchers at the University of Chile at Santiago found that Lambda is better able to escape antibodies created by the CoronaVac vaccine made by Sinovac in China. In the paper, which hasn’t yet been peer-reviewed, researchers tested blood samples from local health care workers in Santiago who had received two doses of the vaccine.

“Our data revealed that the spike protein ... carries mutations conferring increased infectivity and the ability to escape from neutralizing antibodies,” they wrote.

The research team urged countries to continue testing for contagious variants, even in areas with high vaccination rates, so scientists can identify mutations quickly and analyze whether new variants can escape vaccines.

“The world has to get its act together,” Saad Omer, PhD, director of the Yale Institute for Global Health, told NPR. “Otherwise yet another, potentially more dangerous, variant could emerge.”

A version of this article first appeared on WebMD.com.

The Diagnosis: Dowling-Degos Disease

Histopathology demonstrated elongation of the epidermal rete ridges with increased basal pigmentation, suprapapillary epithelial thinning, dermal melanophages, and a mild lymphocytic infiltrate (Figure). Given the clinical and histologic findings, a diagnosis of Dowling-Degos disease (DDD) was made. The patient was counseled on the increased risk for her children developing DDD. Treatment with the erbium:YAG (Er:YAG) laser subsequently was initiated.

Dowling-Degos disease (also known as reticulate pigmented anomaly of the flexures) is an uncommon autosomal-dominant condition characterized by reticular hyperpigmentation involving the flexural and intertriginous sites. Classic DDD commonly is caused by lossof-function mutations in the keratin 5 gene, KRT5¹; however, DDD also may result from loss-of-function mutations in the protein O-fucosyltransferase 1, POFUT1, and protein O-glucosyltransferase 1, POGLUT1, genes.²

Rare cases of DDD associated with hidradenitis suppurativa are caused by mutations in the presenilin enhancer protein 2 gene, PSENEN.³

Of note, a missense mutation in KRT5 is implicated in epidermolysis bullosa simplex with mottled pigmentation. Onset of DDD typically occurs during the third to fourth decades of life. Reticulated hyperpigmented macules initially occur in the axillae and groin and progressively increase over time to involve the neck, inframammary folds, trunk, and flexural surfaces of the arms and thighs. Patients additionally may present with pitted perioral scars, comedolike lesions on the back and neck, epidermoid cysts, and hidradenitis suppurativa. Keratoacanthoma and squamous cell carcinoma rarely have been reported in association with classic DDD.^4,5

Dowling-Degos disease usually is asymptomatic, though pruritus seldom may occur in the affected flexural areas. Histologically, the epidermal rete ridges are elongated in a filiform or antlerlike pattern with increased pigmentation of the basal layer and thinning of the suprapapillary epithelium. Dermal melanosis and a mild perivascular lymphohistiocytic infiltrate also are present with no increase in the number of melanocytes.^6,7 Galli-Galli disease is a variant of DDD that shares similar clinical and histologic features of DDD but is distinguished from DDD by suprabasilar nondyskeratotic acantholysis on histology.⁸

Regarding other differential diagnoses for our patient, acanthosis nigricans may be distinguished clinically by the presence of velvety and/or verrucous plaques, commonly in the neck folds and axillae. Histologically, acanthosis nigricans is distinct from DDD and involves hyperkeratosis, acanthosis, and epidermal papillomatosis. Our patient had no history of diabetes mellitus or insulin resistance. Granular parakeratosis presents with hyperpigmented hyperkeratotic papules and plaques classically confined to the axillary region; however, the involvement of other intertriginous areas may occur. Histologically, granular parakeratosis demonstrates compact parakeratosis with small bluish keratohyalin granules within the stratum corneum. Confluent and reticulated papillomatosis presents with red-brown keratotic papules that initially appear in the intermammary region and spread laterally forming a reticulated pattern. Histology is similar to acanthosis nigricans and demonstrates hyperkeratosis, acanthosis, and papillomatosis. Inverse psoriasis presents with symmetric and sharply demarcated, erythematous, nonscaly plaques in the intertriginous areas. The plaques of inverse psoriasis may be pruritic and/or sore and occasionally may become macerated. Inverse psoriasis shares similar histologic findings compared to classic plaque psoriasis but may have less confluent parakeratosis.

Treatment of DDD essentially is reserved for cosmetic reasons. Topical hydroquinone, tretinoin, and corticosteroids have been used with limited to no success.^5,9 Beneficial results after treatment with the Er:YAG laser have been reported.¹⁰

The Diagnosis: Dowling-Degos Disease

Histopathology demonstrated elongation of the epidermal rete ridges with increased basal pigmentation, suprapapillary epithelial thinning, dermal melanophages, and a mild lymphocytic infiltrate (Figure). Given the clinical and histologic findings, a diagnosis of Dowling-Degos disease (DDD) was made. The patient was counseled on the increased risk for her children developing DDD. Treatment with the erbium:YAG (Er:YAG) laser subsequently was initiated.

Dowling-Degos disease (also known as reticulate pigmented anomaly of the flexures) is an uncommon autosomal-dominant condition characterized by reticular hyperpigmentation involving the flexural and intertriginous sites. Classic DDD commonly is caused by lossof-function mutations in the keratin 5 gene, KRT5¹; however, DDD also may result from loss-of-function mutations in the protein O-fucosyltransferase 1, POFUT1, and protein O-glucosyltransferase 1, POGLUT1, genes.²

Rare cases of DDD associated with hidradenitis suppurativa are caused by mutations in the presenilin enhancer protein 2 gene, PSENEN.³

Of note, a missense mutation in KRT5 is implicated in epidermolysis bullosa simplex with mottled pigmentation. Onset of DDD typically occurs during the third to fourth decades of life. Reticulated hyperpigmented macules initially occur in the axillae and groin and progressively increase over time to involve the neck, inframammary folds, trunk, and flexural surfaces of the arms and thighs. Patients additionally may present with pitted perioral scars, comedolike lesions on the back and neck, epidermoid cysts, and hidradenitis suppurativa. Keratoacanthoma and squamous cell carcinoma rarely have been reported in association with classic DDD.^4,5

Dowling-Degos disease usually is asymptomatic, though pruritus seldom may occur in the affected flexural areas. Histologically, the epidermal rete ridges are elongated in a filiform or antlerlike pattern with increased pigmentation of the basal layer and thinning of the suprapapillary epithelium. Dermal melanosis and a mild perivascular lymphohistiocytic infiltrate also are present with no increase in the number of melanocytes.^6,7 Galli-Galli disease is a variant of DDD that shares similar clinical and histologic features of DDD but is distinguished from DDD by suprabasilar nondyskeratotic acantholysis on histology.⁸

Regarding other differential diagnoses for our patient, acanthosis nigricans may be distinguished clinically by the presence of velvety and/or verrucous plaques, commonly in the neck folds and axillae. Histologically, acanthosis nigricans is distinct from DDD and involves hyperkeratosis, acanthosis, and epidermal papillomatosis. Our patient had no history of diabetes mellitus or insulin resistance. Granular parakeratosis presents with hyperpigmented hyperkeratotic papules and plaques classically confined to the axillary region; however, the involvement of other intertriginous areas may occur. Histologically, granular parakeratosis demonstrates compact parakeratosis with small bluish keratohyalin granules within the stratum corneum. Confluent and reticulated papillomatosis presents with red-brown keratotic papules that initially appear in the intermammary region and spread laterally forming a reticulated pattern. Histology is similar to acanthosis nigricans and demonstrates hyperkeratosis, acanthosis, and papillomatosis. Inverse psoriasis presents with symmetric and sharply demarcated, erythematous, nonscaly plaques in the intertriginous areas. The plaques of inverse psoriasis may be pruritic and/or sore and occasionally may become macerated. Inverse psoriasis shares similar histologic findings compared to classic plaque psoriasis but may have less confluent parakeratosis.

Treatment of DDD essentially is reserved for cosmetic reasons. Topical hydroquinone, tretinoin, and corticosteroids have been used with limited to no success.^5,9 Beneficial results after treatment with the Er:YAG laser have been reported.¹⁰

The Diagnosis: Dowling-Degos Disease

Histopathology demonstrated elongation of the epidermal rete ridges with increased basal pigmentation, suprapapillary epithelial thinning, dermal melanophages, and a mild lymphocytic infiltrate (Figure). Given the clinical and histologic findings, a diagnosis of Dowling-Degos disease (DDD) was made. The patient was counseled on the increased risk for her children developing DDD. Treatment with the erbium:YAG (Er:YAG) laser subsequently was initiated.

Dowling-Degos disease (also known as reticulate pigmented anomaly of the flexures) is an uncommon autosomal-dominant condition characterized by reticular hyperpigmentation involving the flexural and intertriginous sites. Classic DDD commonly is caused by lossof-function mutations in the keratin 5 gene, KRT5¹; however, DDD also may result from loss-of-function mutations in the protein O-fucosyltransferase 1, POFUT1, and protein O-glucosyltransferase 1, POGLUT1, genes.²

Rare cases of DDD associated with hidradenitis suppurativa are caused by mutations in the presenilin enhancer protein 2 gene, PSENEN.³

Of note, a missense mutation in KRT5 is implicated in epidermolysis bullosa simplex with mottled pigmentation. Onset of DDD typically occurs during the third to fourth decades of life. Reticulated hyperpigmented macules initially occur in the axillae and groin and progressively increase over time to involve the neck, inframammary folds, trunk, and flexural surfaces of the arms and thighs. Patients additionally may present with pitted perioral scars, comedolike lesions on the back and neck, epidermoid cysts, and hidradenitis suppurativa. Keratoacanthoma and squamous cell carcinoma rarely have been reported in association with classic DDD.^4,5

Dowling-Degos disease usually is asymptomatic, though pruritus seldom may occur in the affected flexural areas. Histologically, the epidermal rete ridges are elongated in a filiform or antlerlike pattern with increased pigmentation of the basal layer and thinning of the suprapapillary epithelium. Dermal melanosis and a mild perivascular lymphohistiocytic infiltrate also are present with no increase in the number of melanocytes.^6,7 Galli-Galli disease is a variant of DDD that shares similar clinical and histologic features of DDD but is distinguished from DDD by suprabasilar nondyskeratotic acantholysis on histology.⁸

Regarding other differential diagnoses for our patient, acanthosis nigricans may be distinguished clinically by the presence of velvety and/or verrucous plaques, commonly in the neck folds and axillae. Histologically, acanthosis nigricans is distinct from DDD and involves hyperkeratosis, acanthosis, and epidermal papillomatosis. Our patient had no history of diabetes mellitus or insulin resistance. Granular parakeratosis presents with hyperpigmented hyperkeratotic papules and plaques classically confined to the axillary region; however, the involvement of other intertriginous areas may occur. Histologically, granular parakeratosis demonstrates compact parakeratosis with small bluish keratohyalin granules within the stratum corneum. Confluent and reticulated papillomatosis presents with red-brown keratotic papules that initially appear in the intermammary region and spread laterally forming a reticulated pattern. Histology is similar to acanthosis nigricans and demonstrates hyperkeratosis, acanthosis, and papillomatosis. Inverse psoriasis presents with symmetric and sharply demarcated, erythematous, nonscaly plaques in the intertriginous areas. The plaques of inverse psoriasis may be pruritic and/or sore and occasionally may become macerated. Inverse psoriasis shares similar histologic findings compared to classic plaque psoriasis but may have less confluent parakeratosis.

Treatment of DDD essentially is reserved for cosmetic reasons. Topical hydroquinone, tretinoin, and corticosteroids have been used with limited to no success.^5,9 Beneficial results after treatment with the Er:YAG laser have been reported.¹⁰

Violin and viola players can pay a price for the music they create: Many suffer from skin irritation and inflammation where the instruments touch their necks and upper bodies. Now, a new literature review offers insight into this common condition, known as “fiddler’s neck.”

Hill Street Studios/Stone/Getty Images

“These skin conditions are disfiguring, and they also carry so much psychological burden. Not only are these patients under constant pressure to perform at their maximum at all times, it really is troublesome when there is a barrier between you and performing art that you absolutely love,” lead author Henry Lim, an osteopathic medical student at the University of North Texas Health Science Center at Fort Worth, said in an interview.

The results of the literature review were presented in a poster at the Inaugural Symposium for Inflammatory Skin Disease.

Mr. Lim, who has a special interest in skin, said his own musical experience inspired the research. “Throughout my experience as a violinist, I faced many dermatologic issues because of my violin, and it affected my performance,” he said. “As time went on, I recognized that many other stringed instrumentalists were dealing with similar issues but chose to live with it because it came with the territory.”

One physician told Mr. Lim that he needed to quit in order to permanently treat his skin problems. He didn’t accept this answer and instead launched the literature review with colleagues Marshall Hall, MPH, also an osteopathic medical student with an interest in dermatology, and Sajid Surve, DO, codirector of the UNT Texas Center for Performing Arts Health.

Mr. Lim and colleagues evaluated 23 articles, which included case studies and literature reviews, about dermatitis in violinists, violists, cellists, bassists, guitarists and harpists. “Stringed instrumentalists are the highest at-risk population compared to performers who play other types of instruments,” Mr. Lim said.

The poster he presented at the meeting largely focuses on fiddler’s neck, which he defined as “simply dermatitis related to friction and allergic irritation from playing violin or viola.” Many people, he noted, are allergic to nickel, and the bracket that secures the violin’s chin rest “most often contains nickel. Even a very small concentration of nickel can cause massive reactions, and we found that the C string of a viola – the thickest, lowest-sounding string – contains a nickel concentration of up to 37%.”

Gold-coated strings are an alternative option, he said, but they’re more expensive.

Stringed instrumentalists may also be allergic to rosin applied to “bow hairs,” which is the hair – typically from horses – that is used to string bows, also described in the poster. “We found that there is an overall common allergy to the main ingredient called colophony,” Mr. Lim said. The legendary violin maker Antonio Stradivari “was rumored to have used colophony and another irritating ingredient called propolis in the wood varnish of his instruments. Because he was such a great influence on the art of violin crafting, his technique is still used in the modern era, which may be another contributing factor to the allergic reactions seen in stringed instrumentalists.”

(In the poster, the authors refer to one of the articles in the review, which described a violin maker allergic to colophony and propolis, who was treated with cetirizine, mild corticosteroids, and avoidance.)

What should dermatologists know about skin conditions in these musicians? Mr. Hall, one of the coauthors of the report, suggested they invite the patients to play their instruments during a visit. “The musicians may not understand that they are doing certain things with their movements, but looking from a clinical lens, we are able to see how their biomechanics and posture [are] contributing to their dermatitis,” he said.

Dr. Surve, the other coauthor, also suggested speaking to the patient’s teacher, coach, or mentor. “Keeping that person in the loop regarding what you are seeing and recommending will go a long way towards helping your patient,” he said. “If the teacher doesn’t understand or agree with what you’re trying to accomplish, they may try to undermine your plan of care. But if they are on board, they become a valuable tool for facilitating and reinforcing it.”

As for treatments, avoidance of the instruments is the most effective, but is simply not feasible for many musicians. “Certain interventions like creating a barrier between the musician and the instrument can reduce the risk of contact dermatitis without compromising the quality [of playing] as much,” Mr. Hall said. The poster reported that a handkerchief was used for this purpose in one case attributed to nickel sulfate in a 16-year-old .

Purchasing more expensive instrument materials to prevent reactions is another option, he said, and players can also purchase stands. But musicians may be resistant to any treatment that changes how the instruments sound or forces them to adjust the way they do things, he cautioned.

No funding for the study or author disclosures were reported.

Violin and viola players can pay a price for the music they create: Many suffer from skin irritation and inflammation where the instruments touch their necks and upper bodies. Now, a new literature review offers insight into this common condition, known as “fiddler’s neck.”

Hill Street Studios/Stone/Getty Images

“These skin conditions are disfiguring, and they also carry so much psychological burden. Not only are these patients under constant pressure to perform at their maximum at all times, it really is troublesome when there is a barrier between you and performing art that you absolutely love,” lead author Henry Lim, an osteopathic medical student at the University of North Texas Health Science Center at Fort Worth, said in an interview.

The results of the literature review were presented in a poster at the Inaugural Symposium for Inflammatory Skin Disease.

Mr. Lim, who has a special interest in skin, said his own musical experience inspired the research. “Throughout my experience as a violinist, I faced many dermatologic issues because of my violin, and it affected my performance,” he said. “As time went on, I recognized that many other stringed instrumentalists were dealing with similar issues but chose to live with it because it came with the territory.”

One physician told Mr. Lim that he needed to quit in order to permanently treat his skin problems. He didn’t accept this answer and instead launched the literature review with colleagues Marshall Hall, MPH, also an osteopathic medical student with an interest in dermatology, and Sajid Surve, DO, codirector of the UNT Texas Center for Performing Arts Health.

Mr. Lim and colleagues evaluated 23 articles, which included case studies and literature reviews, about dermatitis in violinists, violists, cellists, bassists, guitarists and harpists. “Stringed instrumentalists are the highest at-risk population compared to performers who play other types of instruments,” Mr. Lim said.

The poster he presented at the meeting largely focuses on fiddler’s neck, which he defined as “simply dermatitis related to friction and allergic irritation from playing violin or viola.” Many people, he noted, are allergic to nickel, and the bracket that secures the violin’s chin rest “most often contains nickel. Even a very small concentration of nickel can cause massive reactions, and we found that the C string of a viola – the thickest, lowest-sounding string – contains a nickel concentration of up to 37%.”

Gold-coated strings are an alternative option, he said, but they’re more expensive.

Stringed instrumentalists may also be allergic to rosin applied to “bow hairs,” which is the hair – typically from horses – that is used to string bows, also described in the poster. “We found that there is an overall common allergy to the main ingredient called colophony,” Mr. Lim said. The legendary violin maker Antonio Stradivari “was rumored to have used colophony and another irritating ingredient called propolis in the wood varnish of his instruments. Because he was such a great influence on the art of violin crafting, his technique is still used in the modern era, which may be another contributing factor to the allergic reactions seen in stringed instrumentalists.”

(In the poster, the authors refer to one of the articles in the review, which described a violin maker allergic to colophony and propolis, who was treated with cetirizine, mild corticosteroids, and avoidance.)

What should dermatologists know about skin conditions in these musicians? Mr. Hall, one of the coauthors of the report, suggested they invite the patients to play their instruments during a visit. “The musicians may not understand that they are doing certain things with their movements, but looking from a clinical lens, we are able to see how their biomechanics and posture [are] contributing to their dermatitis,” he said.

Dr. Surve, the other coauthor, also suggested speaking to the patient’s teacher, coach, or mentor. “Keeping that person in the loop regarding what you are seeing and recommending will go a long way towards helping your patient,” he said. “If the teacher doesn’t understand or agree with what you’re trying to accomplish, they may try to undermine your plan of care. But if they are on board, they become a valuable tool for facilitating and reinforcing it.”

As for treatments, avoidance of the instruments is the most effective, but is simply not feasible for many musicians. “Certain interventions like creating a barrier between the musician and the instrument can reduce the risk of contact dermatitis without compromising the quality [of playing] as much,” Mr. Hall said. The poster reported that a handkerchief was used for this purpose in one case attributed to nickel sulfate in a 16-year-old .

Purchasing more expensive instrument materials to prevent reactions is another option, he said, and players can also purchase stands. But musicians may be resistant to any treatment that changes how the instruments sound or forces them to adjust the way they do things, he cautioned.

No funding for the study or author disclosures were reported.

Violin and viola players can pay a price for the music they create: Many suffer from skin irritation and inflammation where the instruments touch their necks and upper bodies. Now, a new literature review offers insight into this common condition, known as “fiddler’s neck.”

Hill Street Studios/Stone/Getty Images

“These skin conditions are disfiguring, and they also carry so much psychological burden. Not only are these patients under constant pressure to perform at their maximum at all times, it really is troublesome when there is a barrier between you and performing art that you absolutely love,” lead author Henry Lim, an osteopathic medical student at the University of North Texas Health Science Center at Fort Worth, said in an interview.

The results of the literature review were presented in a poster at the Inaugural Symposium for Inflammatory Skin Disease.

Mr. Lim, who has a special interest in skin, said his own musical experience inspired the research. “Throughout my experience as a violinist, I faced many dermatologic issues because of my violin, and it affected my performance,” he said. “As time went on, I recognized that many other stringed instrumentalists were dealing with similar issues but chose to live with it because it came with the territory.”

One physician told Mr. Lim that he needed to quit in order to permanently treat his skin problems. He didn’t accept this answer and instead launched the literature review with colleagues Marshall Hall, MPH, also an osteopathic medical student with an interest in dermatology, and Sajid Surve, DO, codirector of the UNT Texas Center for Performing Arts Health.

Mr. Lim and colleagues evaluated 23 articles, which included case studies and literature reviews, about dermatitis in violinists, violists, cellists, bassists, guitarists and harpists. “Stringed instrumentalists are the highest at-risk population compared to performers who play other types of instruments,” Mr. Lim said.

The poster he presented at the meeting largely focuses on fiddler’s neck, which he defined as “simply dermatitis related to friction and allergic irritation from playing violin or viola.” Many people, he noted, are allergic to nickel, and the bracket that secures the violin’s chin rest “most often contains nickel. Even a very small concentration of nickel can cause massive reactions, and we found that the C string of a viola – the thickest, lowest-sounding string – contains a nickel concentration of up to 37%.”

Gold-coated strings are an alternative option, he said, but they’re more expensive.

Stringed instrumentalists may also be allergic to rosin applied to “bow hairs,” which is the hair – typically from horses – that is used to string bows, also described in the poster. “We found that there is an overall common allergy to the main ingredient called colophony,” Mr. Lim said. The legendary violin maker Antonio Stradivari “was rumored to have used colophony and another irritating ingredient called propolis in the wood varnish of his instruments. Because he was such a great influence on the art of violin crafting, his technique is still used in the modern era, which may be another contributing factor to the allergic reactions seen in stringed instrumentalists.”

(In the poster, the authors refer to one of the articles in the review, which described a violin maker allergic to colophony and propolis, who was treated with cetirizine, mild corticosteroids, and avoidance.)

What should dermatologists know about skin conditions in these musicians? Mr. Hall, one of the coauthors of the report, suggested they invite the patients to play their instruments during a visit. “The musicians may not understand that they are doing certain things with their movements, but looking from a clinical lens, we are able to see how their biomechanics and posture [are] contributing to their dermatitis,” he said.

Dr. Surve, the other coauthor, also suggested speaking to the patient’s teacher, coach, or mentor. “Keeping that person in the loop regarding what you are seeing and recommending will go a long way towards helping your patient,” he said. “If the teacher doesn’t understand or agree with what you’re trying to accomplish, they may try to undermine your plan of care. But if they are on board, they become a valuable tool for facilitating and reinforcing it.”

As for treatments, avoidance of the instruments is the most effective, but is simply not feasible for many musicians. “Certain interventions like creating a barrier between the musician and the instrument can reduce the risk of contact dermatitis without compromising the quality [of playing] as much,” Mr. Hall said. The poster reported that a handkerchief was used for this purpose in one case attributed to nickel sulfate in a 16-year-old .

Purchasing more expensive instrument materials to prevent reactions is another option, he said, and players can also purchase stands. But musicians may be resistant to any treatment that changes how the instruments sound or forces them to adjust the way they do things, he cautioned.

No funding for the study or author disclosures were reported.

Hypochondria has been useful to my patients. I mean my own hypochondria. It may not take one to know one, but we hypochondriacs understand each other.

Hypochondriacs worry that we are sick, worry that our fears are foolish and that we will be mocked for worrying about nothing, and worry even more that this time, we finally worried about something after all. Reassurance leaves us sheepish, then elated. Elation soon fades, and a new worry appears. Worry, rinse, repeat. Hypochondriasis presents one kind of patient need that doctors have to deal with. Patients have many needs, some common, others all their own. Some folks are just needy. Soothing the needs of the needy can feel like trying to drain the seven seas with a teaspoon. Those who work with people must either find ways to cope with the spectrum of neediness, or find another kind of work to do.

Some patient needs call for diagnosis and treatment. Other needs go beyond the strictly medical. Beyond knowing whether they are ill, patients have questions like, “Will this get worse?” “Will I be ashamed to go out in public?” “Can I visit my grandchildren, or will my daughter-in-law throw me out as contagious?” “Is this the beginning of the end?” or, worst of all, “Am I losing my hair?”

The list of possible patient needs is long, though not endless. Lining them up one after the other can make them sound melodramatic, even silly. (Other people’s worries often sound silly; your own never do.) Can a small growth or slight itch really cause existential agitation? Anyone who deals with complaints like these knows that the answer is yes.

Hypochondriacs with medical degrees cannot reassure themselves, but we can bring useful experience to help other members of the worry club. Doing so means paying attention not just to what doctors worry about but what patients do.

Sometimes a patient is terrified, the doctor not at all. Gentle sympathy may be enough. But the reverse can also be true: The doctor is concerned, but the patient thinks there is no problem. Sometimes I am worried enough to ask a patient to call or email an update. Patients who have already stopped worrying may not bother to answer the phone or shoot back an email. Failure to respond may mean they are fine, or in intensive care. Silence is hard to interpret.

Skin doctors have one advantageous disadvantage: Few tests help us beyond a skin scraping, the odd blood test, or a biopsy. Otherwise, most of the time all we can do is look, and perhaps apply “tincture of time,” watching the clinical course. We cannot send patients for the complex and expensive tests our colleagues use “just to be sure,” because we have no such tests to send them for.

Practice and experience help us recognize needs and worries that patients might not express. For instance, a man may show up with pimples on his back. His concerns seem intense. “What worries you?” we ask. The patient whispers, “It couldn’t be ... shingles, could it?” No, it couldn’t be shingles, because it is bilateral and for many other reasons.

The question is not whether he has shingles but why he thinks he does. Maybe his aunt suggested it. Or an article told him to watch out for it. Or his pharmacy is promoting zoster vaccination by showing huge, full-color photos of shingles cases worthy of horror movies. (Shingles the 13th!) Because he wants to visit his grandkids and his daughter is in her fourth month of pregnancy. In other words, along with the fear of cancer, fear of shingles is just out there. There are other such public concerns. Over time, we come to recognize them.

Anyone can worry, but anxiety paralyzes some to such an extent that referral to a mental health professional seems reasonable. The problem with advising it is that patients who somaticize may take exception to suggestions, however delicately put, that make us sound dismissive, locating their concern “all in the head.” Over the years, my attempts to make such referrals have met with limited success.

Dealing with needs – and neediness – can take up more of a doctor’s day than making specific diagnoses and prescribing helpful treatments. Besides, addressing needs and neediness demands skills not always stressed at school.

Practice at noting neediness makes you better at it, but no doctor nails the true wellsprings of worry all the time. We hypochondriacs can be devilishly inventive.


Dr. Rockoff, who wrote the Dermatology News column “Under My Skin,” is now semiretired, after 40 years of practice in Brookline, Mass. He served on the clinical faculty at Tufts University, Boston, and taught senior medical students and other trainees for 30 years. His latest book, “Doctoring from the Outside In,” was recently published. Write to him at [email protected].

Hypochondria has been useful to my patients. I mean my own hypochondria. It may not take one to know one, but we hypochondriacs understand each other.

Hypochondriacs worry that we are sick, worry that our fears are foolish and that we will be mocked for worrying about nothing, and worry even more that this time, we finally worried about something after all. Reassurance leaves us sheepish, then elated. Elation soon fades, and a new worry appears. Worry, rinse, repeat. Hypochondriasis presents one kind of patient need that doctors have to deal with. Patients have many needs, some common, others all their own. Some folks are just needy. Soothing the needs of the needy can feel like trying to drain the seven seas with a teaspoon. Those who work with people must either find ways to cope with the spectrum of neediness, or find another kind of work to do.

Some patient needs call for diagnosis and treatment. Other needs go beyond the strictly medical. Beyond knowing whether they are ill, patients have questions like, “Will this get worse?” “Will I be ashamed to go out in public?” “Can I visit my grandchildren, or will my daughter-in-law throw me out as contagious?” “Is this the beginning of the end?” or, worst of all, “Am I losing my hair?”

The list of possible patient needs is long, though not endless. Lining them up one after the other can make them sound melodramatic, even silly. (Other people’s worries often sound silly; your own never do.) Can a small growth or slight itch really cause existential agitation? Anyone who deals with complaints like these knows that the answer is yes.

Hypochondriacs with medical degrees cannot reassure themselves, but we can bring useful experience to help other members of the worry club. Doing so means paying attention not just to what doctors worry about but what patients do.

Sometimes a patient is terrified, the doctor not at all. Gentle sympathy may be enough. But the reverse can also be true: The doctor is concerned, but the patient thinks there is no problem. Sometimes I am worried enough to ask a patient to call or email an update. Patients who have already stopped worrying may not bother to answer the phone or shoot back an email. Failure to respond may mean they are fine, or in intensive care. Silence is hard to interpret.

Skin doctors have one advantageous disadvantage: Few tests help us beyond a skin scraping, the odd blood test, or a biopsy. Otherwise, most of the time all we can do is look, and perhaps apply “tincture of time,” watching the clinical course. We cannot send patients for the complex and expensive tests our colleagues use “just to be sure,” because we have no such tests to send them for.

Practice and experience help us recognize needs and worries that patients might not express. For instance, a man may show up with pimples on his back. His concerns seem intense. “What worries you?” we ask. The patient whispers, “It couldn’t be ... shingles, could it?” No, it couldn’t be shingles, because it is bilateral and for many other reasons.

The question is not whether he has shingles but why he thinks he does. Maybe his aunt suggested it. Or an article told him to watch out for it. Or his pharmacy is promoting zoster vaccination by showing huge, full-color photos of shingles cases worthy of horror movies. (Shingles the 13th!) Because he wants to visit his grandkids and his daughter is in her fourth month of pregnancy. In other words, along with the fear of cancer, fear of shingles is just out there. There are other such public concerns. Over time, we come to recognize them.

Anyone can worry, but anxiety paralyzes some to such an extent that referral to a mental health professional seems reasonable. The problem with advising it is that patients who somaticize may take exception to suggestions, however delicately put, that make us sound dismissive, locating their concern “all in the head.” Over the years, my attempts to make such referrals have met with limited success.

Dealing with needs – and neediness – can take up more of a doctor’s day than making specific diagnoses and prescribing helpful treatments. Besides, addressing needs and neediness demands skills not always stressed at school.

Practice at noting neediness makes you better at it, but no doctor nails the true wellsprings of worry all the time. We hypochondriacs can be devilishly inventive.


Dr. Rockoff, who wrote the Dermatology News column “Under My Skin,” is now semiretired, after 40 years of practice in Brookline, Mass. He served on the clinical faculty at Tufts University, Boston, and taught senior medical students and other trainees for 30 years. His latest book, “Doctoring from the Outside In,” was recently published. Write to him at [email protected].

Hypochondria has been useful to my patients. I mean my own hypochondria. It may not take one to know one, but we hypochondriacs understand each other.

Hypochondriacs worry that we are sick, worry that our fears are foolish and that we will be mocked for worrying about nothing, and worry even more that this time, we finally worried about something after all. Reassurance leaves us sheepish, then elated. Elation soon fades, and a new worry appears. Worry, rinse, repeat. Hypochondriasis presents one kind of patient need that doctors have to deal with. Patients have many needs, some common, others all their own. Some folks are just needy. Soothing the needs of the needy can feel like trying to drain the seven seas with a teaspoon. Those who work with people must either find ways to cope with the spectrum of neediness, or find another kind of work to do.

Some patient needs call for diagnosis and treatment. Other needs go beyond the strictly medical. Beyond knowing whether they are ill, patients have questions like, “Will this get worse?” “Will I be ashamed to go out in public?” “Can I visit my grandchildren, or will my daughter-in-law throw me out as contagious?” “Is this the beginning of the end?” or, worst of all, “Am I losing my hair?”

The list of possible patient needs is long, though not endless. Lining them up one after the other can make them sound melodramatic, even silly. (Other people’s worries often sound silly; your own never do.) Can a small growth or slight itch really cause existential agitation? Anyone who deals with complaints like these knows that the answer is yes.

Hypochondriacs with medical degrees cannot reassure themselves, but we can bring useful experience to help other members of the worry club. Doing so means paying attention not just to what doctors worry about but what patients do.

Sometimes a patient is terrified, the doctor not at all. Gentle sympathy may be enough. But the reverse can also be true: The doctor is concerned, but the patient thinks there is no problem. Sometimes I am worried enough to ask a patient to call or email an update. Patients who have already stopped worrying may not bother to answer the phone or shoot back an email. Failure to respond may mean they are fine, or in intensive care. Silence is hard to interpret.

Skin doctors have one advantageous disadvantage: Few tests help us beyond a skin scraping, the odd blood test, or a biopsy. Otherwise, most of the time all we can do is look, and perhaps apply “tincture of time,” watching the clinical course. We cannot send patients for the complex and expensive tests our colleagues use “just to be sure,” because we have no such tests to send them for.

Practice and experience help us recognize needs and worries that patients might not express. For instance, a man may show up with pimples on his back. His concerns seem intense. “What worries you?” we ask. The patient whispers, “It couldn’t be ... shingles, could it?” No, it couldn’t be shingles, because it is bilateral and for many other reasons.

The question is not whether he has shingles but why he thinks he does. Maybe his aunt suggested it. Or an article told him to watch out for it. Or his pharmacy is promoting zoster vaccination by showing huge, full-color photos of shingles cases worthy of horror movies. (Shingles the 13th!) Because he wants to visit his grandkids and his daughter is in her fourth month of pregnancy. In other words, along with the fear of cancer, fear of shingles is just out there. There are other such public concerns. Over time, we come to recognize them.

Anyone can worry, but anxiety paralyzes some to such an extent that referral to a mental health professional seems reasonable. The problem with advising it is that patients who somaticize may take exception to suggestions, however delicately put, that make us sound dismissive, locating their concern “all in the head.” Over the years, my attempts to make such referrals have met with limited success.

Dealing with needs – and neediness – can take up more of a doctor’s day than making specific diagnoses and prescribing helpful treatments. Besides, addressing needs and neediness demands skills not always stressed at school.

Practice at noting neediness makes you better at it, but no doctor nails the true wellsprings of worry all the time. We hypochondriacs can be devilishly inventive.


Dr. Rockoff, who wrote the Dermatology News column “Under My Skin,” is now semiretired, after 40 years of practice in Brookline, Mass. He served on the clinical faculty at Tufts University, Boston, and taught senior medical students and other trainees for 30 years. His latest book, “Doctoring from the Outside In,” was recently published. Write to him at [email protected].

“What’s my number?” When I hear this from my financial planning clients, I know they mean: “What investment net worth do I need to be financially independent and make practicing medicine optional?” In my 20-year career, this “magic number” is by far the most common thing physicians want to know.

Wiroj Sidhisoradej/EyeEm/Getty Images

If you look online, articles may recommend having a portfolio valued at $2 million, $5 million, and not uncommonly $10 million or more to retire. Really? $10 million? You might be thinking that surely not everyone needs that amount. Luckily, that’s true.

There’s no magic number your portfolio should be – just your number.

It’s human nature to want a simple, clear target to shoot for. But unfortunately, there’s no generic answer when it comes to saving for retirement. Even after a comprehensive hour-long review of a client’s financial plan – including insurance, investments, estate planning, and other items – the most honest answer I can give is: “It depends.” Not satisfying, I know. But there are still too many holes to fill.

By far the most important factor in getting beyond “it depends” is having an accurate estimate of annual retirement expenses. I have clients who live comfortably on $50,000 a year in retirement and others who need $250,000 or more. Knowing how much you need – your personal number – depends on the individual’s unique dream for retirement and calculating what that dream will cost.

Form a guesstimate based on savings and anticipated expenses

The total portfolio value needed to sustain an annual expense of $50,000 a year in retirement spending versus the portfolio size needed for $250,000 or more, blows apart the fiction of a universal “magic number.” It’s just not that simple. While it’s hard to gauge exactly what you will need, the right information can lead to a logical guesstimate about what size portfolio will provide you with financial independence.

In the end, it’s up to you to determine your desired retirement lifestyle. Then, the only way to get there is to calculate how much it will cost and save up for it by following a well-informed financial plan. This plan will be based on strategy that shifts from the middle to the later stages of your medical career and into retirement.

Let’s see how it works.
 

Early to mid-career: Focus on building up retirement savings

We ultimately want to save enough to meet our retirement expenses. But figuring out how much to save when you’re in your 40s and 50s is difficult. A mid-career physician likely has significant family- and child-related expenses. When we become empty-nesters, those expenses will decline. In retirement they may disappear entirely, but new expenses may arise.

With large variations in expenses at different life stages, it’s hard to calculate exactly how much you will need to save. Early on, the most sensible thing is putting aside a “reasonable” percentage of gross income for retirement savings.

What is a ‘reasonable’ savings goal for retirement?

As is often the case with high-income earners, many of our clients don’t have a budget or a clear picture of their current expenses and spending habits. That’s alright as long as they are building up a reasonable nest egg for the future – which begs the question of what is reasonable.

For mid-career docs, a reasonable goal to aim for is putting aside 20% of gross income for retirement. What you spend the rest of your money on is less important than how much you’re saving.

This is quite different from how you’ll handle expenses during retirement, when you no longer have a steady stream of income; rather, you have a pot of money that needs to last you another 20, 30, or even 40 years. At that point, thinking about specific expenses becomes more important (more on this topic later). That said, if you’re a mid-career doctor who is not meeting this 20% savings goal, it’s time to make a plan that will free up cash for retirement savings and investments.
 

Later-career docs: Calculate your spending level in retirement

Financial success means having a portfolio that can support your retirement dreams – with the confidence that your money will last and you won’t need to watch every dollar you spend. As you near retirement, your focus will shift away from accumulating savings to calculating the annual expenses you will have to meet in retirement.

A good place to start is figuring out which expenses will be necessary and which will be more flexible. To do this, separate your anticipated spending into these two categories:

• Fixed expenses: You can confidently forecast your “must-have” fixed expenses – such as property taxes, property/casualty insurance, health care costs, utilities, and groceries – because they remain steady from month to month.
• Discretionary expenses: These “like-to-have” expenses vary from month to month. This makes them harder to predict but easier to control. They might include dining out, travel, and charitable contributions.

As a retiree, understanding your fixed and discretionary expenses can help you prepare for a bear market, when the stock market can decline by 20% or more. Your portfolio won’t consist entirely of stocks, so it shouldn’t drop to that degree. Still, it will decline significantly. You may need to cut back on spending for a year or 2 to allow your portfolio to recover, particularly if the portfolio declines early in retirement.

Are you ready for retirement?

During the long bull market preceding the great recession of 2007 and 2009, many physicians retired –only to return to their practices when their portfolio values plummeted. In the exuberance of the moment, many failed to heed the warnings of many economists and got caught flat-footed.

Right now it’s a bull market, but we’re seeing concerning signs, such as an out-of-control housing market and rumblings about inflation and rising consumer costs. Sound familiar? If you hope to retire soon, take the time to objectively look around the corner so you can plan appropriately – whether your goal is to retire completely, stay in practice part-time, or even take on a new opportunity.

In an “it-depends” world, don’t be lured by a fictitious magic number, no matter what comes up when you Google: “When can I retire?” Instead, save early, imagine your dream retirement, and calculate expenses later to see what’s possible.

Dr. Greenwald is a graduate of the Albert Einstein College of Medicine, New York. Dr. Greenwald completed his internal medicine residency at the University of Minnesota, Minneapolis. He practiced internal medicine in the Twin Cities for 11 years before making the transition to financial planning for physicians, beginning in 1998.

A version of this article first appeared on Medscape.com.

“What’s my number?” When I hear this from my financial planning clients, I know they mean: “What investment net worth do I need to be financially independent and make practicing medicine optional?” In my 20-year career, this “magic number” is by far the most common thing physicians want to know.

Wiroj Sidhisoradej/EyeEm/Getty Images

If you look online, articles may recommend having a portfolio valued at $2 million, $5 million, and not uncommonly $10 million or more to retire. Really? $10 million? You might be thinking that surely not everyone needs that amount. Luckily, that’s true.

There’s no magic number your portfolio should be – just your number.

It’s human nature to want a simple, clear target to shoot for. But unfortunately, there’s no generic answer when it comes to saving for retirement. Even after a comprehensive hour-long review of a client’s financial plan – including insurance, investments, estate planning, and other items – the most honest answer I can give is: “It depends.” Not satisfying, I know. But there are still too many holes to fill.

By far the most important factor in getting beyond “it depends” is having an accurate estimate of annual retirement expenses. I have clients who live comfortably on $50,000 a year in retirement and others who need $250,000 or more. Knowing how much you need – your personal number – depends on the individual’s unique dream for retirement and calculating what that dream will cost.

Form a guesstimate based on savings and anticipated expenses

The total portfolio value needed to sustain an annual expense of $50,000 a year in retirement spending versus the portfolio size needed for $250,000 or more, blows apart the fiction of a universal “magic number.” It’s just not that simple. While it’s hard to gauge exactly what you will need, the right information can lead to a logical guesstimate about what size portfolio will provide you with financial independence.

In the end, it’s up to you to determine your desired retirement lifestyle. Then, the only way to get there is to calculate how much it will cost and save up for it by following a well-informed financial plan. This plan will be based on strategy that shifts from the middle to the later stages of your medical career and into retirement.

Let’s see how it works.
 

Early to mid-career: Focus on building up retirement savings

We ultimately want to save enough to meet our retirement expenses. But figuring out how much to save when you’re in your 40s and 50s is difficult. A mid-career physician likely has significant family- and child-related expenses. When we become empty-nesters, those expenses will decline. In retirement they may disappear entirely, but new expenses may arise.

With large variations in expenses at different life stages, it’s hard to calculate exactly how much you will need to save. Early on, the most sensible thing is putting aside a “reasonable” percentage of gross income for retirement savings.

What is a ‘reasonable’ savings goal for retirement?

As is often the case with high-income earners, many of our clients don’t have a budget or a clear picture of their current expenses and spending habits. That’s alright as long as they are building up a reasonable nest egg for the future – which begs the question of what is reasonable.

For mid-career docs, a reasonable goal to aim for is putting aside 20% of gross income for retirement. What you spend the rest of your money on is less important than how much you’re saving.

This is quite different from how you’ll handle expenses during retirement, when you no longer have a steady stream of income; rather, you have a pot of money that needs to last you another 20, 30, or even 40 years. At that point, thinking about specific expenses becomes more important (more on this topic later). That said, if you’re a mid-career doctor who is not meeting this 20% savings goal, it’s time to make a plan that will free up cash for retirement savings and investments.
 

Later-career docs: Calculate your spending level in retirement

Financial success means having a portfolio that can support your retirement dreams – with the confidence that your money will last and you won’t need to watch every dollar you spend. As you near retirement, your focus will shift away from accumulating savings to calculating the annual expenses you will have to meet in retirement.

A good place to start is figuring out which expenses will be necessary and which will be more flexible. To do this, separate your anticipated spending into these two categories:

• Fixed expenses: You can confidently forecast your “must-have” fixed expenses – such as property taxes, property/casualty insurance, health care costs, utilities, and groceries – because they remain steady from month to month.
• Discretionary expenses: These “like-to-have” expenses vary from month to month. This makes them harder to predict but easier to control. They might include dining out, travel, and charitable contributions.

As a retiree, understanding your fixed and discretionary expenses can help you prepare for a bear market, when the stock market can decline by 20% or more. Your portfolio won’t consist entirely of stocks, so it shouldn’t drop to that degree. Still, it will decline significantly. You may need to cut back on spending for a year or 2 to allow your portfolio to recover, particularly if the portfolio declines early in retirement.

Are you ready for retirement?

During the long bull market preceding the great recession of 2007 and 2009, many physicians retired –only to return to their practices when their portfolio values plummeted. In the exuberance of the moment, many failed to heed the warnings of many economists and got caught flat-footed.

Right now it’s a bull market, but we’re seeing concerning signs, such as an out-of-control housing market and rumblings about inflation and rising consumer costs. Sound familiar? If you hope to retire soon, take the time to objectively look around the corner so you can plan appropriately – whether your goal is to retire completely, stay in practice part-time, or even take on a new opportunity.

In an “it-depends” world, don’t be lured by a fictitious magic number, no matter what comes up when you Google: “When can I retire?” Instead, save early, imagine your dream retirement, and calculate expenses later to see what’s possible.

Dr. Greenwald is a graduate of the Albert Einstein College of Medicine, New York. Dr. Greenwald completed his internal medicine residency at the University of Minnesota, Minneapolis. He practiced internal medicine in the Twin Cities for 11 years before making the transition to financial planning for physicians, beginning in 1998.

A version of this article first appeared on Medscape.com.

“What’s my number?” When I hear this from my financial planning clients, I know they mean: “What investment net worth do I need to be financially independent and make practicing medicine optional?” In my 20-year career, this “magic number” is by far the most common thing physicians want to know.

Wiroj Sidhisoradej/EyeEm/Getty Images

If you look online, articles may recommend having a portfolio valued at $2 million, $5 million, and not uncommonly $10 million or more to retire. Really? $10 million? You might be thinking that surely not everyone needs that amount. Luckily, that’s true.

There’s no magic number your portfolio should be – just your number.

It’s human nature to want a simple, clear target to shoot for. But unfortunately, there’s no generic answer when it comes to saving for retirement. Even after a comprehensive hour-long review of a client’s financial plan – including insurance, investments, estate planning, and other items – the most honest answer I can give is: “It depends.” Not satisfying, I know. But there are still too many holes to fill.

By far the most important factor in getting beyond “it depends” is having an accurate estimate of annual retirement expenses. I have clients who live comfortably on $50,000 a year in retirement and others who need $250,000 or more. Knowing how much you need – your personal number – depends on the individual’s unique dream for retirement and calculating what that dream will cost.

Form a guesstimate based on savings and anticipated expenses

The total portfolio value needed to sustain an annual expense of $50,000 a year in retirement spending versus the portfolio size needed for $250,000 or more, blows apart the fiction of a universal “magic number.” It’s just not that simple. While it’s hard to gauge exactly what you will need, the right information can lead to a logical guesstimate about what size portfolio will provide you with financial independence.

In the end, it’s up to you to determine your desired retirement lifestyle. Then, the only way to get there is to calculate how much it will cost and save up for it by following a well-informed financial plan. This plan will be based on strategy that shifts from the middle to the later stages of your medical career and into retirement.

Let’s see how it works.
 

Early to mid-career: Focus on building up retirement savings

We ultimately want to save enough to meet our retirement expenses. But figuring out how much to save when you’re in your 40s and 50s is difficult. A mid-career physician likely has significant family- and child-related expenses. When we become empty-nesters, those expenses will decline. In retirement they may disappear entirely, but new expenses may arise.

With large variations in expenses at different life stages, it’s hard to calculate exactly how much you will need to save. Early on, the most sensible thing is putting aside a “reasonable” percentage of gross income for retirement savings.

What is a ‘reasonable’ savings goal for retirement?

As is often the case with high-income earners, many of our clients don’t have a budget or a clear picture of their current expenses and spending habits. That’s alright as long as they are building up a reasonable nest egg for the future – which begs the question of what is reasonable.

For mid-career docs, a reasonable goal to aim for is putting aside 20% of gross income for retirement. What you spend the rest of your money on is less important than how much you’re saving.

This is quite different from how you’ll handle expenses during retirement, when you no longer have a steady stream of income; rather, you have a pot of money that needs to last you another 20, 30, or even 40 years. At that point, thinking about specific expenses becomes more important (more on this topic later). That said, if you’re a mid-career doctor who is not meeting this 20% savings goal, it’s time to make a plan that will free up cash for retirement savings and investments.
 

Later-career docs: Calculate your spending level in retirement

Financial success means having a portfolio that can support your retirement dreams – with the confidence that your money will last and you won’t need to watch every dollar you spend. As you near retirement, your focus will shift away from accumulating savings to calculating the annual expenses you will have to meet in retirement.

A good place to start is figuring out which expenses will be necessary and which will be more flexible. To do this, separate your anticipated spending into these two categories:

• Fixed expenses: You can confidently forecast your “must-have” fixed expenses – such as property taxes, property/casualty insurance, health care costs, utilities, and groceries – because they remain steady from month to month.
• Discretionary expenses: These “like-to-have” expenses vary from month to month. This makes them harder to predict but easier to control. They might include dining out, travel, and charitable contributions.

As a retiree, understanding your fixed and discretionary expenses can help you prepare for a bear market, when the stock market can decline by 20% or more. Your portfolio won’t consist entirely of stocks, so it shouldn’t drop to that degree. Still, it will decline significantly. You may need to cut back on spending for a year or 2 to allow your portfolio to recover, particularly if the portfolio declines early in retirement.

Are you ready for retirement?

During the long bull market preceding the great recession of 2007 and 2009, many physicians retired –only to return to their practices when their portfolio values plummeted. In the exuberance of the moment, many failed to heed the warnings of many economists and got caught flat-footed.

Right now it’s a bull market, but we’re seeing concerning signs, such as an out-of-control housing market and rumblings about inflation and rising consumer costs. Sound familiar? If you hope to retire soon, take the time to objectively look around the corner so you can plan appropriately – whether your goal is to retire completely, stay in practice part-time, or even take on a new opportunity.

In an “it-depends” world, don’t be lured by a fictitious magic number, no matter what comes up when you Google: “When can I retire?” Instead, save early, imagine your dream retirement, and calculate expenses later to see what’s possible.

Dr. Greenwald is a graduate of the Albert Einstein College of Medicine, New York. Dr. Greenwald completed his internal medicine residency at the University of Minnesota, Minneapolis. He practiced internal medicine in the Twin Cities for 11 years before making the transition to financial planning for physicians, beginning in 1998.

A version of this article first appeared on Medscape.com.