Contact Dermatitis

To the Editor:

First identified by Samuel Wilks in 1852, trichorrhexis nodosa (TN) is a congenital or acquired hair shaft disorder that is characterized by fragile and easily broken hair.¹ Congenital TN is rare and can occur in syndromes such as pseudomonilethrix, Netherton syndrome, pili annulati,² argininosuccinic aciduria,³ trichothiodystrophy,⁴ Menkes syndrome,⁵ and trichohepatoenteric syndrome.⁶ The primary congenital form of TN is inherited as an autosomal-dominant trait in some families. Acquired TN is the most common hair shaft abnormality and often is overlooked. It is provoked by hair injury, usually mechanical or physical, or chemical trauma.^7,8

Chemical trauma is caused by the use of permanent hair liquids or dyes. Mechanical injuries are the result of frequent brushing, scalp massage, or lengthy backcombing, and physical damage includes excessive UV exposure or repeated application of heat. Habit tics, trichotillomania, and the scratching and pulling associated with pruritic dermatoses also can result in sufficient damage to provoke TN. Furthermore, this acquired disorder may develop from malnutrition, particularly iron deficiency, or endocrinopathy such as hypothyroidism.⁹ Seasonal recurrence of TN has been reported from the cumulative effect of repeated soaking in salt water and exposure to UV light. Macroscopically, hair shafts affected by TN contain small white nodes at irregular intervals throughout the length of the hair shaft. These nodes represent areas of cuticular cell disruption, which allows the underlying cortical fibers to separate and fray and gives the node the microscopic appearance of 2 brooms or paintbrushes thrusting together end-to-end by the bristles. The classic description is known as paintbrush fracture.¹⁰ Generally, complete breakage occurs at these nodes.

A 21-year-old white woman presented to our clinic with hair fragility and inability to grow long hair of 2 years’ duration. The hair was lusterless and dry. Dermoscopic examination revealed broken blunt-ended hair of uneven length with minute pinpoint grayish white nodules (Figure 1). Small fragments could be easily broken off with gentle tugging on the distal ends. She reported a history of severe sunlight and seawater exposure during the last 2 summers and the continuous use of a flat iron in the last year. Microscopic examination of hair samples with a scanning electron microscope showed the characteristic paintbrush fracture (Figure 2). She had no history of diseases, and blood examinations including complete blood cell count, thyroid function test, and iron levels were within reference range.

Figure 1. Dermoscopy revealed broken blunt-ended hair of uneven length with minute pinpoint grayish white nodules (original magnification ×30). Figure 2. Scanning electron microscopy showed characteristic paintbrush fracture of the hair shaft (original magnification ×748).

We hypothesize that the seasonal damage caused by exposure to UV light and salt water with repeated trauma from the heat of the flat iron caused distal TN. The patient was given an explanation about the diagnosis of TN and was instructed to avoid the practices that were suspected causes of the condition. Use of a gentle shampoo and conditioner also was recommended. At 6-month follow-up, we noticed an improvement of the quality of hair with a reduction in the whitish nodules and a revival of hair growth.

Acquired TN has been classified into 3 clinical forms: proximal, distal, and localized.¹ Proximal TN is common in black individuals who use caustic chemicals when styling the hair. The involved hairs develop the characteristic nodes that break within a few centimeters from the scalp, especially in areas subject to friction from combing or sleeping. Distal TN primarily occurs in white or Asian individuals. In this disorder, nodes and breakage occur near the ends of the hairs that appear dull, dry, and uneven. Breakage commonly is associated with trichoptilosis, or longitudinal splitting, commonly referred to as split ends. This breakage may reflect frequent use of shampoo or heat treatments. The distal acquired form may simulate dandruff or pediculosis and the detection of this hair defect often is casual.

Localized TN, described by Raymond Sabouraud in 1921, is a rare disorder. It occurs in a patch that is usually a few centimeters long. It generally is accompanied by a pruritic dermatosis, such as circumscribed neurodermatitis, contact dermatitis, or atopic dermatitis. Scratching and rubbing most likely are the ultimate causes.

Trichorrhexis nodosa can spontaneously resolve. In all cases, diagnosis depends on careful microscopy examination and, if possible, scanning electron microscopy. Treatment is aimed at minimizing mechanical and physical injury, and chemical trauma. Excessive brushing, hot-combing, permanent waving, and other harsh hair treatments should be avoided. If the hair is long and the damage is distal, it may be sufficient to cut the distal fraction and to change cosmetic practices to prevent relapse.

Dermatologists who see patients with hair fragility and inability to grow long hair should consider the diagnosis of TN. Acquired TN often is reversible. Complete resolution may take 2 to 4 years depending on the growth of new anagen hairs. All patients with a history of white flecking on the scalp, abnormal fragility of the hair, and failure to attain normal hair length should be questioned about their routine hair care habits as well as environmental or chemical exposures to determine and remove the source of physical or chemical trauma.

To the Editor:

First identified by Samuel Wilks in 1852, trichorrhexis nodosa (TN) is a congenital or acquired hair shaft disorder that is characterized by fragile and easily broken hair.¹ Congenital TN is rare and can occur in syndromes such as pseudomonilethrix, Netherton syndrome, pili annulati,² argininosuccinic aciduria,³ trichothiodystrophy,⁴ Menkes syndrome,⁵ and trichohepatoenteric syndrome.⁶ The primary congenital form of TN is inherited as an autosomal-dominant trait in some families. Acquired TN is the most common hair shaft abnormality and often is overlooked. It is provoked by hair injury, usually mechanical or physical, or chemical trauma.^7,8

Chemical trauma is caused by the use of permanent hair liquids or dyes. Mechanical injuries are the result of frequent brushing, scalp massage, or lengthy backcombing, and physical damage includes excessive UV exposure or repeated application of heat. Habit tics, trichotillomania, and the scratching and pulling associated with pruritic dermatoses also can result in sufficient damage to provoke TN. Furthermore, this acquired disorder may develop from malnutrition, particularly iron deficiency, or endocrinopathy such as hypothyroidism.⁹ Seasonal recurrence of TN has been reported from the cumulative effect of repeated soaking in salt water and exposure to UV light. Macroscopically, hair shafts affected by TN contain small white nodes at irregular intervals throughout the length of the hair shaft. These nodes represent areas of cuticular cell disruption, which allows the underlying cortical fibers to separate and fray and gives the node the microscopic appearance of 2 brooms or paintbrushes thrusting together end-to-end by the bristles. The classic description is known as paintbrush fracture.¹⁰ Generally, complete breakage occurs at these nodes.

A 21-year-old white woman presented to our clinic with hair fragility and inability to grow long hair of 2 years’ duration. The hair was lusterless and dry. Dermoscopic examination revealed broken blunt-ended hair of uneven length with minute pinpoint grayish white nodules (Figure 1). Small fragments could be easily broken off with gentle tugging on the distal ends. She reported a history of severe sunlight and seawater exposure during the last 2 summers and the continuous use of a flat iron in the last year. Microscopic examination of hair samples with a scanning electron microscope showed the characteristic paintbrush fracture (Figure 2). She had no history of diseases, and blood examinations including complete blood cell count, thyroid function test, and iron levels were within reference range.

Figure 1. Dermoscopy revealed broken blunt-ended hair of uneven length with minute pinpoint grayish white nodules (original magnification ×30). Figure 2. Scanning electron microscopy showed characteristic paintbrush fracture of the hair shaft (original magnification ×748).

We hypothesize that the seasonal damage caused by exposure to UV light and salt water with repeated trauma from the heat of the flat iron caused distal TN. The patient was given an explanation about the diagnosis of TN and was instructed to avoid the practices that were suspected causes of the condition. Use of a gentle shampoo and conditioner also was recommended. At 6-month follow-up, we noticed an improvement of the quality of hair with a reduction in the whitish nodules and a revival of hair growth.

Acquired TN has been classified into 3 clinical forms: proximal, distal, and localized.¹ Proximal TN is common in black individuals who use caustic chemicals when styling the hair. The involved hairs develop the characteristic nodes that break within a few centimeters from the scalp, especially in areas subject to friction from combing or sleeping. Distal TN primarily occurs in white or Asian individuals. In this disorder, nodes and breakage occur near the ends of the hairs that appear dull, dry, and uneven. Breakage commonly is associated with trichoptilosis, or longitudinal splitting, commonly referred to as split ends. This breakage may reflect frequent use of shampoo or heat treatments. The distal acquired form may simulate dandruff or pediculosis and the detection of this hair defect often is casual.

Localized TN, described by Raymond Sabouraud in 1921, is a rare disorder. It occurs in a patch that is usually a few centimeters long. It generally is accompanied by a pruritic dermatosis, such as circumscribed neurodermatitis, contact dermatitis, or atopic dermatitis. Scratching and rubbing most likely are the ultimate causes.

Trichorrhexis nodosa can spontaneously resolve. In all cases, diagnosis depends on careful microscopy examination and, if possible, scanning electron microscopy. Treatment is aimed at minimizing mechanical and physical injury, and chemical trauma. Excessive brushing, hot-combing, permanent waving, and other harsh hair treatments should be avoided. If the hair is long and the damage is distal, it may be sufficient to cut the distal fraction and to change cosmetic practices to prevent relapse.

Dermatologists who see patients with hair fragility and inability to grow long hair should consider the diagnosis of TN. Acquired TN often is reversible. Complete resolution may take 2 to 4 years depending on the growth of new anagen hairs. All patients with a history of white flecking on the scalp, abnormal fragility of the hair, and failure to attain normal hair length should be questioned about their routine hair care habits as well as environmental or chemical exposures to determine and remove the source of physical or chemical trauma.

To the Editor:

First identified by Samuel Wilks in 1852, trichorrhexis nodosa (TN) is a congenital or acquired hair shaft disorder that is characterized by fragile and easily broken hair.¹ Congenital TN is rare and can occur in syndromes such as pseudomonilethrix, Netherton syndrome, pili annulati,² argininosuccinic aciduria,³ trichothiodystrophy,⁴ Menkes syndrome,⁵ and trichohepatoenteric syndrome.⁶ The primary congenital form of TN is inherited as an autosomal-dominant trait in some families. Acquired TN is the most common hair shaft abnormality and often is overlooked. It is provoked by hair injury, usually mechanical or physical, or chemical trauma.^7,8

Chemical trauma is caused by the use of permanent hair liquids or dyes. Mechanical injuries are the result of frequent brushing, scalp massage, or lengthy backcombing, and physical damage includes excessive UV exposure or repeated application of heat. Habit tics, trichotillomania, and the scratching and pulling associated with pruritic dermatoses also can result in sufficient damage to provoke TN. Furthermore, this acquired disorder may develop from malnutrition, particularly iron deficiency, or endocrinopathy such as hypothyroidism.⁹ Seasonal recurrence of TN has been reported from the cumulative effect of repeated soaking in salt water and exposure to UV light. Macroscopically, hair shafts affected by TN contain small white nodes at irregular intervals throughout the length of the hair shaft. These nodes represent areas of cuticular cell disruption, which allows the underlying cortical fibers to separate and fray and gives the node the microscopic appearance of 2 brooms or paintbrushes thrusting together end-to-end by the bristles. The classic description is known as paintbrush fracture.¹⁰ Generally, complete breakage occurs at these nodes.

A 21-year-old white woman presented to our clinic with hair fragility and inability to grow long hair of 2 years’ duration. The hair was lusterless and dry. Dermoscopic examination revealed broken blunt-ended hair of uneven length with minute pinpoint grayish white nodules (Figure 1). Small fragments could be easily broken off with gentle tugging on the distal ends. She reported a history of severe sunlight and seawater exposure during the last 2 summers and the continuous use of a flat iron in the last year. Microscopic examination of hair samples with a scanning electron microscope showed the characteristic paintbrush fracture (Figure 2). She had no history of diseases, and blood examinations including complete blood cell count, thyroid function test, and iron levels were within reference range.

Figure 1. Dermoscopy revealed broken blunt-ended hair of uneven length with minute pinpoint grayish white nodules (original magnification ×30). Figure 2. Scanning electron microscopy showed characteristic paintbrush fracture of the hair shaft (original magnification ×748).

We hypothesize that the seasonal damage caused by exposure to UV light and salt water with repeated trauma from the heat of the flat iron caused distal TN. The patient was given an explanation about the diagnosis of TN and was instructed to avoid the practices that were suspected causes of the condition. Use of a gentle shampoo and conditioner also was recommended. At 6-month follow-up, we noticed an improvement of the quality of hair with a reduction in the whitish nodules and a revival of hair growth.

Acquired TN has been classified into 3 clinical forms: proximal, distal, and localized.¹ Proximal TN is common in black individuals who use caustic chemicals when styling the hair. The involved hairs develop the characteristic nodes that break within a few centimeters from the scalp, especially in areas subject to friction from combing or sleeping. Distal TN primarily occurs in white or Asian individuals. In this disorder, nodes and breakage occur near the ends of the hairs that appear dull, dry, and uneven. Breakage commonly is associated with trichoptilosis, or longitudinal splitting, commonly referred to as split ends. This breakage may reflect frequent use of shampoo or heat treatments. The distal acquired form may simulate dandruff or pediculosis and the detection of this hair defect often is casual.

Localized TN, described by Raymond Sabouraud in 1921, is a rare disorder. It occurs in a patch that is usually a few centimeters long. It generally is accompanied by a pruritic dermatosis, such as circumscribed neurodermatitis, contact dermatitis, or atopic dermatitis. Scratching and rubbing most likely are the ultimate causes.

Trichorrhexis nodosa can spontaneously resolve. In all cases, diagnosis depends on careful microscopy examination and, if possible, scanning electron microscopy. Treatment is aimed at minimizing mechanical and physical injury, and chemical trauma. Excessive brushing, hot-combing, permanent waving, and other harsh hair treatments should be avoided. If the hair is long and the damage is distal, it may be sufficient to cut the distal fraction and to change cosmetic practices to prevent relapse.

Dermatologists who see patients with hair fragility and inability to grow long hair should consider the diagnosis of TN. Acquired TN often is reversible. Complete resolution may take 2 to 4 years depending on the growth of new anagen hairs. All patients with a history of white flecking on the scalp, abnormal fragility of the hair, and failure to attain normal hair length should be questioned about their routine hair care habits as well as environmental or chemical exposures to determine and remove the source of physical or chemical trauma.

To the Editor:

Liposomal doxorubicin hydrochloride is an anthracycline topoisomerase inhibitor indicated for ovarian cancer, AIDS-related Kaposi sarcoma, and multiple myeloma.¹ It also has been used with limited success in a clinical trial of previously treated patients with endometrial cancer.² The most common adverse reactions include asthenia, fatigue, fever, anorexia, nausea, vomiting, stomatitis, diarrhea, constipation, hand-and-foot syndrome, rash, neutropenia, thrombocytopenia, and anemia.¹

A 58-year-old woman with a history of stage IIIA endometrial cancer underwent a total abdominal hysterectomy and bilateral salpingo-oophorectomy soon after diagnosis. She then completed 5 high-dose-rate brachytherapy treatments and 6 cycles of paclitaxel and carboplatin. Follow-up imaging revealed pulmonary metastasis. The patient was then enrolled in a clinical trial but was switched to 40 mg/m² liposomal doxorubicin given once every 28 days for 5 cycles after progression of disease.

After each dose of doxorubicin, she developed redness of the palms and soles. Following the third cycle of doxorubicin, a painful rash involving the thighs and axilla appeared with some desquamation in the left axilla. Three weeks after the fourth dose of doxorubicin, she presented with severe worsening of the rash to involve the extensor elbows (Figure 1), back, and lower legs with bilateral axillary desquamation. The bilateral medial thighs were erythematous with maceration that was tender and blanchable (Figure 2). The total affected body surface area was 10% to 15%. There was no involvement of the mucosa. She was treated with hydrogel sheet dressings and silver sulfadiazine cream 1%.

Figure 1. Extensor surface of the elbow with an erythematous patch 3 weeks after the fourth dose of doxorubicin.

Figure 2. Medial thigh with erythema and maceration.

The patient’s rash was thought to be due to doxorubicin toxicity; however, a 4-mm punch biopsy specimen from the left thigh was taken for culture and hemotoxylin and eosin stain to rule out other possibilities. Biopsy was consistent with a drug reaction, revealing superficial perivascular dermatitis with keratinocyte atypia of the epidermis. Doxorubicin was discontinued and the rash resolved completely within 2 weeks, except for some thickening of the skin on the palms, soles, and thighs. After a delay of approximately 1 week, doxorubicin was resumed at a lower dose of 30 mg/m². No dermatologic symptoms followed treatment at this dose.

Four clinical patterns of doxorubicin toxicity are recognized. The most common pattern is acral erythema, also known as hand-and-foot syndrome, which is followed by desquamation of the palms and soles, occurring in approximately 50% of patients. Ten percent of patients experience a diffuse follicular rash with mild, diffuse, scaly erythema and follicular accentuation that often occurs over the lateral limbs but also may occur over the trunk. New melanotic macules may appear on the trunk or extremities including palms and soles.³ Finally, an intertrigolike eruption exacerbated by friction with erythematous patches over skin folds or in areas of friction also has been described.^3-5 Our patient presented with a combination of dermatologic toxicities including acral erythema and intertrigolike eruption. Acral erythema occurred in 24 of 60 patients and intertrigolike eruption occurred in 5 of 60 patients in one study.³ Another report documented both occurring together.⁵

Treatment of doxorubicin skin toxicity consists of reduction of the dose of doxorubicin, supportive care, and patient education. Specific treatments include topical wound care, emollient creams, and pain management with analgesics. Other interventions include wearing loose clothing, avoiding vigorous exercise, and sitting on padded surfaces.⁶

Doxorubicin skin toxicity presents in several clinical patterns. Although acral erythema is the most common pattern, severe intertrigolike eruptions similar to our case may occur. Physicians caring for patients receiving doxorubicin should be aware of the variety of presentations of skin toxicity and the possible need for dose reduction to decrease symptoms.

To the Editor:

Liposomal doxorubicin hydrochloride is an anthracycline topoisomerase inhibitor indicated for ovarian cancer, AIDS-related Kaposi sarcoma, and multiple myeloma.¹ It also has been used with limited success in a clinical trial of previously treated patients with endometrial cancer.² The most common adverse reactions include asthenia, fatigue, fever, anorexia, nausea, vomiting, stomatitis, diarrhea, constipation, hand-and-foot syndrome, rash, neutropenia, thrombocytopenia, and anemia.¹

A 58-year-old woman with a history of stage IIIA endometrial cancer underwent a total abdominal hysterectomy and bilateral salpingo-oophorectomy soon after diagnosis. She then completed 5 high-dose-rate brachytherapy treatments and 6 cycles of paclitaxel and carboplatin. Follow-up imaging revealed pulmonary metastasis. The patient was then enrolled in a clinical trial but was switched to 40 mg/m² liposomal doxorubicin given once every 28 days for 5 cycles after progression of disease.

After each dose of doxorubicin, she developed redness of the palms and soles. Following the third cycle of doxorubicin, a painful rash involving the thighs and axilla appeared with some desquamation in the left axilla. Three weeks after the fourth dose of doxorubicin, she presented with severe worsening of the rash to involve the extensor elbows (Figure 1), back, and lower legs with bilateral axillary desquamation. The bilateral medial thighs were erythematous with maceration that was tender and blanchable (Figure 2). The total affected body surface area was 10% to 15%. There was no involvement of the mucosa. She was treated with hydrogel sheet dressings and silver sulfadiazine cream 1%.

Figure 1. Extensor surface of the elbow with an erythematous patch 3 weeks after the fourth dose of doxorubicin.

Figure 2. Medial thigh with erythema and maceration.

The patient’s rash was thought to be due to doxorubicin toxicity; however, a 4-mm punch biopsy specimen from the left thigh was taken for culture and hemotoxylin and eosin stain to rule out other possibilities. Biopsy was consistent with a drug reaction, revealing superficial perivascular dermatitis with keratinocyte atypia of the epidermis. Doxorubicin was discontinued and the rash resolved completely within 2 weeks, except for some thickening of the skin on the palms, soles, and thighs. After a delay of approximately 1 week, doxorubicin was resumed at a lower dose of 30 mg/m². No dermatologic symptoms followed treatment at this dose.

Four clinical patterns of doxorubicin toxicity are recognized. The most common pattern is acral erythema, also known as hand-and-foot syndrome, which is followed by desquamation of the palms and soles, occurring in approximately 50% of patients. Ten percent of patients experience a diffuse follicular rash with mild, diffuse, scaly erythema and follicular accentuation that often occurs over the lateral limbs but also may occur over the trunk. New melanotic macules may appear on the trunk or extremities including palms and soles.³ Finally, an intertrigolike eruption exacerbated by friction with erythematous patches over skin folds or in areas of friction also has been described.^3-5 Our patient presented with a combination of dermatologic toxicities including acral erythema and intertrigolike eruption. Acral erythema occurred in 24 of 60 patients and intertrigolike eruption occurred in 5 of 60 patients in one study.³ Another report documented both occurring together.⁵

Treatment of doxorubicin skin toxicity consists of reduction of the dose of doxorubicin, supportive care, and patient education. Specific treatments include topical wound care, emollient creams, and pain management with analgesics. Other interventions include wearing loose clothing, avoiding vigorous exercise, and sitting on padded surfaces.⁶

Doxorubicin skin toxicity presents in several clinical patterns. Although acral erythema is the most common pattern, severe intertrigolike eruptions similar to our case may occur. Physicians caring for patients receiving doxorubicin should be aware of the variety of presentations of skin toxicity and the possible need for dose reduction to decrease symptoms.

To the Editor:

Liposomal doxorubicin hydrochloride is an anthracycline topoisomerase inhibitor indicated for ovarian cancer, AIDS-related Kaposi sarcoma, and multiple myeloma.¹ It also has been used with limited success in a clinical trial of previously treated patients with endometrial cancer.² The most common adverse reactions include asthenia, fatigue, fever, anorexia, nausea, vomiting, stomatitis, diarrhea, constipation, hand-and-foot syndrome, rash, neutropenia, thrombocytopenia, and anemia.¹

A 58-year-old woman with a history of stage IIIA endometrial cancer underwent a total abdominal hysterectomy and bilateral salpingo-oophorectomy soon after diagnosis. She then completed 5 high-dose-rate brachytherapy treatments and 6 cycles of paclitaxel and carboplatin. Follow-up imaging revealed pulmonary metastasis. The patient was then enrolled in a clinical trial but was switched to 40 mg/m² liposomal doxorubicin given once every 28 days for 5 cycles after progression of disease.

After each dose of doxorubicin, she developed redness of the palms and soles. Following the third cycle of doxorubicin, a painful rash involving the thighs and axilla appeared with some desquamation in the left axilla. Three weeks after the fourth dose of doxorubicin, she presented with severe worsening of the rash to involve the extensor elbows (Figure 1), back, and lower legs with bilateral axillary desquamation. The bilateral medial thighs were erythematous with maceration that was tender and blanchable (Figure 2). The total affected body surface area was 10% to 15%. There was no involvement of the mucosa. She was treated with hydrogel sheet dressings and silver sulfadiazine cream 1%.

Figure 1. Extensor surface of the elbow with an erythematous patch 3 weeks after the fourth dose of doxorubicin.

Figure 2. Medial thigh with erythema and maceration.

The patient’s rash was thought to be due to doxorubicin toxicity; however, a 4-mm punch biopsy specimen from the left thigh was taken for culture and hemotoxylin and eosin stain to rule out other possibilities. Biopsy was consistent with a drug reaction, revealing superficial perivascular dermatitis with keratinocyte atypia of the epidermis. Doxorubicin was discontinued and the rash resolved completely within 2 weeks, except for some thickening of the skin on the palms, soles, and thighs. After a delay of approximately 1 week, doxorubicin was resumed at a lower dose of 30 mg/m². No dermatologic symptoms followed treatment at this dose.

Four clinical patterns of doxorubicin toxicity are recognized. The most common pattern is acral erythema, also known as hand-and-foot syndrome, which is followed by desquamation of the palms and soles, occurring in approximately 50% of patients. Ten percent of patients experience a diffuse follicular rash with mild, diffuse, scaly erythema and follicular accentuation that often occurs over the lateral limbs but also may occur over the trunk. New melanotic macules may appear on the trunk or extremities including palms and soles.³ Finally, an intertrigolike eruption exacerbated by friction with erythematous patches over skin folds or in areas of friction also has been described.^3-5 Our patient presented with a combination of dermatologic toxicities including acral erythema and intertrigolike eruption. Acral erythema occurred in 24 of 60 patients and intertrigolike eruption occurred in 5 of 60 patients in one study.³ Another report documented both occurring together.⁵

Treatment of doxorubicin skin toxicity consists of reduction of the dose of doxorubicin, supportive care, and patient education. Specific treatments include topical wound care, emollient creams, and pain management with analgesics. Other interventions include wearing loose clothing, avoiding vigorous exercise, and sitting on padded surfaces.⁶

Doxorubicin skin toxicity presents in several clinical patterns. Although acral erythema is the most common pattern, severe intertrigolike eruptions similar to our case may occur. Physicians caring for patients receiving doxorubicin should be aware of the variety of presentations of skin toxicity and the possible need for dose reduction to decrease symptoms.

The panniculitides can be a complex dermatologic entity for both dermatologists and dermatopathologists. The history, clinical examination, and histology need to be correlated to arrive at a differential diagnosis that will ultimately provide a diagnosis for the subcutaneous lesions. Panniculitis is an inflammation of the subcutaneous adipose tissue and can be associated with systemic diseases. According to Peters and Su,¹ “Anatomic location of lesions, presence or absence of ulceration, occurrence of lipoatrophy, history of trauma, association with immunologic or metabolic disorders, and age of the patient are important clinical data to consider in conjunction with the microscopic features.” The panniculitides histologic differences may be subtle because they all include septal and lobular components, but one is usually more dominant in leading to a diagnosis along with the clinical findings.²

Cold panniculitis is a form of traumatic panniculitis. We present a unique case of this condition that was caused by use of a cold therapy unit following surgery to relieve pain.

Case Report

A 37-year-old woman presented for a routine postoperative visit 15 days following arthroscopic repair of a superior labrum anterior posterior tear in the left shoulder with a single suture anchor. The patient reported a rash that had developed 10 days postoperatively on the left upper arm. The rash started as red dots that progressively became larger, painful, and warm to the touch. The rash did not spread anywhere else on the patient’s body, and she denied fever, chills, and pruritus. She had tried using diphenhydramine without relief. The only new medication the patient had started prior to the eruption was oxycodone, which was initiated immediately following surgery. Prior to surgery, the entire left upper extremity including the shoulder had been prepared with a preoperative surgical skin antiseptic. There were no visible signs of the antiseptic on the skin at the time of presentation. The patient reported that she had applied a cold therapy unit to the left upper arm over her clothing for 1 hour every night since surgery. The cold therapy unit frequently is used to help decrease postoperative pain, swelling, inflammation, and narcotic use following surgical procedures.

Physical examination revealed multiple well-defined, erythematous, tender, indurated, warm nodules on the lateral aspect of the left upper arm (Figure 1). No other areas of eruption were noted on the body, and there was no swelling of the left elbow, forearm, wrist, or hand. The left upper extremity demonstrated intact sensation, rapid capillary refill, and a palpable radial pulse. Her weight was 230.1 lb with a body mass index of 35.

Figure 1. Multiple well-defined, erythematous, tender, indurated nodules presented on the lateral aspect of the left upper arm. Figure 2. Punch biopsy showed a superficial and deep perivascular and periadnexal lymphoid infiltrate with involvement of the subcutis (H&E, original magnification ×40).

A 5-mm punch biopsy from a nodule on the left upper arm was performed, and pathology demonstrated vacuolar interface changes with patchy parakeratosis, spongiosis, and dyskeratosis on staining with hematoxylin and eosin. Pandermal and subcutaneous perivascular, periadnexal, and mild interstitial lymphohistiocytic infiltrate with occasional neutrophils and eosinophils were noted (Figure 2). The inflammation extended to the subcutaneous fat involving both septae and lobules with a primarily lobular distribution.

Clinical and pathologic correlation was required to arrive at a definitive diagnosis of cold panniculitis. The epidermal and dermal changes were consistent with a pernio or chilblains type of insult, and the septal and lobular panniculitis was indicative of cold panniculitis. The patient was advised to discontinue use of the cold therapy device as well as any other form of icing of the left shoulder or arm. She continued the oxycodone for pain control. Four weeks postoperatively, only desquamation remained where the nodules had previously appeared, which also eventually resolved.

Comment

Infants and small children are more predisposed to cold panniculitis than adults. In their 2008 review, Quesada-Cortés et al³ found the first report of cold panniculitis by Hochsinger in 1902 in a German pediatric journal, followed by reports from Lemez in 1928 and Haxthausen in 1941, which subsequently described similar cases in infants. Adult cases were not reported until 1963 by Solomon and Beerman⁴ and then in 1980 by Beacham et al.⁵

Etiologies for children have included popsicles, ice packs applied to the face to control supraventricular tachycardia or to the lower extremities after vaccinations, and cold weather exposure.⁶ The chemical composition of fat tissue plays a role in pediatric patients. According to Quesada-Cortés et al,³ subcutaneous fat in newborns is rich in saturated oils such as palmitic and stearic acids that have a higher solidification point. A small decrease in an infant’s temperature may result in crystallization of fat. The subcutaneous fat tends to become more unsaturated with aging with more oleic acid, and the solidification temperature diminishes.⁷

Cryoglobulins and cold agglutinins have not been demonstrated to be a cause of cold panniculitis in infants.⁷ Severe cold exposure or predisposition to certain conditions such as cryofibrinogenemia may occur in some adult patients. Gender does not seem to be a factor in children; however, in adults, women tend to be more predisposed to cold panniculitis secondary to obesity and participation in activities such as cycling, motorcycling, or horseback riding in cold conditions.³

On clinical examination, cold panniculitis features erythematous, firm, tender nodules on the cheeks and chin in infants and small children.² These areas often are exposed to cold weather or wind because they typically are not covered with protective clothing.³ Nodules generally occur 1 to 3 days following exposure to cold and usually resolve spontaneously within 2 weeks.⁸ Popsicle panniculitis is characterized by a reddish discoloration on both cheeks 1 or 2 days after sucking on popsicles or ice cubes. This reaction can be reproduced in a half day by applying an ice cube to the volar forearm for 2 minutes, which can help diagnose and differentiate this subset of cold panniuculits.³ The red area in cold panniculitis eventually turns purple, becomes less indurated, and fades in approximately 3 months, but occasionally residual hyperpigmentation will last for a few months. Ice packs used as treatment of congenital cardiac arrhythmias in some cardiac surgeries and as surface cooling for management of birth asphyxia can produce a similar physical presentation.³

Equestrian panniculitis is characterized by erythematous, violaceous, tender plaques on the upper lateral thighs of young females who participate in horseback riding in the winter while wearing tight-fitting pants.^2,5 These plaques typically occur within several hours and over the next week become painful, violaceous, and indurated or develop red nodules or plaques that can ulcerate or become crusted.³ These lesions usually will spontaneously resolve within 3 weeks, but new areas may occur again during the winter on further exposure with occasional persistent hyperpigmentation. These areas usually disappear at the end of winter with warmer weather or when horseback riding is discontinued. Perniosis also needs to be considered in the differential diagnosis due to the location and appearance of the lesions.³

It is important to obtain the correct specimen for biopsy. According to Peters and Su,¹ a deep excisional biopsy that includes multiple fat lobules in addition to dermis and epidermis is critical. On histology, cold panniculitis usually demonstrates a primarily lobular inflammation. There typically is a superficial and deep perivascular lymphocytic infiltrate in the papillary dermis with edema noted in the connective tissue around the eccrine glands that can appear similar to perniosis on histopathology.⁹ Deposition of mucin, focal panniculitis surrounded by fatty tissue without inflammatory changes within the same field, and fat necrosis with pseudocysts and numerous lipophages also are characteristic features of cold panniculitis.¹⁰ Needlelike clefts are not present in cold panniculitis but appear in subcutaneous fat necrosis of the newborn.¹

Different treatments have been tried, but no substantial impact on the rate of dissipation of the lesions has been noted. The plaques slowly resolve without scarring over 2 to 3 weeks if the cold source is removed.² Application of a heating pad to the affected area has been used with limited success. Vasodilators such as nifedipine have been used but have not been found to be effective.³ Antihistamines also have failed to control the lesions.¹¹

Treatment of cold panniculitis is based on the prevention of further insult versus trying to cure the condition. Avoidance of cold and wind exposure as well as direct contact with ice are key methods in preventing cold panniculitis.

Our patient’s presentation of this condition was unique. Although cold panniculitis lesions usually develop 1 to 3 days after cold exposure, our patient did not develop lesions until 10 days following surgery. The cold therapy unit used by our patient was evaluated in our office and also by the manufacturer and was found to be functioning normally with no defects. The late onset of the lesions was attributed to limited application of the cold therapy unit; our patient used it for only 1 hour every night, whereas application for 6 to 8 hours continuously is normally recommended. The lesions may have occurred sooner had the patient been using a solid ice pack versus the continuous cold circulating water of the cold therapy unit. Pathology was consistent with the patient’s history and physical examination indicating a diagnosis of cold panniculitis. The challenge of treatment was to alleviate the pain of the lesions as well as the postoperative shoulder pain without the aid of any form of cold therapy. The patient only needed a tincture of time, as the lesions resolved after 4 weeks. Patient education was provided on future prevention of this condition by avoiding exposure to cold or applying cold packs directly to the skin.

Acknowledgment

The authors thank the staff at the Office of Scientific Writing and Publication at the Marshfield Clinic Research Foundation, Wisconsin, for their editorial assistance in the preparation of this manuscript.

The panniculitides can be a complex dermatologic entity for both dermatologists and dermatopathologists. The history, clinical examination, and histology need to be correlated to arrive at a differential diagnosis that will ultimately provide a diagnosis for the subcutaneous lesions. Panniculitis is an inflammation of the subcutaneous adipose tissue and can be associated with systemic diseases. According to Peters and Su,¹ “Anatomic location of lesions, presence or absence of ulceration, occurrence of lipoatrophy, history of trauma, association with immunologic or metabolic disorders, and age of the patient are important clinical data to consider in conjunction with the microscopic features.” The panniculitides histologic differences may be subtle because they all include septal and lobular components, but one is usually more dominant in leading to a diagnosis along with the clinical findings.²

Cold panniculitis is a form of traumatic panniculitis. We present a unique case of this condition that was caused by use of a cold therapy unit following surgery to relieve pain.

Case Report

A 37-year-old woman presented for a routine postoperative visit 15 days following arthroscopic repair of a superior labrum anterior posterior tear in the left shoulder with a single suture anchor. The patient reported a rash that had developed 10 days postoperatively on the left upper arm. The rash started as red dots that progressively became larger, painful, and warm to the touch. The rash did not spread anywhere else on the patient’s body, and she denied fever, chills, and pruritus. She had tried using diphenhydramine without relief. The only new medication the patient had started prior to the eruption was oxycodone, which was initiated immediately following surgery. Prior to surgery, the entire left upper extremity including the shoulder had been prepared with a preoperative surgical skin antiseptic. There were no visible signs of the antiseptic on the skin at the time of presentation. The patient reported that she had applied a cold therapy unit to the left upper arm over her clothing for 1 hour every night since surgery. The cold therapy unit frequently is used to help decrease postoperative pain, swelling, inflammation, and narcotic use following surgical procedures.

Physical examination revealed multiple well-defined, erythematous, tender, indurated, warm nodules on the lateral aspect of the left upper arm (Figure 1). No other areas of eruption were noted on the body, and there was no swelling of the left elbow, forearm, wrist, or hand. The left upper extremity demonstrated intact sensation, rapid capillary refill, and a palpable radial pulse. Her weight was 230.1 lb with a body mass index of 35.

Figure 1. Multiple well-defined, erythematous, tender, indurated nodules presented on the lateral aspect of the left upper arm. Figure 2. Punch biopsy showed a superficial and deep perivascular and periadnexal lymphoid infiltrate with involvement of the subcutis (H&E, original magnification ×40).

A 5-mm punch biopsy from a nodule on the left upper arm was performed, and pathology demonstrated vacuolar interface changes with patchy parakeratosis, spongiosis, and dyskeratosis on staining with hematoxylin and eosin. Pandermal and subcutaneous perivascular, periadnexal, and mild interstitial lymphohistiocytic infiltrate with occasional neutrophils and eosinophils were noted (Figure 2). The inflammation extended to the subcutaneous fat involving both septae and lobules with a primarily lobular distribution.

Clinical and pathologic correlation was required to arrive at a definitive diagnosis of cold panniculitis. The epidermal and dermal changes were consistent with a pernio or chilblains type of insult, and the septal and lobular panniculitis was indicative of cold panniculitis. The patient was advised to discontinue use of the cold therapy device as well as any other form of icing of the left shoulder or arm. She continued the oxycodone for pain control. Four weeks postoperatively, only desquamation remained where the nodules had previously appeared, which also eventually resolved.

Comment

Infants and small children are more predisposed to cold panniculitis than adults. In their 2008 review, Quesada-Cortés et al³ found the first report of cold panniculitis by Hochsinger in 1902 in a German pediatric journal, followed by reports from Lemez in 1928 and Haxthausen in 1941, which subsequently described similar cases in infants. Adult cases were not reported until 1963 by Solomon and Beerman⁴ and then in 1980 by Beacham et al.⁵

Etiologies for children have included popsicles, ice packs applied to the face to control supraventricular tachycardia or to the lower extremities after vaccinations, and cold weather exposure.⁶ The chemical composition of fat tissue plays a role in pediatric patients. According to Quesada-Cortés et al,³ subcutaneous fat in newborns is rich in saturated oils such as palmitic and stearic acids that have a higher solidification point. A small decrease in an infant’s temperature may result in crystallization of fat. The subcutaneous fat tends to become more unsaturated with aging with more oleic acid, and the solidification temperature diminishes.⁷

Cryoglobulins and cold agglutinins have not been demonstrated to be a cause of cold panniculitis in infants.⁷ Severe cold exposure or predisposition to certain conditions such as cryofibrinogenemia may occur in some adult patients. Gender does not seem to be a factor in children; however, in adults, women tend to be more predisposed to cold panniculitis secondary to obesity and participation in activities such as cycling, motorcycling, or horseback riding in cold conditions.³

On clinical examination, cold panniculitis features erythematous, firm, tender nodules on the cheeks and chin in infants and small children.² These areas often are exposed to cold weather or wind because they typically are not covered with protective clothing.³ Nodules generally occur 1 to 3 days following exposure to cold and usually resolve spontaneously within 2 weeks.⁸ Popsicle panniculitis is characterized by a reddish discoloration on both cheeks 1 or 2 days after sucking on popsicles or ice cubes. This reaction can be reproduced in a half day by applying an ice cube to the volar forearm for 2 minutes, which can help diagnose and differentiate this subset of cold panniuculits.³ The red area in cold panniculitis eventually turns purple, becomes less indurated, and fades in approximately 3 months, but occasionally residual hyperpigmentation will last for a few months. Ice packs used as treatment of congenital cardiac arrhythmias in some cardiac surgeries and as surface cooling for management of birth asphyxia can produce a similar physical presentation.³

Equestrian panniculitis is characterized by erythematous, violaceous, tender plaques on the upper lateral thighs of young females who participate in horseback riding in the winter while wearing tight-fitting pants.^2,5 These plaques typically occur within several hours and over the next week become painful, violaceous, and indurated or develop red nodules or plaques that can ulcerate or become crusted.³ These lesions usually will spontaneously resolve within 3 weeks, but new areas may occur again during the winter on further exposure with occasional persistent hyperpigmentation. These areas usually disappear at the end of winter with warmer weather or when horseback riding is discontinued. Perniosis also needs to be considered in the differential diagnosis due to the location and appearance of the lesions.³

It is important to obtain the correct specimen for biopsy. According to Peters and Su,¹ a deep excisional biopsy that includes multiple fat lobules in addition to dermis and epidermis is critical. On histology, cold panniculitis usually demonstrates a primarily lobular inflammation. There typically is a superficial and deep perivascular lymphocytic infiltrate in the papillary dermis with edema noted in the connective tissue around the eccrine glands that can appear similar to perniosis on histopathology.⁹ Deposition of mucin, focal panniculitis surrounded by fatty tissue without inflammatory changes within the same field, and fat necrosis with pseudocysts and numerous lipophages also are characteristic features of cold panniculitis.¹⁰ Needlelike clefts are not present in cold panniculitis but appear in subcutaneous fat necrosis of the newborn.¹

Different treatments have been tried, but no substantial impact on the rate of dissipation of the lesions has been noted. The plaques slowly resolve without scarring over 2 to 3 weeks if the cold source is removed.² Application of a heating pad to the affected area has been used with limited success. Vasodilators such as nifedipine have been used but have not been found to be effective.³ Antihistamines also have failed to control the lesions.¹¹

Treatment of cold panniculitis is based on the prevention of further insult versus trying to cure the condition. Avoidance of cold and wind exposure as well as direct contact with ice are key methods in preventing cold panniculitis.

Our patient’s presentation of this condition was unique. Although cold panniculitis lesions usually develop 1 to 3 days after cold exposure, our patient did not develop lesions until 10 days following surgery. The cold therapy unit used by our patient was evaluated in our office and also by the manufacturer and was found to be functioning normally with no defects. The late onset of the lesions was attributed to limited application of the cold therapy unit; our patient used it for only 1 hour every night, whereas application for 6 to 8 hours continuously is normally recommended. The lesions may have occurred sooner had the patient been using a solid ice pack versus the continuous cold circulating water of the cold therapy unit. Pathology was consistent with the patient’s history and physical examination indicating a diagnosis of cold panniculitis. The challenge of treatment was to alleviate the pain of the lesions as well as the postoperative shoulder pain without the aid of any form of cold therapy. The patient only needed a tincture of time, as the lesions resolved after 4 weeks. Patient education was provided on future prevention of this condition by avoiding exposure to cold or applying cold packs directly to the skin.

Acknowledgment

The authors thank the staff at the Office of Scientific Writing and Publication at the Marshfield Clinic Research Foundation, Wisconsin, for their editorial assistance in the preparation of this manuscript.

The panniculitides can be a complex dermatologic entity for both dermatologists and dermatopathologists. The history, clinical examination, and histology need to be correlated to arrive at a differential diagnosis that will ultimately provide a diagnosis for the subcutaneous lesions. Panniculitis is an inflammation of the subcutaneous adipose tissue and can be associated with systemic diseases. According to Peters and Su,¹ “Anatomic location of lesions, presence or absence of ulceration, occurrence of lipoatrophy, history of trauma, association with immunologic or metabolic disorders, and age of the patient are important clinical data to consider in conjunction with the microscopic features.” The panniculitides histologic differences may be subtle because they all include septal and lobular components, but one is usually more dominant in leading to a diagnosis along with the clinical findings.²

Cold panniculitis is a form of traumatic panniculitis. We present a unique case of this condition that was caused by use of a cold therapy unit following surgery to relieve pain.

Case Report

A 37-year-old woman presented for a routine postoperative visit 15 days following arthroscopic repair of a superior labrum anterior posterior tear in the left shoulder with a single suture anchor. The patient reported a rash that had developed 10 days postoperatively on the left upper arm. The rash started as red dots that progressively became larger, painful, and warm to the touch. The rash did not spread anywhere else on the patient’s body, and she denied fever, chills, and pruritus. She had tried using diphenhydramine without relief. The only new medication the patient had started prior to the eruption was oxycodone, which was initiated immediately following surgery. Prior to surgery, the entire left upper extremity including the shoulder had been prepared with a preoperative surgical skin antiseptic. There were no visible signs of the antiseptic on the skin at the time of presentation. The patient reported that she had applied a cold therapy unit to the left upper arm over her clothing for 1 hour every night since surgery. The cold therapy unit frequently is used to help decrease postoperative pain, swelling, inflammation, and narcotic use following surgical procedures.

Physical examination revealed multiple well-defined, erythematous, tender, indurated, warm nodules on the lateral aspect of the left upper arm (Figure 1). No other areas of eruption were noted on the body, and there was no swelling of the left elbow, forearm, wrist, or hand. The left upper extremity demonstrated intact sensation, rapid capillary refill, and a palpable radial pulse. Her weight was 230.1 lb with a body mass index of 35.

Figure 1. Multiple well-defined, erythematous, tender, indurated nodules presented on the lateral aspect of the left upper arm. Figure 2. Punch biopsy showed a superficial and deep perivascular and periadnexal lymphoid infiltrate with involvement of the subcutis (H&E, original magnification ×40).

A 5-mm punch biopsy from a nodule on the left upper arm was performed, and pathology demonstrated vacuolar interface changes with patchy parakeratosis, spongiosis, and dyskeratosis on staining with hematoxylin and eosin. Pandermal and subcutaneous perivascular, periadnexal, and mild interstitial lymphohistiocytic infiltrate with occasional neutrophils and eosinophils were noted (Figure 2). The inflammation extended to the subcutaneous fat involving both septae and lobules with a primarily lobular distribution.

Clinical and pathologic correlation was required to arrive at a definitive diagnosis of cold panniculitis. The epidermal and dermal changes were consistent with a pernio or chilblains type of insult, and the septal and lobular panniculitis was indicative of cold panniculitis. The patient was advised to discontinue use of the cold therapy device as well as any other form of icing of the left shoulder or arm. She continued the oxycodone for pain control. Four weeks postoperatively, only desquamation remained where the nodules had previously appeared, which also eventually resolved.

Comment

Infants and small children are more predisposed to cold panniculitis than adults. In their 2008 review, Quesada-Cortés et al³ found the first report of cold panniculitis by Hochsinger in 1902 in a German pediatric journal, followed by reports from Lemez in 1928 and Haxthausen in 1941, which subsequently described similar cases in infants. Adult cases were not reported until 1963 by Solomon and Beerman⁴ and then in 1980 by Beacham et al.⁵

Etiologies for children have included popsicles, ice packs applied to the face to control supraventricular tachycardia or to the lower extremities after vaccinations, and cold weather exposure.⁶ The chemical composition of fat tissue plays a role in pediatric patients. According to Quesada-Cortés et al,³ subcutaneous fat in newborns is rich in saturated oils such as palmitic and stearic acids that have a higher solidification point. A small decrease in an infant’s temperature may result in crystallization of fat. The subcutaneous fat tends to become more unsaturated with aging with more oleic acid, and the solidification temperature diminishes.⁷

Cryoglobulins and cold agglutinins have not been demonstrated to be a cause of cold panniculitis in infants.⁷ Severe cold exposure or predisposition to certain conditions such as cryofibrinogenemia may occur in some adult patients. Gender does not seem to be a factor in children; however, in adults, women tend to be more predisposed to cold panniculitis secondary to obesity and participation in activities such as cycling, motorcycling, or horseback riding in cold conditions.³

On clinical examination, cold panniculitis features erythematous, firm, tender nodules on the cheeks and chin in infants and small children.² These areas often are exposed to cold weather or wind because they typically are not covered with protective clothing.³ Nodules generally occur 1 to 3 days following exposure to cold and usually resolve spontaneously within 2 weeks.⁸ Popsicle panniculitis is characterized by a reddish discoloration on both cheeks 1 or 2 days after sucking on popsicles or ice cubes. This reaction can be reproduced in a half day by applying an ice cube to the volar forearm for 2 minutes, which can help diagnose and differentiate this subset of cold panniuculits.³ The red area in cold panniculitis eventually turns purple, becomes less indurated, and fades in approximately 3 months, but occasionally residual hyperpigmentation will last for a few months. Ice packs used as treatment of congenital cardiac arrhythmias in some cardiac surgeries and as surface cooling for management of birth asphyxia can produce a similar physical presentation.³

Equestrian panniculitis is characterized by erythematous, violaceous, tender plaques on the upper lateral thighs of young females who participate in horseback riding in the winter while wearing tight-fitting pants.^2,5 These plaques typically occur within several hours and over the next week become painful, violaceous, and indurated or develop red nodules or plaques that can ulcerate or become crusted.³ These lesions usually will spontaneously resolve within 3 weeks, but new areas may occur again during the winter on further exposure with occasional persistent hyperpigmentation. These areas usually disappear at the end of winter with warmer weather or when horseback riding is discontinued. Perniosis also needs to be considered in the differential diagnosis due to the location and appearance of the lesions.³

It is important to obtain the correct specimen for biopsy. According to Peters and Su,¹ a deep excisional biopsy that includes multiple fat lobules in addition to dermis and epidermis is critical. On histology, cold panniculitis usually demonstrates a primarily lobular inflammation. There typically is a superficial and deep perivascular lymphocytic infiltrate in the papillary dermis with edema noted in the connective tissue around the eccrine glands that can appear similar to perniosis on histopathology.⁹ Deposition of mucin, focal panniculitis surrounded by fatty tissue without inflammatory changes within the same field, and fat necrosis with pseudocysts and numerous lipophages also are characteristic features of cold panniculitis.¹⁰ Needlelike clefts are not present in cold panniculitis but appear in subcutaneous fat necrosis of the newborn.¹

Different treatments have been tried, but no substantial impact on the rate of dissipation of the lesions has been noted. The plaques slowly resolve without scarring over 2 to 3 weeks if the cold source is removed.² Application of a heating pad to the affected area has been used with limited success. Vasodilators such as nifedipine have been used but have not been found to be effective.³ Antihistamines also have failed to control the lesions.¹¹

Treatment of cold panniculitis is based on the prevention of further insult versus trying to cure the condition. Avoidance of cold and wind exposure as well as direct contact with ice are key methods in preventing cold panniculitis.

Our patient’s presentation of this condition was unique. Although cold panniculitis lesions usually develop 1 to 3 days after cold exposure, our patient did not develop lesions until 10 days following surgery. The cold therapy unit used by our patient was evaluated in our office and also by the manufacturer and was found to be functioning normally with no defects. The late onset of the lesions was attributed to limited application of the cold therapy unit; our patient used it for only 1 hour every night, whereas application for 6 to 8 hours continuously is normally recommended. The lesions may have occurred sooner had the patient been using a solid ice pack versus the continuous cold circulating water of the cold therapy unit. Pathology was consistent with the patient’s history and physical examination indicating a diagnosis of cold panniculitis. The challenge of treatment was to alleviate the pain of the lesions as well as the postoperative shoulder pain without the aid of any form of cold therapy. The patient only needed a tincture of time, as the lesions resolved after 4 weeks. Patient education was provided on future prevention of this condition by avoiding exposure to cold or applying cold packs directly to the skin.

Acknowledgment

The authors thank the staff at the Office of Scientific Writing and Publication at the Marshfield Clinic Research Foundation, Wisconsin, for their editorial assistance in the preparation of this manuscript.

To the Editor:

Cutaneous aspergillosis mostly has been reported in immunosuppressed hosts and usually is caused by Aspergillus flavus or Aspergillus fumigatus. We report the occurrence of primary cutaneous aspergillosis (PCA) caused by a relatively rare species, Aspergillus nidulans, in a middle-aged patient without overt immunosuppression or history of trauma.

A 57-year-old woman was referred to the dermatology outpatient department for evaluation of a lesion on the right hand of 1 month's duration. On examination the lesion measured approximately 4×3 cm with central necrosis (Figure 1). Her medical history was unremarkable and routine laboratory test results were within reference range.

The patient was an agricultural worker with no history of trauma. Her history was unremarkable. A 20% potassium hydroxide mount of the tissue revealed septate, branched, hyaline hyphae. A soft, wooly, greenish brown growth was observed after 3 days of incubation on Sabouraud dextrose agar (Figure 2). No growth was observed on dermatophyte test medium. A lactophenol cotton blue mount revealed columnar conidial heads with brown, short, smooth-walled conidiophores (Figures 3–6). Vesicles were hemispheric and small (8–12 µm in diameter), with metulae and phialides occurring in the upper portion. Conidia were globose (3–4 µm) and rough. Based on these findings the fungus was identified as A nidulans. The patient did not respond to daily oral ketoconazole, and after 1 month of therapy the lesion did not regress. She was eventually treated with oral itraconazole and the lesion completely healed within 15 weeks.

An overwhelming majority of the cases of cutaneous aspergillosis have been reported either in immunocompromised hosts (ie, leukemia, cutaneous T-cell lymphoma, Hodgkin disease, human immunodeficiency virus/AIDS, solid-organ or hematopoietic stem cell transplant recipients) or in patients with contributing risk factors (ie, severe burns, diabetes mellitus, preterm or underweight neonates, elderly patients). Two outbreaks of this condition have been reported in neonatal intensive care units, with the source of contamination being linked to nonsterile disposable gloves, incubators, and humidity chambers.^1,2 However, PCA is a relatively rare condition and often is associated with disruption of dermal integrity by trauma or maceration, followed by colonization of the wound by Aspergillus spores that are ubiquitously present in soil and decomposed vegetation.^3-5 Our case was remarkable, as the patient was not immunosuppressed and did not have a history of trauma. However, we surmise that fungal inoculation might have inadvertently occurred through some trivial trauma sustained through her professional work.

The 2 species that have most commonly been associated with PCA are A flavus and A fumigatus.^6,7 There have been isolated reports of PCA caused by other organisms such as Aspergillus niger,^8,9 Aspergillus terreus,¹⁰Aspergillus ustus,¹¹ or Aspergillus calidoustus.¹² In a report of a neutropenic 56-year-old patient suffering from acute myeloblastic leukemia, PCA developed in association with a double-lumen Hickman catheter after a period of prolonged hospitalization.¹³ A study by the National Institutes of Health (1976-1997) revealed 6 life-threatening cases of A nidulans infection in patients with chronic granulomatous disease.¹⁴

We did not perform antifungal susceptibility testing on the isolate in our patient. However, we observed disease that was refractory to ketoconazole therapy but successfully resolved with oral itraconazole. Antifungal susceptibility was noted in a large number of reported cases of Aspergillus infections that were resistant to conventional treatment, such as voriconazole, itraconazole, and amphotericin B.¹⁵ Thus antifungal susceptibility testing is necessary before starting treatment. There also have been reports of recurrence of cutaneous aspergillosis following incomplete and irregular treatment.¹⁶ Our case of PCA also failed to respond to ketoconazole therapy, thus stressing the need for thorough mycological characterization, including the determination of an antifungal susceptibility profile, for successful and complete management of this condition.

Acknowledgment
The authors would like to thank Arunaloke Chakraborti, MD, Chandigarh, India, for the help extended for identification of the fungus.

To the Editor:

Cutaneous aspergillosis mostly has been reported in immunosuppressed hosts and usually is caused by Aspergillus flavus or Aspergillus fumigatus. We report the occurrence of primary cutaneous aspergillosis (PCA) caused by a relatively rare species, Aspergillus nidulans, in a middle-aged patient without overt immunosuppression or history of trauma.

A 57-year-old woman was referred to the dermatology outpatient department for evaluation of a lesion on the right hand of 1 month's duration. On examination the lesion measured approximately 4×3 cm with central necrosis (Figure 1). Her medical history was unremarkable and routine laboratory test results were within reference range.

The patient was an agricultural worker with no history of trauma. Her history was unremarkable. A 20% potassium hydroxide mount of the tissue revealed septate, branched, hyaline hyphae. A soft, wooly, greenish brown growth was observed after 3 days of incubation on Sabouraud dextrose agar (Figure 2). No growth was observed on dermatophyte test medium. A lactophenol cotton blue mount revealed columnar conidial heads with brown, short, smooth-walled conidiophores (Figures 3–6). Vesicles were hemispheric and small (8–12 µm in diameter), with metulae and phialides occurring in the upper portion. Conidia were globose (3–4 µm) and rough. Based on these findings the fungus was identified as A nidulans. The patient did not respond to daily oral ketoconazole, and after 1 month of therapy the lesion did not regress. She was eventually treated with oral itraconazole and the lesion completely healed within 15 weeks.

An overwhelming majority of the cases of cutaneous aspergillosis have been reported either in immunocompromised hosts (ie, leukemia, cutaneous T-cell lymphoma, Hodgkin disease, human immunodeficiency virus/AIDS, solid-organ or hematopoietic stem cell transplant recipients) or in patients with contributing risk factors (ie, severe burns, diabetes mellitus, preterm or underweight neonates, elderly patients). Two outbreaks of this condition have been reported in neonatal intensive care units, with the source of contamination being linked to nonsterile disposable gloves, incubators, and humidity chambers.^1,2 However, PCA is a relatively rare condition and often is associated with disruption of dermal integrity by trauma or maceration, followed by colonization of the wound by Aspergillus spores that are ubiquitously present in soil and decomposed vegetation.^3-5 Our case was remarkable, as the patient was not immunosuppressed and did not have a history of trauma. However, we surmise that fungal inoculation might have inadvertently occurred through some trivial trauma sustained through her professional work.

The 2 species that have most commonly been associated with PCA are A flavus and A fumigatus.^6,7 There have been isolated reports of PCA caused by other organisms such as Aspergillus niger,^8,9 Aspergillus terreus,¹⁰Aspergillus ustus,¹¹ or Aspergillus calidoustus.¹² In a report of a neutropenic 56-year-old patient suffering from acute myeloblastic leukemia, PCA developed in association with a double-lumen Hickman catheter after a period of prolonged hospitalization.¹³ A study by the National Institutes of Health (1976-1997) revealed 6 life-threatening cases of A nidulans infection in patients with chronic granulomatous disease.¹⁴

We did not perform antifungal susceptibility testing on the isolate in our patient. However, we observed disease that was refractory to ketoconazole therapy but successfully resolved with oral itraconazole. Antifungal susceptibility was noted in a large number of reported cases of Aspergillus infections that were resistant to conventional treatment, such as voriconazole, itraconazole, and amphotericin B.¹⁵ Thus antifungal susceptibility testing is necessary before starting treatment. There also have been reports of recurrence of cutaneous aspergillosis following incomplete and irregular treatment.¹⁶ Our case of PCA also failed to respond to ketoconazole therapy, thus stressing the need for thorough mycological characterization, including the determination of an antifungal susceptibility profile, for successful and complete management of this condition.

Acknowledgment
The authors would like to thank Arunaloke Chakraborti, MD, Chandigarh, India, for the help extended for identification of the fungus.

To the Editor:

Cutaneous aspergillosis mostly has been reported in immunosuppressed hosts and usually is caused by Aspergillus flavus or Aspergillus fumigatus. We report the occurrence of primary cutaneous aspergillosis (PCA) caused by a relatively rare species, Aspergillus nidulans, in a middle-aged patient without overt immunosuppression or history of trauma.

A 57-year-old woman was referred to the dermatology outpatient department for evaluation of a lesion on the right hand of 1 month's duration. On examination the lesion measured approximately 4×3 cm with central necrosis (Figure 1). Her medical history was unremarkable and routine laboratory test results were within reference range.

The patient was an agricultural worker with no history of trauma. Her history was unremarkable. A 20% potassium hydroxide mount of the tissue revealed septate, branched, hyaline hyphae. A soft, wooly, greenish brown growth was observed after 3 days of incubation on Sabouraud dextrose agar (Figure 2). No growth was observed on dermatophyte test medium. A lactophenol cotton blue mount revealed columnar conidial heads with brown, short, smooth-walled conidiophores (Figures 3–6). Vesicles were hemispheric and small (8–12 µm in diameter), with metulae and phialides occurring in the upper portion. Conidia were globose (3–4 µm) and rough. Based on these findings the fungus was identified as A nidulans. The patient did not respond to daily oral ketoconazole, and after 1 month of therapy the lesion did not regress. She was eventually treated with oral itraconazole and the lesion completely healed within 15 weeks.

An overwhelming majority of the cases of cutaneous aspergillosis have been reported either in immunocompromised hosts (ie, leukemia, cutaneous T-cell lymphoma, Hodgkin disease, human immunodeficiency virus/AIDS, solid-organ or hematopoietic stem cell transplant recipients) or in patients with contributing risk factors (ie, severe burns, diabetes mellitus, preterm or underweight neonates, elderly patients). Two outbreaks of this condition have been reported in neonatal intensive care units, with the source of contamination being linked to nonsterile disposable gloves, incubators, and humidity chambers.^1,2 However, PCA is a relatively rare condition and often is associated with disruption of dermal integrity by trauma or maceration, followed by colonization of the wound by Aspergillus spores that are ubiquitously present in soil and decomposed vegetation.^3-5 Our case was remarkable, as the patient was not immunosuppressed and did not have a history of trauma. However, we surmise that fungal inoculation might have inadvertently occurred through some trivial trauma sustained through her professional work.

The 2 species that have most commonly been associated with PCA are A flavus and A fumigatus.^6,7 There have been isolated reports of PCA caused by other organisms such as Aspergillus niger,^8,9 Aspergillus terreus,¹⁰Aspergillus ustus,¹¹ or Aspergillus calidoustus.¹² In a report of a neutropenic 56-year-old patient suffering from acute myeloblastic leukemia, PCA developed in association with a double-lumen Hickman catheter after a period of prolonged hospitalization.¹³ A study by the National Institutes of Health (1976-1997) revealed 6 life-threatening cases of A nidulans infection in patients with chronic granulomatous disease.¹⁴

We did not perform antifungal susceptibility testing on the isolate in our patient. However, we observed disease that was refractory to ketoconazole therapy but successfully resolved with oral itraconazole. Antifungal susceptibility was noted in a large number of reported cases of Aspergillus infections that were resistant to conventional treatment, such as voriconazole, itraconazole, and amphotericin B.¹⁵ Thus antifungal susceptibility testing is necessary before starting treatment. There also have been reports of recurrence of cutaneous aspergillosis following incomplete and irregular treatment.¹⁶ Our case of PCA also failed to respond to ketoconazole therapy, thus stressing the need for thorough mycological characterization, including the determination of an antifungal susceptibility profile, for successful and complete management of this condition.

Acknowledgment
The authors would like to thank Arunaloke Chakraborti, MD, Chandigarh, India, for the help extended for identification of the fungus.