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Excoriated Papules and Plaques on the Arms and Legs
The Diagnosis: Reactive Perforating Collagenosis
Reactive perforating collagenosis (RPC) may be either acquired or inherited. It is 1 of 4 classical forms of transepithelial elimination, which also includes elastosis perforans serpiginosa (EPS) as well as perforating folliculitis and Kyrle disease. These 4 forms of transepithelial elimination share characteristics of the elimination of altered dermal components through the epidermis.1 The acquired subtype of RPC frequently occurs in patients with diabetes mellitus and end-stage renal disease,2 both present in our patient.
Clinical presentation typically shows pruritic hyperkeratotic papules with a central crater filled with crust that frequently are distributed on the extensor surfaces of the extremities, often in a linear pattern.3 The perforating papules and nodules occasionally may involve the trunk and face.4 Histopathologic examination is characterized by the elimination of altered collagen through the epidermis. Established lesions may show a cup-shaped depression of the epidermis filled with a keratin plug. The underlying dermis will show vertically oriented basophilic collagen fibers with focal extrusion through the epidermis, and elastic fibers will be absent.5 The exact pathophysiology of this disease is unknown, but it may represent a cutaneous response to superficial trauma caused by intense scratching.6
Standard treatment protocols are not well established for this condition, but some evidence shows that a combination of treatments can help ameliorate symptoms, even if they are not curative.7 Treatments without strong evidence have included a wide range of topical, systemic, and other therapies. Case series and anecdotal reports have used retinoids, corticosteroids, menthol, antibiotics, allopurinol antihistamines, cryotherapy, and lasers.8 One case was treated with a combination of narrowband UVB phototherapy and doxycycline with resolution in approximately 6 weeks.9 Other cases have been cured using triple therapy with antihistamines, topical or injected steroids, and emollients or oral antibiotics.7 Evidence shows that there may be benefit to combining multiple different treatment types that target pruritus, inflammation, and collagen damage.7,9 This disease usually cannot be cured, but it may be improved by the available treatments.
The differential diagnosis includes delusional parasitosis, EPS, perforating folliculitis, and prurigo nodularis. Delusional parasitosis also can be characterized by excoriated plaques and a sensation of parasites infesting the skin, as our patient described.10 However, it can be differentiated from RPC by the fact that it is a diagnosis of exclusion, which would not have the histopathologic findings of the elimination of collagen from the epidermis, as was demonstrated in our patient.11 Elastosis perforans serpiginosa is in the same family of perforating diseases as RPC; however, EPS typically appears in children or young adults and often is associated with other genetic disorders. Physical examination in a patient with EPS would reveal keratotic papules in a serpiginous pattern, whereas our patient had discrete lesions without any serpiginous pattern. The histopathologic appearance of EPS would reveal plugs of elastic fibers rather than collagen fibers, as was demonstrated in our patient.8 Perforating folliculitis, while also demonstrating transepithelial elimination similar to RPC, would appear as erythematous follicular papules with small central keratotic plugs and histopathologic findings of a widely dilated follicle with a mass of keratotic debris.12 Prurigo nodularis would appear as dome-shaped papulonodules with varying degrees of scale, crust, and erosion, with a histopathologic appearance of hyperplasia and thick hyperkeratosis.11
Overall, the histopathology is paramount in differentiating RPC from the alternative diagnoses, with the extrusion of collagen from the epidermis not being seen in these other conditions. The coupling of the medical history (type 2 diabetes mellitus and end-stage renal disease) with the clinical presentation and skin biopsy findings confirmed the diagnosis of RPC.
- Fei C, Wang Y, Gong Y, et al. Acquired reactive perforating collagenosis: a report of a typical case. Medicine (Baltimore). 2016;95:E4305.
- Matsui A, Nakano H, Aizu T, et al. Treatment of acquired reactive perforating collagenosis with 308‐nm excimer laser. Clin Exp Dermatol. 2016;41:820-821.
- Dey AK. Reactive perforating collagenosis: an important differential diagnosis in hemodialysis patients. Saudi J Kidney Dis Transpl. 2018;29:422-425.
- Kang S, Amagai M, Bruckner AL, et al, eds. Fitzpatrick’s Dermatology in General Medicine. 9th ed. McGraw-Hill Education LLC; 2012.
- Plaza JA, Prieto VG. Inflammatory Skin Disorders. Demos Medical Publishing LLC; 2012.
- Kreuter A, Gambichler T. Acquired reactive perforating collagenosis. CMAJ. 2010;182:E184.
- Zhang X, Yang Y, Shao S. Acquired reactive perforating collagenosis: a case report and review of the literature. Medicine (Baltimore). 2020;99:E20391.
- Rapini RP. Perforating diseases. In: Bolognia JL, Schaffer JV, Cerroni L, eds. Dermatology. 4th ed. Elsevier; 2018:1690-1696.
- Gao L, Gu L, Chen Z, et al. Doxycycline combined with NB-UVB phototherapy for acquired reactive perforating collagenosis. Ther Clin Risk Manag. 2020;16:917-921.
- Bolognia JL, Schaffer JV, Duncan KO, et al. Psychocutaneous disorders. Dermatology Essentials. Elsevier; 2014:50-55. 11. Bolognia JL, Schaffer JV, Duncan KO, et al. Pruritus and dysesthesia. Dermatology Essentials. Elsevier; 2014:39-49. 12. Rubio FA, Herranz P, Robayna G, et al. Perforating folliculitis: report of a case in an HIV-infected man. J Am Acad Dermatol. 1999;40:300-302.
The Diagnosis: Reactive Perforating Collagenosis
Reactive perforating collagenosis (RPC) may be either acquired or inherited. It is 1 of 4 classical forms of transepithelial elimination, which also includes elastosis perforans serpiginosa (EPS) as well as perforating folliculitis and Kyrle disease. These 4 forms of transepithelial elimination share characteristics of the elimination of altered dermal components through the epidermis.1 The acquired subtype of RPC frequently occurs in patients with diabetes mellitus and end-stage renal disease,2 both present in our patient.
Clinical presentation typically shows pruritic hyperkeratotic papules with a central crater filled with crust that frequently are distributed on the extensor surfaces of the extremities, often in a linear pattern.3 The perforating papules and nodules occasionally may involve the trunk and face.4 Histopathologic examination is characterized by the elimination of altered collagen through the epidermis. Established lesions may show a cup-shaped depression of the epidermis filled with a keratin plug. The underlying dermis will show vertically oriented basophilic collagen fibers with focal extrusion through the epidermis, and elastic fibers will be absent.5 The exact pathophysiology of this disease is unknown, but it may represent a cutaneous response to superficial trauma caused by intense scratching.6
Standard treatment protocols are not well established for this condition, but some evidence shows that a combination of treatments can help ameliorate symptoms, even if they are not curative.7 Treatments without strong evidence have included a wide range of topical, systemic, and other therapies. Case series and anecdotal reports have used retinoids, corticosteroids, menthol, antibiotics, allopurinol antihistamines, cryotherapy, and lasers.8 One case was treated with a combination of narrowband UVB phototherapy and doxycycline with resolution in approximately 6 weeks.9 Other cases have been cured using triple therapy with antihistamines, topical or injected steroids, and emollients or oral antibiotics.7 Evidence shows that there may be benefit to combining multiple different treatment types that target pruritus, inflammation, and collagen damage.7,9 This disease usually cannot be cured, but it may be improved by the available treatments.
The differential diagnosis includes delusional parasitosis, EPS, perforating folliculitis, and prurigo nodularis. Delusional parasitosis also can be characterized by excoriated plaques and a sensation of parasites infesting the skin, as our patient described.10 However, it can be differentiated from RPC by the fact that it is a diagnosis of exclusion, which would not have the histopathologic findings of the elimination of collagen from the epidermis, as was demonstrated in our patient.11 Elastosis perforans serpiginosa is in the same family of perforating diseases as RPC; however, EPS typically appears in children or young adults and often is associated with other genetic disorders. Physical examination in a patient with EPS would reveal keratotic papules in a serpiginous pattern, whereas our patient had discrete lesions without any serpiginous pattern. The histopathologic appearance of EPS would reveal plugs of elastic fibers rather than collagen fibers, as was demonstrated in our patient.8 Perforating folliculitis, while also demonstrating transepithelial elimination similar to RPC, would appear as erythematous follicular papules with small central keratotic plugs and histopathologic findings of a widely dilated follicle with a mass of keratotic debris.12 Prurigo nodularis would appear as dome-shaped papulonodules with varying degrees of scale, crust, and erosion, with a histopathologic appearance of hyperplasia and thick hyperkeratosis.11
Overall, the histopathology is paramount in differentiating RPC from the alternative diagnoses, with the extrusion of collagen from the epidermis not being seen in these other conditions. The coupling of the medical history (type 2 diabetes mellitus and end-stage renal disease) with the clinical presentation and skin biopsy findings confirmed the diagnosis of RPC.
The Diagnosis: Reactive Perforating Collagenosis
Reactive perforating collagenosis (RPC) may be either acquired or inherited. It is 1 of 4 classical forms of transepithelial elimination, which also includes elastosis perforans serpiginosa (EPS) as well as perforating folliculitis and Kyrle disease. These 4 forms of transepithelial elimination share characteristics of the elimination of altered dermal components through the epidermis.1 The acquired subtype of RPC frequently occurs in patients with diabetes mellitus and end-stage renal disease,2 both present in our patient.
Clinical presentation typically shows pruritic hyperkeratotic papules with a central crater filled with crust that frequently are distributed on the extensor surfaces of the extremities, often in a linear pattern.3 The perforating papules and nodules occasionally may involve the trunk and face.4 Histopathologic examination is characterized by the elimination of altered collagen through the epidermis. Established lesions may show a cup-shaped depression of the epidermis filled with a keratin plug. The underlying dermis will show vertically oriented basophilic collagen fibers with focal extrusion through the epidermis, and elastic fibers will be absent.5 The exact pathophysiology of this disease is unknown, but it may represent a cutaneous response to superficial trauma caused by intense scratching.6
Standard treatment protocols are not well established for this condition, but some evidence shows that a combination of treatments can help ameliorate symptoms, even if they are not curative.7 Treatments without strong evidence have included a wide range of topical, systemic, and other therapies. Case series and anecdotal reports have used retinoids, corticosteroids, menthol, antibiotics, allopurinol antihistamines, cryotherapy, and lasers.8 One case was treated with a combination of narrowband UVB phototherapy and doxycycline with resolution in approximately 6 weeks.9 Other cases have been cured using triple therapy with antihistamines, topical or injected steroids, and emollients or oral antibiotics.7 Evidence shows that there may be benefit to combining multiple different treatment types that target pruritus, inflammation, and collagen damage.7,9 This disease usually cannot be cured, but it may be improved by the available treatments.
The differential diagnosis includes delusional parasitosis, EPS, perforating folliculitis, and prurigo nodularis. Delusional parasitosis also can be characterized by excoriated plaques and a sensation of parasites infesting the skin, as our patient described.10 However, it can be differentiated from RPC by the fact that it is a diagnosis of exclusion, which would not have the histopathologic findings of the elimination of collagen from the epidermis, as was demonstrated in our patient.11 Elastosis perforans serpiginosa is in the same family of perforating diseases as RPC; however, EPS typically appears in children or young adults and often is associated with other genetic disorders. Physical examination in a patient with EPS would reveal keratotic papules in a serpiginous pattern, whereas our patient had discrete lesions without any serpiginous pattern. The histopathologic appearance of EPS would reveal plugs of elastic fibers rather than collagen fibers, as was demonstrated in our patient.8 Perforating folliculitis, while also demonstrating transepithelial elimination similar to RPC, would appear as erythematous follicular papules with small central keratotic plugs and histopathologic findings of a widely dilated follicle with a mass of keratotic debris.12 Prurigo nodularis would appear as dome-shaped papulonodules with varying degrees of scale, crust, and erosion, with a histopathologic appearance of hyperplasia and thick hyperkeratosis.11
Overall, the histopathology is paramount in differentiating RPC from the alternative diagnoses, with the extrusion of collagen from the epidermis not being seen in these other conditions. The coupling of the medical history (type 2 diabetes mellitus and end-stage renal disease) with the clinical presentation and skin biopsy findings confirmed the diagnosis of RPC.
- Fei C, Wang Y, Gong Y, et al. Acquired reactive perforating collagenosis: a report of a typical case. Medicine (Baltimore). 2016;95:E4305.
- Matsui A, Nakano H, Aizu T, et al. Treatment of acquired reactive perforating collagenosis with 308‐nm excimer laser. Clin Exp Dermatol. 2016;41:820-821.
- Dey AK. Reactive perforating collagenosis: an important differential diagnosis in hemodialysis patients. Saudi J Kidney Dis Transpl. 2018;29:422-425.
- Kang S, Amagai M, Bruckner AL, et al, eds. Fitzpatrick’s Dermatology in General Medicine. 9th ed. McGraw-Hill Education LLC; 2012.
- Plaza JA, Prieto VG. Inflammatory Skin Disorders. Demos Medical Publishing LLC; 2012.
- Kreuter A, Gambichler T. Acquired reactive perforating collagenosis. CMAJ. 2010;182:E184.
- Zhang X, Yang Y, Shao S. Acquired reactive perforating collagenosis: a case report and review of the literature. Medicine (Baltimore). 2020;99:E20391.
- Rapini RP. Perforating diseases. In: Bolognia JL, Schaffer JV, Cerroni L, eds. Dermatology. 4th ed. Elsevier; 2018:1690-1696.
- Gao L, Gu L, Chen Z, et al. Doxycycline combined with NB-UVB phototherapy for acquired reactive perforating collagenosis. Ther Clin Risk Manag. 2020;16:917-921.
- Bolognia JL, Schaffer JV, Duncan KO, et al. Psychocutaneous disorders. Dermatology Essentials. Elsevier; 2014:50-55. 11. Bolognia JL, Schaffer JV, Duncan KO, et al. Pruritus and dysesthesia. Dermatology Essentials. Elsevier; 2014:39-49. 12. Rubio FA, Herranz P, Robayna G, et al. Perforating folliculitis: report of a case in an HIV-infected man. J Am Acad Dermatol. 1999;40:300-302.
- Fei C, Wang Y, Gong Y, et al. Acquired reactive perforating collagenosis: a report of a typical case. Medicine (Baltimore). 2016;95:E4305.
- Matsui A, Nakano H, Aizu T, et al. Treatment of acquired reactive perforating collagenosis with 308‐nm excimer laser. Clin Exp Dermatol. 2016;41:820-821.
- Dey AK. Reactive perforating collagenosis: an important differential diagnosis in hemodialysis patients. Saudi J Kidney Dis Transpl. 2018;29:422-425.
- Kang S, Amagai M, Bruckner AL, et al, eds. Fitzpatrick’s Dermatology in General Medicine. 9th ed. McGraw-Hill Education LLC; 2012.
- Plaza JA, Prieto VG. Inflammatory Skin Disorders. Demos Medical Publishing LLC; 2012.
- Kreuter A, Gambichler T. Acquired reactive perforating collagenosis. CMAJ. 2010;182:E184.
- Zhang X, Yang Y, Shao S. Acquired reactive perforating collagenosis: a case report and review of the literature. Medicine (Baltimore). 2020;99:E20391.
- Rapini RP. Perforating diseases. In: Bolognia JL, Schaffer JV, Cerroni L, eds. Dermatology. 4th ed. Elsevier; 2018:1690-1696.
- Gao L, Gu L, Chen Z, et al. Doxycycline combined with NB-UVB phototherapy for acquired reactive perforating collagenosis. Ther Clin Risk Manag. 2020;16:917-921.
- Bolognia JL, Schaffer JV, Duncan KO, et al. Psychocutaneous disorders. Dermatology Essentials. Elsevier; 2014:50-55. 11. Bolognia JL, Schaffer JV, Duncan KO, et al. Pruritus and dysesthesia. Dermatology Essentials. Elsevier; 2014:39-49. 12. Rubio FA, Herranz P, Robayna G, et al. Perforating folliculitis: report of a case in an HIV-infected man. J Am Acad Dermatol. 1999;40:300-302.
A 73-year-old woman presented for evaluation of a rash on the arms and legs of 3 months’ duration. The rash had developed abruptly, and she believed it was caused by bugs in the skin; her husband noted that she constantly picked at her arms and legs. She had a medical history of hypertension, type 2 diabetes mellitus, and endstage renal disease on dialysis. Physical examination revealed multiple pigmented papules and plaques, some with keratotic scale, on the lower legs (left) and arms, with greater involvement on the left arm (right). The lesions were of various sizes and shapes, some with a central keratotic core, and several lesions demonstrated erosion, excoriation, or ulceration. Histopathologic examination revealed slight attenuation of the epidermis with loss of normal rete peg architecture, alternating areas of hypergranulosis and hypogranulosis, central ulceration with inflammatory cells, and a basophilic hue to the ulcer base with sweeping up of the collagen fibers.
Periorbital Swelling and Rash Following Trauma
The Diagnosis: Herpes Zoster Opthalmicus
Due to the potential concern of vision loss, the patient was directed to a local emergency department for immediate ophthalmologic evaluation. He was diagnosed with herpes zoster ophthalmicus (HZO) and treated with oral acyclovir and prednisone. The rash and periorbital swelling resolved within 2 weeks of treatment, and he remained asymptomatic at follow-up 3 months later.
Herpes zoster ophthalmicus presents with an erythematous and vesicular rash in the distribution of cranial nerve V1. The herpetiform grouping of lesions on the forehead is diagnostic of HZO. Varicella-zoster virus (VZV) infection presents in 2 distinct forms. Primary infection (commonly known as chickenpox) presents clinically as a vesicular rash usually located on the face, arms, and trunk. Although the initial presentation usually occurs in childhood and is self-limited, the virus becomes latent in the dorsal root ganglia of sensory neurons. Varicella-zoster virus may become reactivated later in life and is termed herpes zoster (commonly known as shingles). It most often presents as a painful vesicular rash that may later form pustules.
Zoster outbreaks typically do not cross the midline but may in disseminated disease. Patients may experience a prodrome in the form of pain or less commonly pruritus or paresthesia along the dermatome between 1 and 10 days before the rash appears. Triggers for herpes zoster include illness, medications, malnutrition, surgery, or the natural decline in immune function due to aging. Trauma is another important precipitating event for VZV reactivation; one case-control study showed that zoster patients were 3.4 times more likely than controls to have had trauma the week prior.1 Patients with cranial zoster are more than 25 times more likely to have experienced trauma in the preceding week. Local trauma may predispose these patients to VZV reactivation by stimulating local sensory nerves or by disrupting local cutaneous immunity.2
Herpes zoster ophthalmicus occurs when zoster presents in the ophthalmic division of the fifth cranial nerve. It is a serious, vision-threatening condition with a presentation that can include conjunctivitis, scleritis, keratitis, optic neuritis, exophthalmos, lid retraction, ptosis, and extraocular muscle palsies. Treatment includes antiviral medication (eg, acyclovir, valacyclovir, famciclovir) and prompt ophthalmologic consultation due to potential vision-threatening complications, such as acute retinal necrosis. Acute pain control may be necessary with nonsteroidal anti-inflammatory drugs, opioids, steroids, tricyclic antidepressants, or anticonvulsants.3 Wet-to-dry dressings with sterile saline or Burow solution and/or calamine lotion can provide symptomatic relief of itching.
Periorbital and preseptal cellulitis typically present with more erythema of the skin surrounding the eye and without the accompanying rash. Periorbital cellulitis is the more serious infection and may be clinically distinguished by the presence of pain with extraocular muscle movement. Contact dermatitis and pemphigus vulgaris are possibilities, but both were less likely than HZO in this case presentation given the distribution of the rash and the patient history. Contact dermatitis typically presents with no prodrome with a main concern of pruritus. Pemphigus vulgaris nearly always includes involvement of the oral mucous membranes.
- Goh CL, Khoo L. A retrospective study of the clinical presentation and outcome of herpes zoster in a tertiary dermatology outpatient referral clinic. Int J Dermatol. 1997;36:667-672.
- Zhang JX, Joesoef RM, Bialek S, et al. Association of physical trauma with risk of herpes zoster among Medicare beneficiaries in the United States. J Infect Dis. 2013;207:1007-1011.
- Rousseau A, Bourcier T, Colin J, et al. Herpes zoster ophthalmicus--diagnosis and management. US Ophthalm Rev. 2013;6:119-124.
The Diagnosis: Herpes Zoster Opthalmicus
Due to the potential concern of vision loss, the patient was directed to a local emergency department for immediate ophthalmologic evaluation. He was diagnosed with herpes zoster ophthalmicus (HZO) and treated with oral acyclovir and prednisone. The rash and periorbital swelling resolved within 2 weeks of treatment, and he remained asymptomatic at follow-up 3 months later.
Herpes zoster ophthalmicus presents with an erythematous and vesicular rash in the distribution of cranial nerve V1. The herpetiform grouping of lesions on the forehead is diagnostic of HZO. Varicella-zoster virus (VZV) infection presents in 2 distinct forms. Primary infection (commonly known as chickenpox) presents clinically as a vesicular rash usually located on the face, arms, and trunk. Although the initial presentation usually occurs in childhood and is self-limited, the virus becomes latent in the dorsal root ganglia of sensory neurons. Varicella-zoster virus may become reactivated later in life and is termed herpes zoster (commonly known as shingles). It most often presents as a painful vesicular rash that may later form pustules.
Zoster outbreaks typically do not cross the midline but may in disseminated disease. Patients may experience a prodrome in the form of pain or less commonly pruritus or paresthesia along the dermatome between 1 and 10 days before the rash appears. Triggers for herpes zoster include illness, medications, malnutrition, surgery, or the natural decline in immune function due to aging. Trauma is another important precipitating event for VZV reactivation; one case-control study showed that zoster patients were 3.4 times more likely than controls to have had trauma the week prior.1 Patients with cranial zoster are more than 25 times more likely to have experienced trauma in the preceding week. Local trauma may predispose these patients to VZV reactivation by stimulating local sensory nerves or by disrupting local cutaneous immunity.2
Herpes zoster ophthalmicus occurs when zoster presents in the ophthalmic division of the fifth cranial nerve. It is a serious, vision-threatening condition with a presentation that can include conjunctivitis, scleritis, keratitis, optic neuritis, exophthalmos, lid retraction, ptosis, and extraocular muscle palsies. Treatment includes antiviral medication (eg, acyclovir, valacyclovir, famciclovir) and prompt ophthalmologic consultation due to potential vision-threatening complications, such as acute retinal necrosis. Acute pain control may be necessary with nonsteroidal anti-inflammatory drugs, opioids, steroids, tricyclic antidepressants, or anticonvulsants.3 Wet-to-dry dressings with sterile saline or Burow solution and/or calamine lotion can provide symptomatic relief of itching.
Periorbital and preseptal cellulitis typically present with more erythema of the skin surrounding the eye and without the accompanying rash. Periorbital cellulitis is the more serious infection and may be clinically distinguished by the presence of pain with extraocular muscle movement. Contact dermatitis and pemphigus vulgaris are possibilities, but both were less likely than HZO in this case presentation given the distribution of the rash and the patient history. Contact dermatitis typically presents with no prodrome with a main concern of pruritus. Pemphigus vulgaris nearly always includes involvement of the oral mucous membranes.
The Diagnosis: Herpes Zoster Opthalmicus
Due to the potential concern of vision loss, the patient was directed to a local emergency department for immediate ophthalmologic evaluation. He was diagnosed with herpes zoster ophthalmicus (HZO) and treated with oral acyclovir and prednisone. The rash and periorbital swelling resolved within 2 weeks of treatment, and he remained asymptomatic at follow-up 3 months later.
Herpes zoster ophthalmicus presents with an erythematous and vesicular rash in the distribution of cranial nerve V1. The herpetiform grouping of lesions on the forehead is diagnostic of HZO. Varicella-zoster virus (VZV) infection presents in 2 distinct forms. Primary infection (commonly known as chickenpox) presents clinically as a vesicular rash usually located on the face, arms, and trunk. Although the initial presentation usually occurs in childhood and is self-limited, the virus becomes latent in the dorsal root ganglia of sensory neurons. Varicella-zoster virus may become reactivated later in life and is termed herpes zoster (commonly known as shingles). It most often presents as a painful vesicular rash that may later form pustules.
Zoster outbreaks typically do not cross the midline but may in disseminated disease. Patients may experience a prodrome in the form of pain or less commonly pruritus or paresthesia along the dermatome between 1 and 10 days before the rash appears. Triggers for herpes zoster include illness, medications, malnutrition, surgery, or the natural decline in immune function due to aging. Trauma is another important precipitating event for VZV reactivation; one case-control study showed that zoster patients were 3.4 times more likely than controls to have had trauma the week prior.1 Patients with cranial zoster are more than 25 times more likely to have experienced trauma in the preceding week. Local trauma may predispose these patients to VZV reactivation by stimulating local sensory nerves or by disrupting local cutaneous immunity.2
Herpes zoster ophthalmicus occurs when zoster presents in the ophthalmic division of the fifth cranial nerve. It is a serious, vision-threatening condition with a presentation that can include conjunctivitis, scleritis, keratitis, optic neuritis, exophthalmos, lid retraction, ptosis, and extraocular muscle palsies. Treatment includes antiviral medication (eg, acyclovir, valacyclovir, famciclovir) and prompt ophthalmologic consultation due to potential vision-threatening complications, such as acute retinal necrosis. Acute pain control may be necessary with nonsteroidal anti-inflammatory drugs, opioids, steroids, tricyclic antidepressants, or anticonvulsants.3 Wet-to-dry dressings with sterile saline or Burow solution and/or calamine lotion can provide symptomatic relief of itching.
Periorbital and preseptal cellulitis typically present with more erythema of the skin surrounding the eye and without the accompanying rash. Periorbital cellulitis is the more serious infection and may be clinically distinguished by the presence of pain with extraocular muscle movement. Contact dermatitis and pemphigus vulgaris are possibilities, but both were less likely than HZO in this case presentation given the distribution of the rash and the patient history. Contact dermatitis typically presents with no prodrome with a main concern of pruritus. Pemphigus vulgaris nearly always includes involvement of the oral mucous membranes.
- Goh CL, Khoo L. A retrospective study of the clinical presentation and outcome of herpes zoster in a tertiary dermatology outpatient referral clinic. Int J Dermatol. 1997;36:667-672.
- Zhang JX, Joesoef RM, Bialek S, et al. Association of physical trauma with risk of herpes zoster among Medicare beneficiaries in the United States. J Infect Dis. 2013;207:1007-1011.
- Rousseau A, Bourcier T, Colin J, et al. Herpes zoster ophthalmicus--diagnosis and management. US Ophthalm Rev. 2013;6:119-124.
- Goh CL, Khoo L. A retrospective study of the clinical presentation and outcome of herpes zoster in a tertiary dermatology outpatient referral clinic. Int J Dermatol. 1997;36:667-672.
- Zhang JX, Joesoef RM, Bialek S, et al. Association of physical trauma with risk of herpes zoster among Medicare beneficiaries in the United States. J Infect Dis. 2013;207:1007-1011.
- Rousseau A, Bourcier T, Colin J, et al. Herpes zoster ophthalmicus--diagnosis and management. US Ophthalm Rev. 2013;6:119-124.
A 56-year-old man presented to an urgent care clinic with right periorbital swelling. He reported hitting his head on the door to a storage unit 2 days prior but did not lose consciousness. The swelling presented 2 days later. He reported mild headache and swelling around the right eye that coincided with an uncomfortable rash on the face and scalp. He also reported visual disruption due to the swelling but denied any eye pain, discharge from the eye, or painful eye movements. He had no lesions on the lips or inside the mouth. He denied any history of skin conditions. He further denied fever, joint pain, or any other systemic symptoms. His chronic medical conditions included diabetes mellitus, hypertension, and hyperlipidemia that were stable on metformin, carvedilol, amlodipine, enalapril, and simvastatin, which he had taken for several years. He had not started any new medications, and there were no recent changes in the dosing of his medications.
