Review Article
Open Access
Erosive and Pustular Dermatitis of the Scalp, an Under
Recognized Condition. Case Reports and Review
Carol R. Drucker*
Department of Dermatology, The University of Texas M. D. Anderson Cancer Center, Houston, Texas, USA
*Corresponding author: Carol R. Drucker, MD, Department of Dermatology, The University of Texas M. D. Anderson Cancer Center, 1515 Holcombe
Blvd. Unit 1452, Houston, Texas 77381, USA, Tel: 713-745-5736; Fax: 713-745-3597; E-mail:
@
Received: April 01, 2016; Accepted: April 20, 2016; Published: April 28, 2016
Citation: Drucker CR (2016) Erosive and Pustular Dermatitis of the Scalp, an Under Recognized Condition. Case Reports and Review.
Clin Res Dermatol Open Access 3(2): 1-5. DOI: http://dx.doi.org/10.15226/2378-1726/3/2/00127
Abstract
Erosive pustular dermatitis of the scalp has been reported as a
rare chronic and progressive inflammatory condition of the actinically
damaged scalp characterized by crusts, erosions and pustules.
Less than 150 cases have been reported worldwide. I present 4
representative cases, review the world literature on the condition
and postulate the condition is more common than diagnosed. No
single treatment has been constantly acceptable, but a review of
treatments used to date can help clinicians deal with this difficult to
treat chronic condition. Increased awareness of and proper diagnosis
of this condition changes the approach to treatment of these patients
and while giving them a better outcome, keeps the clinician vigilant of
squamous cell carcinomas that can arise in this skin.
Introduction
Erosive Pustular Dermatosis of the Scalp (EPDS) is an
inflammatory process of unknown etiology. It is characterized
by pustules, erosions and crusts on atrophic, actinically damaged
skin in areas of alopecia. It tends to occur on the scalp of older
people who have usually been treated for diffuse actinic damage
and actinic keratoses. Some have had squamous cell carcinoma
in the field involved. All have been reported to occur after
trauma, including previous treatments for actinic keratoses
and generally after stronger or more extensive treatments. As
such, the condition tends to initially be approached as chronic
and extensive actinically damaged skin with actinic keratoses,
some hyperkeratotic, with the need to be clinically alert for
development of squamous cell carcinomas.
In the chronic course of this treatment, after an inciting trauma of one type or another, the patient's scalp quits responding to typical treatment for actinic keratoses, and becomes a chronic process of inflammation, erosions, crusts and pustules on a background of atrophic, actinically damaged skin, sometimes resulting in scarring alopecia.
Notoriously difficult to treat, these cases tend to be chronic and progressive. These patients often present after repeated treatments to actinic keratoses which have not lead to clearing, but to persistent new lesions and perpetuation of the process. I postulate the disease process is more common than is implied by the 150 or so reported cases would imply. Most likely a number of these patients continue to receive treatment for actinic keratoses, but eventually it becomes apparent the lesions are no longer responding, maybe even worsening with the treatment. I believe the presentation of the review of this entity should serve to increase awareness among those of us who treat these patients so that more appropriate treatment can be instituted.
Recognition of the process can help steer treatment away from destructive treatments to anti-inflammatory treatments. I present four representative cases and a review of the disease, its precipitating traumas, its histology, and reported treatments in an effort to increase awareness of the condition so that proper treatment may ensue.
In the chronic course of this treatment, after an inciting trauma of one type or another, the patient's scalp quits responding to typical treatment for actinic keratoses, and becomes a chronic process of inflammation, erosions, crusts and pustules on a background of atrophic, actinically damaged skin, sometimes resulting in scarring alopecia.
Notoriously difficult to treat, these cases tend to be chronic and progressive. These patients often present after repeated treatments to actinic keratoses which have not lead to clearing, but to persistent new lesions and perpetuation of the process. I postulate the disease process is more common than is implied by the 150 or so reported cases would imply. Most likely a number of these patients continue to receive treatment for actinic keratoses, but eventually it becomes apparent the lesions are no longer responding, maybe even worsening with the treatment. I believe the presentation of the review of this entity should serve to increase awareness among those of us who treat these patients so that more appropriate treatment can be instituted.
Recognition of the process can help steer treatment away from destructive treatments to anti-inflammatory treatments. I present four representative cases and a review of the disease, its precipitating traumas, its histology, and reported treatments in an effort to increase awareness of the condition so that proper treatment may ensue.
Patient 1
An 82 year old man presented with dermatitis of the scalp
having been seen for years for actinic keratoses. He had numerous
treatments with cryotherapy, trichloracetic acid peels, and 5
fluorouracil field therapy. In the year before presentation, he had
developed a chronic crusting of the scalp. Sometimes pustules
developed but it always remained crusty. Several biopsies were
done and variously showed actinic keratoses, inflammation, and
granulation tissue.
Compresses with Domeboro did not help. January 2014, he was started on tacrolimus ointment for erosive pustular dermatitis of the scalp. It burned upon application and lesions sometimes bled, but dramatic results were noted in the first month. He discontinued it within the month because of the intolerable burning with application. The burn occurred even if he applied Aquaphor first. April 2014 he presented with red and painful scalp, and minocycline for secondary infection cleared that. Later that month, he was started on acitretin 10 mg daily. His scalp improved markedly, and he stayed on this until October 2014. After he stopped it, crusting and drainage worsened. He was restarted on acitretin within one month at a higher dose of 17.5 mg. Although the scalp continued to be involved, he had improvement with crust but without drainage, bleeding or pain; it did itch.
At that point underlying metastatic bladder cell carcinoma progressed. He was placed on hospice care, and with markedly increasing fatigue, he discontinued the acitretin. Topical steroids and emollients did not help, and the crusting and drainage worsened.
Compresses with Domeboro did not help. January 2014, he was started on tacrolimus ointment for erosive pustular dermatitis of the scalp. It burned upon application and lesions sometimes bled, but dramatic results were noted in the first month. He discontinued it within the month because of the intolerable burning with application. The burn occurred even if he applied Aquaphor first. April 2014 he presented with red and painful scalp, and minocycline for secondary infection cleared that. Later that month, he was started on acitretin 10 mg daily. His scalp improved markedly, and he stayed on this until October 2014. After he stopped it, crusting and drainage worsened. He was restarted on acitretin within one month at a higher dose of 17.5 mg. Although the scalp continued to be involved, he had improvement with crust but without drainage, bleeding or pain; it did itch.
At that point underlying metastatic bladder cell carcinoma progressed. He was placed on hospice care, and with markedly increasing fatigue, he discontinued the acitretin. Topical steroids and emollients did not help, and the crusting and drainage worsened.
Patient 2
A 78 year old female was referred with a history of nonhealing
lesion of the scalp. This site had biopsy shown squamous
cell carcinoma in November 2011. Pathology from the original
MOHS surgery December 2011 showed skin and subcutis with
dermal scar and chronic inflammation with no squamous cell
carcinoma identified. When next seen in February 2013, the
site had never healed. Biopsy of the non-healing skin showed
granulation tissue and ulceration. This site was treated with
silver nitrate and improved but persisted. Repeat biopsy of the
site June 2013 showed squamous cell carcinoma in situ arising
in association with actinic keratosis. The positive margins
were treated with cryotherapy. She presented October 2013
with persistent non healing of the site; another biopsy showed
superficial dermal scar and actinic changes. When she was seen
again with the persistent wound February 2014, she was thought
to have inflammatory and pustular dermatitis of the scalp.
Tacrolimus was prescribed but not filled by the patient due to the
cost. Follow up was delayed due to other medical issues requiring
hospitalization and intravenous antibiotics. Conservative
treatment was used during this time with steroid ointment. The
site improved. When last seen in May 2015 the vertex scalp had
two adherent hard whitish scales with no visible growth beneath
them. No erosions or pustules were noted, and she felt the site
had improved markedly. She was managed conservatively
with Aquaphor. Unfortunately she succumbed to septic shock
September 2015.
Patient 3
A 62 year old male presented in November 2010 with a
history of chronic actinic keratoses of the vertex scalp, treated
repeatedly with cryotherapy. Biopsy in 2007 showed spongiotic
dermatitis and in 2008 another biopsy showed the surface
of probable folliculitis. On presentation November 2010 the
scalp showed erythema with at least 3 very adherent white
hyperkeratotic scales on erythematous bases, and biopsy showed
actinic keratosis and dermal scar both present at the edges
of the biopsy specimen. He received cryotherapy to the sites.
When he was seen again December 2011 vertex scalp showed
confluent erythema with smaller distinct hyperkeratotic lesions.
The isolated lesions were treated with cryotherapy, and he was
started on minocycline. By February 2012 his problem of skin
lesions continued to clinically appear to be hypertrophic actinic
keratoses but did not respond like them, and with a diagnosis of
inflammatory process with scarring, he was started on clobetasol
foam. On his next follow up April 2012 he was responding to the
topical steroid. Follow up two months later showed fewer crusts
and he was continued on the topical steroid, and by April 2015
the scalp was essentially resolved with the topical steroids and
was thought to have been EPDS.
Patient 4
A 68 year old male was first seen with a history of squamous
cell carcinoma of the scalp and a history of many actinic keratoses
of the scalp previously treated with cryotherapy. A year later,
among other actinic keratoses treated with cryotherapy, another
squamous cell carcinoma was diagnosed and treated with
curettage and electrodessication. A recheck of the site a month
later showed granulation tissue and silver nitrate application
cleared this. Further cryotherapy was used to multiple actinic
keratoses on his scalp over the next year, but by February 2015
it was felt the treatment was not working anymore. Biopsy
then showed dermal fibrosis and atypia of basal keratinocytes
present at the edges of the specimen. Curettage and desiccation
of another squamous cell carcinoma at the frontal scalp resulted
in granulation tissue and was treated with silver nitrate and
responded. At the next follow up, hyperkeratotic and erosive
lesions persisted and with the diagnosis of EPDS, the patient opted
to follow for progressing lesions of squamous cell carcinoma but
discontinue the regular cryotherapy to existing lesions. Further
visits are pending.
Clinical Review
EPDS was first described by Burton [1] in 1987 and Pye et
al [2] in 1979. Over 100 cases have been reported worldwide
since, with the first cases reported in the United States by Patton
et al [3]. The typical presentation is in the setting of chronically
and markedly actinically damaged skin of the scalp, with crusty
and eroded lesions which can be mistaken for actinic keratoses
or squamous cell carcinomas. Importantly, most patients start
with actinic lesions of the scalp and have been serially treated
for actinic keratoses; some have had development of squamous
cell carcinomas. However, at some point during treatment, the
lesions become more chronic, progressive and inflammatory,
and they no longer respond to previously used treatments for
the actinic keratoses. This marked change has been regularly
attributed to a specific precipitating trauma, usually a treatment
aimed at the actinic lesions.
Preceding Traumas
The traumas which have been reported to precede the
development of this chronic progressive process are usually
related to the destruction of the original actinic lesions, but some
cases have been reported to unrelated traumas.
A review of the culprit trauma preceding the development of EPDS includes:
Cryotherapy [3-5] fluorouracil [3,5,6] imiquimod [7,8] tretinoin [4], ingenol mebutate [9], radiation therapy [10-12] CO2 Laser [3,13] photodynamic therapy [14,15] surgery [16- 18], skin grafting [17,19-21], hair transplantation [22], minoxidil treatment [23], lantanoprost application [24], herpes zoster [25- 28], birth trauma [29].
The disease itself is characterized by erosions and crusts; pustules can be found and are initially sterile [30]. Treatment of secondary infection, most commonly staphylococcal aureus [31] does not clear the process.
A review of the culprit trauma preceding the development of EPDS includes:
Cryotherapy [3-5] fluorouracil [3,5,6] imiquimod [7,8] tretinoin [4], ingenol mebutate [9], radiation therapy [10-12] CO2 Laser [3,13] photodynamic therapy [14,15] surgery [16- 18], skin grafting [17,19-21], hair transplantation [22], minoxidil treatment [23], lantanoprost application [24], herpes zoster [25- 28], birth trauma [29].
The disease itself is characterized by erosions and crusts; pustules can be found and are initially sterile [30]. Treatment of secondary infection, most commonly staphylococcal aureus [31] does not clear the process.
Comorbidities
Isolated cases in patients with concomitant autoimmune
diseases are sometimes noted including rheumatoid arthritis
[32,33], autoimmune hepatitis, Hashimoto's thyroiditis, Takayasu
arteritis [34], myasthenia gravis [35]. Positive antibodies for
autoimmune diseases are sometimes found [36-38] but are not
considered necessary for or germane to the diagnosis.
Likewise, other isolated cases of associated comorbidities including myelodysplastic syndrome [39], metastatic lung cancer [11], and metastatic renal cell carcinoma (Patient 1) have been reported. However, considering the population prone to this disorder is largely the elderly, comorbidities would not be unusual and would not suggest significance of association.
Likewise, other isolated cases of associated comorbidities including myelodysplastic syndrome [39], metastatic lung cancer [11], and metastatic renal cell carcinoma (Patient 1) have been reported. However, considering the population prone to this disorder is largely the elderly, comorbidities would not be unusual and would not suggest significance of association.
Histology
Histology is not diagnostic. Pathology shows actinic damage
and the presence of enlarged keratinocytes at the edges of ulcers
which may lead to the misdiagnosis of actinic keratosis or poor
healing in actinically damaged skin.
The epidermis may be normal, with hyperkeratosis and parakeratosis, erosion, or atrophy; with or without edema and subcorneal pustules [40, 36]. The dermis may contain chronic inflammatory infiltrate and plasma cells with neutrophils, especially in the upper dermis [40, 34]. Phagocytosis and giant cells can be seen around hair shafts in the deep dermis with follicle destruction. Dermal fibrosis and atrophy of hair follicles with loss of elastic tissue can be seen [36]. Granulation tissue changes have also been seen.
The epidermis may be normal, with hyperkeratosis and parakeratosis, erosion, or atrophy; with or without edema and subcorneal pustules [40, 36]. The dermis may contain chronic inflammatory infiltrate and plasma cells with neutrophils, especially in the upper dermis [40, 34]. Phagocytosis and giant cells can be seen around hair shafts in the deep dermis with follicle destruction. Dermal fibrosis and atrophy of hair follicles with loss of elastic tissue can be seen [36]. Granulation tissue changes have also been seen.
Treatment
A number of treatments have been reported used to treat
EPDS. An occasional treatment, such as photodynamic therapy,
has been reported to precipitate [14, 15] and to treat [41-43]
the condition. Treatments reported have not been consistently
effective or been adopted to be used as a standard.
Treatments reported to help have included potent topical steroids [44, 2], oral steroids [45, 15], and intralesional steroids [46] but relapse with discontinuation is common [47]. Other reported treatments have been oral isotretinoin [47, 36, 5], oral zinc sulfate [24, 48], calcipotriol [49], tacrolimus [32, 39, 45, 50, 51, 25, 16, 46, 52, 53], topical dapsone [54], acitretin [55, current cases], cyclopsorin [56], surgery [57].
Treatments reported to help have included potent topical steroids [44, 2], oral steroids [45, 15], and intralesional steroids [46] but relapse with discontinuation is common [47]. Other reported treatments have been oral isotretinoin [47, 36, 5], oral zinc sulfate [24, 48], calcipotriol [49], tacrolimus [32, 39, 45, 50, 51, 25, 16, 46, 52, 53], topical dapsone [54], acitretin [55, current cases], cyclopsorin [56], surgery [57].
Discussion
EPDS has no pathognomonic laboratory or histologic findings
and is a clinical diagnosis of exclusion [55].
EPDS has been considered rare but is likely more common but under recognized. Since it commonly develops in the actinically damaged scalp skin and manifests as superficial erosion and crusts with or without pustules on atrophic skin, proper diagnosis is important as further destructive treatments to suspected actinic keratoses perpetuate the process. The disease must be followed closely clinically as squamous cell carcinomas do occur in this setting. No distinct treatment has been successful in all cases, but patients need treatment for pain and pruritus associated with the process.
Dermatologists should be on alert for EPDS when treating the common actinically damaged scalp, as these two similarly appearing clinical conditions require markedly different approach to management.
EPDS has been considered rare but is likely more common but under recognized. Since it commonly develops in the actinically damaged scalp skin and manifests as superficial erosion and crusts with or without pustules on atrophic skin, proper diagnosis is important as further destructive treatments to suspected actinic keratoses perpetuate the process. The disease must be followed closely clinically as squamous cell carcinomas do occur in this setting. No distinct treatment has been successful in all cases, but patients need treatment for pain and pruritus associated with the process.
Dermatologists should be on alert for EPDS when treating the common actinically damaged scalp, as these two similarly appearing clinical conditions require markedly different approach to management.
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