Annals of Puzzling Purpuras

Percussion Purpura -- Taiko Purpura
Submitted by Trudi Shim, San Antonio, Texas

History: The patient is a 63 year-old Japanese-Hawaiian woman who plays Taiko drums as a hobby. She has a past history of porphyria cutanea tarda (PCT) from estrogens which is now quiescent. A few years back, she developed tendonitis of her wrists and received cortisone injections near each wrist from two different physicians. When she developed a hypopigmented patch of skin on her right forearm she attributed it to the cortisone injection. The patch was characterized by an large, flat, smooth area of hypopigmentation, and occasionally some round, bright red spots appeared in the hypopigmented area. They would disappear after a week or two. She consulted a dermatologist a year ago because she worried that this might be contagious. He diagnosed tinea, but did no KOH prep and she has been faithfully applying clotrimazole ever since, but without relief. The dermatologist also raised the spectre of Hansen's Disease which worried the patient, a retired public health nurse, greatly. She does not have any known skin problems elsewhere on her body at this time.

On Examination: The patch is now predominately reddish in color, with sharp irregular borders. The skin is fragile in the sense that if she hits her arm against something, it will break and take a while to heal. - similar to what used to happen way back when she had PCT. This only occurs in the localized area of hypopigmentation.

Clinical Photos:
Patient and Taiko




Discussion: This case presentation contains some interesting points. The patient is a late middle-aged Japanese-Hawaiian woman who has lived in the sub-tropics for her entire life. Thus, she has a fair amount of solar elastosis. The intra-articular corticosteroid most likely caused more localized atrophy and the trauma the arm experienced doing heavy drumming was all she needed to cause purpura. The diagnosis of tinea without a KOH prep showed a certain cavalier approach on the part of her practitioner; and the suggestion of the possibility of Hansen's Disease should not have been made unless a biopsy followed. Leprosy in economically comfortable people born in Hawaii is very unusual. Most cases seen in the Hawaiian Islands today are in immigrants from the Philippines, Oceania and Southeast Asia. Purpura is not a usual finding, but rather a hypopigmented anesthetic plaque (tuberculoid leprosy). Lepromatous leprosy would often appear more dramatically. The patient's PCT is likely not related, but she should have regular liver function studies and ferritin levels looked at. In the absence of other findings urinary porphyrins may not be necessary. "Percussion Purpura" while likely not super rare, has not been reported before.

Comments: Your thoughts and questions will be most welcome.

Parastomal Ulceration

Presented by Amanda Oakley, Hamilton, NZ

The patient is a 44 year old man with parastomal ulceration over the last 12 months.
He had a stable stoma for 12 years, following colostomy to remove rectal tumour (carcinoid) and is healthy otherwise with no bowel problems and no skin disease elsewhere.

Last year he received IV antibiotics for peristomal cellulitis, with complete recovery. A month or so later the peristomal skin began ulcerating. Partial healing is followed by skin lifting off at bag changes alternate days, leaving painful ulceration. Meticulous hygiene resulted in no improvement with different devices or topical steroid for one month, applied as beclomethasone nasal spray. Now trying clobetasol solution on appliance, allowed to dry before fitting to skin. He is on no medications.

Swab: group G streptococcus on two swabs - no deep fungi or mycobacteria.
Blood screen: all normal - no sign carcinoid or other disease

Clinical Photos (July '09 (top) and February '09 bottom):


Histology: paucicellular; subepidermal clefting. Not diagnostic.

Dr. Oakley's Comments: Most stomal rashes are dealt with by stoma nurses and a dermatologist's opinion is rarely sought; so we don't see many of them. I see irritant dermatitis from time to time and it responds to topical steroids. He has no risk factors for pyoderma gangrenosum, and the histology is not typical of that.

Questions: Could group G streptococcus do this? There is no cellulitis or abscess formation and I have prescribed antibiotics without improvement.
Any suggestions re: diagnosis and treatment will be gratefully received! I am hoping some dermatologists have greater exposure to stomal disease and I can benefit from their experience.

Reference:
Yeo H, Abir F, Longo WE. Management of parastomal ulcers.
World J Gastroenterol. 2006 28;12(20):3133-7.
Management of surgically placed ostomies is an important aspect of any general surgical or colon and rectal surgery practice. Complications with surgically placed ostomies are common and their causes are multifactorial. Parastomal ulceration, although rare, is a particularly difficult management problem. We conducted a literature search using MD Consult, Science Direct, OVID, Medline, and Cochrane Databases to review the causes and management options of parastomal ulceration. Both the etiology and treatments are varied. Different physicians and ostomy specialists have used a large array of methods to manage parastomal ulcers; these including local wound care; steroid creams; systemic steroids; and, when conservative measures fail, surgery. Most patients with parastomal ulcers who do not have associated IBD or peristomal pyoderma gangrenosum (PPG) often respond quickly to local wound care and conservative management. Patients with PPG, IBD, or other systemic causes of their ulceration need both systemic and local care and are more likely to need long term treatment and possibly surgical revision of the ostomy. The treatment is complicated, but improved with the help of ostomy specialists. Note: This reference is available as free full text from the publisher.

Localized Bullae

This healthy 83 year-old man has had a one year history of bullae and vesicles on the medial aspect of the left knee. They come and go. He is on no new medications and does not take any drugss on an as necessary or intermittent basis. His medications consist of valsartan (Diovan), simvastatin and omeprazole (Prilosec).

O/E: A collection of vesicles and bullae left knee.

Clinical Photo:


Lab and Path:
Bacterial Culture 8/14/o9 Negative
Biopsies were done by two other dermatologists (will try to get results). Apparently, no firm diagnosis was made.

Path Report: 9/30/08 Perivascular and interstitial dermatitis with mixed cell infiltrate including eosiniphils. Dermal hypersensitivity reaction. "These findings may be seen in the prebullous lesions of pemphigoid." DIF was negative.

Diagnosis:
Consider localized bullous pemphigoid.

Discussion: This is an 82 yo man with a one year history of a localized bullous disorder. The initial pathology showed an inflammatory process with eosinophils. The bullous process has stayed localized to the left knee. It seems likely that this is localized bullous pemphigoid. There is a "pretibial variant" and this may be related. Apparently, many of these patients have negative direct immunofluorescence (See ref. below)
Plan to treat initially with clobetasol ointment and if does well follow with tactolimus ointment 0.1%.

Questions: What do you think? What else is in your differential diagnosis? Therapeutic options?

Reference:

Kurzhals G, et. al. [Localized cicatricial bullous
pemphigoid of the Brunsting-Perry type] Hautartz.
1993 Feb;44(2):110-3 [Article in German]
Localized cicatricial pemphigoid of the Brunsting-
Perry type is a very rare bullous condition, which
has so far been reported in 51 cases. It is
characterized by scarring blisters confined to the
head, scalp and neck.  Diagnosis can be difficult
because of the discrete skin lesions, often repeatedly
false-negative direct immunofluorescence, and the
absence of circulating antibodies. We report on a
87-year-old male patient with the typical clinical
feature of a cicatricial pemphigoid of the Brunsting-
Perry type and give a reviewof the 51 cases published
in the world literature.

Follow-up Photo (08/21/09):  The patient was seen after a week for a second visit.  No
treatment had been rendered and the bullae had resolved.  One wonders
what triggers the bullae?  He's a tennis player, so could it be minor
trauma, UVL?

Tan Papules in a Child

Abstract: Eight year old boy with six month hx of tan macules

HPI: This otherwise healthy boy has had a six-month history of asymptomatic tan macules on his torso. Takes no meds by mouth and is asymptomatic.

O/E: Six - eight smooth surfaced tan macules measuring from 5 mm to 15 mm in diameter on torso. After lesions are rubbed they urticate mildly and are faint pink. Dermographia is negative.

Photos:




























Pathology:

Diagnosis:

Photodermatitis in a Teenage Girl

Abstract: 8 yr history of photodermatitis in a 17 yo girl

HPI: This 17 yo student has an 8 year history of a summer eruption. She has a pruritic eruption of her hands and distal forearms starting in spring and lasting till late fall. In winter her skin is perfectly normal. She has used triamcinalone 0.1% ointment without relief and similarly has not been helped with sunscreens.

O/E: Mild lichenification and a fine micro-papular eruption on the dorsum of the hands. A few serum crusts. No vesicles or h/o vesicles.

Photos (7/16/09)






Note no facial lesions


Diagnosis: Atypical Photodermatitis in a teenaged girl. Consider PCT, Hydroa variant, photoactivated atopoic dermatitis (nothing fits perfectly at this time)

Plan: 24 hour urine for porphyrins. Broad spectrum sunscreen for hands and clobetasol ointment after a 20 minute soak. Not sure biopsy will be helpful, but will do at next visit. PCT would be unusual but the porphyrias need to be ruled out.

Comments and suggestions?

Recurrent Toxic Erythema vx. Cellulitis

H.P.I. The patient is a 70 yo woman who has had ~ 10 episodes of a cellulitis-like picture of her legs over the past ten years. She has never had fever or constitutional signs. The process can affect one or both lower extremities. I saw her in 2001 for this and then she was referred by the emergency room yesterday with the same picture. It began with a fall two days ago. She hit her hip -- was in pain and took ibuprofen before this episode. She said she does not recall taking this before other episodes.

O/E: Patchy, fiery erythema of left lower extremity. Very mild erythems of right lower leg (mostly around the ankle).

Clinical Photos:





Labs: Biopsy obtained and CBC ordered

Diagnosis: Is this an atypical cellulitis, or toxic erythema secondary to and NSAID?

Discussion: If the patient remains afebrile and wbc is normal, I'd be inclined to just watch and wait.

Unusual Pigmentation of Legs

The patient is a healthy 51 yo woman with a 5 - 6 year history of asymptomatic progressive hyperpigmentation of the legs. She is in good general health and takes no medications by mouth. The process started on the calves and has spread proximally to the knees. She has rosacea in addition. She thinks her father has a similar problem.

O/E: Both legs from just above the ankles to the knees show punctate hyperpigmentation. The skin here has a slightly pebbly feel. Other than erythematous papules on both cheeks, the remainder of the cutaneous exam is normal. (There is no sclerodactyly, telangiectasas or sclerotic changes).

Photos:
Affected skin


Digital Zoom


Normal Skin (adjacent)


Dermoscopic Image


Lab: Biopsies of affected and normal skin were taken.

Diagnosis: Punctate Hyperpigmentation of the Legs. This does not look like the "salt and pepper" picture of scleroderma. Could this be an unusual genodermatosis?

Plan: Present to VGRD. Perhaps get serologies for scleroderma.

References: Nothing helpful found on PubMed.

Amytrophic (?) Dermatomyositis

Presented by Henry Foong
Ipoh, Malaysia

HPI: A 82 yr old housewife presented with 6 month history of skin eruptions on her face, neck and hands. They were aggravated with exposure to sun. She was diagnosed with carcinoma of the stomach in 2007 and completed chemotherapy about 3 months ago. While on chemotherapy she noticed weakness in getting up and putting on her shirt. She has improved since then. She has a history of diabetes mellitus, and IHD for more than 10 years.

O/E: Pertinent findings: bilateral and symmetrical erythematous macules and plaques on the dorsum of the PIP, DIO and MCP jpints. They have a violaceous hue and were non tender. Erythematous discoloration was noted
bilaterally and symmetrically around the eyes, nose and forehead.

Photos:


Lab:
TWBC 5,500
CK 41 U/l (<201) style="font-weight: bold;">Clinical Diagnosis: Dermatomyositis in Ca stomach
Could this be amytrophic dermatomyositis?
ANA + 1:320 Speckled and homogeneous

Questions: How would you proceed? Would you do a skin biopsy?
Would you treat her? Oral prednisolone or plaquenil alone?

Reference: (from eMedicine.com) Dr. Jeff Callen

Dermatomyositis sine myositis, also known as amyopathic dermatomyositis, is diagnosed in patients with typical cutaneous disease in whom no evidence of muscle weakness exists and in whom serum muscle enzyme levels are repeatedly normal for a 2-year period in the absence of disease-modifying therapies such as corticosteroids, immunosuppressive agents, or both. When studied, some patients with amyopathic dermatomyositis have abnormal ultrasound, MRI or magnetic resonance spectroscopy, or muscle biopsy findings. These patients have muscle involvement, and their condition may be better classified as hypomyopathic dermatomyositis. Patients with these variations may also reflect an underlying malignancy, and some develop severe pulmonary disease, particularly persons from Asian countries.
Patients exist in whom myositis resolves following therapy but whose skin disease remains as an active, important feature of the disease. These patients are not classified as having amyopathic dermatomyositis, despite the fact that, at this point in time, the skin is the major and often only manifestation of the disease. Sontheimer has suggested the term postmyopathic dermatomyositis for these patients.

Therapy for the cutaneous disease is often difficult. Patients who present primarily with skin disease (amyopathic dermatomyositis) and those in whom the muscle component is controlled but who still have significant skin disease exist. The first-line of therapy is recognizing that the patient is photosensitive and advising the patient to avoid sun exposure and to use sun protective measures, including broad-spectrum sunscreens. Hydroxychloroquine and chloroquine have been beneficial in small open-label case studies. Methotrexate is also useful. Mycophenolate mofetil has been reported to be useful. IvIg not only benefited the muscle but also cleared the skin lesions in the patients in whom it was used. Rituximab has been used for skin disease, but the results are mixed. Efalizumab has been used and may have some benefit. Efalizumab (Raptiva), a drug indicated for psoriasis, is being withdrawn from the US market and will no longer be available after June 8, 2009, because of potential risk for progressive multifocal leukoencephalopathy (PML). PML is a rapidly progressive infection of the central nervous system caused by the JC virus that leads to death or severe disability. Demyelination associated with PML is a result from the JC virus infection. JC virus belongs to the genus Polyomavirus of the Papovaviridae.

Lyme Tick

This 60 yo man came in for a skin cancer check. He had a basal cell removed from his forehead two years ago. The exam was negative until I checked his leg and noted a funny looking lesion. On closer examination, I realized it was a tick. It's head was embedded in the patient's leg. I removed the tick and gave the patient 200 mg. of doxycycline. This latter might be unnecessary, but a study published in the NEJM gives support to this fairly benign prophylaxis.

Reference:
Prophylaxis with single-dose doxycycline for the prevention of Lyme disease after
an Ixodes scapularis tick bite.

Nadelman RB, wt. al. Tick Bite Study Group.

Department of Medicine, New York Medical College, Valhalla 10595, USA.

BACKGROUND: It is unclear whether antimicrobial treatment after an Ixodes scapularis tick bite will prevent Lyme disease. METHODS: In an area of New York where Lyme disease is hyperendemic we conducted a randomized, double-blind, placebo-controlled trial of treatment with a single 200-mg dose of doxycycline in 482 subjects who had removed attached I. scapularis ticks from their bodies within the previous 72 hours. At base line, three weeks, and six weeks, subjects were interviewed and examined, and serum antibody tests were performed, along with blood cultures for Borrelia burgdorferi. Entomologists confirmed the species of the ticks and classified them according to sex, stage, and degree of engorgement. RESULTS: Erythema migrans developed at the site of the tick bite in a significantly smaller proportion of the subjects in the doxycycline group than of those in the placebo group (1 of 235 subjects [0.4 percent] vs. 8 of 247 subjects [3.2 percent], P<0.04). p="0.02)" p="0.02)." style="font-weight: bold;">CONCLUSIONS: A single 200-mg dose of doxycycline given within 72 hours after an I. scapularis tick bite can prevent the development of Lyme disease.

Abdominal Sinuses in a 23 yo Man

Three month history of draining sinuses lower abdomen.

HPI: This college student developed abdominal pain and bloody diarrhea in August of 2008. A diagnosis of ulcerative colitis was made and a number of theapies were tried (including prednisone and Remicaid). All were ineffective and he had a subtotal colectomy and ileostomy performed in December of 2008. Subsequent to that he continues to have some pain in the rectal stump and is scheduled for a J-pouch procedure in a few weeks. Three months ago, he developed painful draining tracts in the lower abdomen.

O/E: The patient is a healthy-appearing 23 yo man. The cutaneous findings are 5 - 10 mm in diameter sinus tracts with sero-sanguinous drainage. There are four active lesions at this time. The remainder of the cutaneous exam is negative.

Photos: (June 9, 2009)


Lab and Path: Nil

Diagnosis: Could this be an extra-intestinal manifestation of inflammatory bowel disease? This is more common with Crohn's disease than U.C. My working diagnosis is sinus tracts or abdomino-cutaneous fistulae. The patient was referred for the question of pyoderma gangrenosum. If this is P.g., it is a very atypical case.

Questions:
Has anyone seen and treated a similar patient?
He is scheduled to have a resection of the rectal stump with a re-anastamosis of small bowel to the rectum allowing closure of his ileostomy (I am not sure of exact procedure). Perhaps this will help. Your thoughts are appreciated.

Trichoepithelioma

A Dermatologic Vignette.

The patient is a 78 yo woman with a few year history of an enlarging lesion on the nasal tip. Excellent health.

Eight mm in diameter pearly papule nasal tip. Clinically and dermoscopically BCC.



Pathology shows this to be a trichoeoithelioma:






Question: Observe, refer to Mohs, radiate?
Would surgery be deforming in this site? vs. Is radiotherapy overkill?

Reference: There are very few references which address this type of lesion, unless we consider this to be like a BCC. But here is one.

Aygun C, Blum JE. Trichoepithelioma 100 years later: a case report supporting the use of radiotherapy. Dermatology. 1993;187(3):209-12.
Trichoepitheliomas are rare skin tumors which can cause significant cosmetic and functional impairment when they occur in the head and neck area. Multiple methods of treatment including plastic surgery, dermabrasion, cryosurgery and laser surgery have been reported in the literature. A 32-year-old male with multiple coalesced lesions in his ear canals was treated with radiation therapy after he failed more conventional methods of treatment. He is free of tumor in the radiated area 17.5 months after treatment with significant functional improvement. Various aspects of this tumor were reviewed. More data are still needed to define the proper place for radiation in the management of this disease.

Remember Dorinda and Walter Shelley's poem:
Who knows
Who's nose
Needs Mohs

Dissecting Cellulitis of the Scalp

Abstract: 18 yo man with three year history of cystic lesions scalp, axillae, chin

HPI: This 18 year-old man has had dissecting cellulitis of the scalp for three years. He has been treated with doxycycline 100 mg b.i.d. and excisions of cysts and sinuses by a plastic surgeon. He presented in May of 2009 for another opinion. He has had a few cysts of the axillae and chin. The patient has observed that his scalp is worse after wearing a helmet for football.

O/E: The patient is a healthy, moderately obese African-American teenager. He has painful cysts, nodules and draining sinuses mostly on the occipital portion of the scalp and around the vertex. He has a hypertrophic scar at the site of an excision in the occipital region. He has a few hyperpigmented nodules in the axillae and some small acne cysts on his chin in the bearded area.

Clinical Photos:


Lab: Nil
Path: Nil

Diagnosis: Dissecting Cellulitis of the Scalp in the setting of Follicular Triad Syndrome. An older name for the scalp process is the hard to remember "Perifolliculitis Capitis Abscedens et Suffodiens

Treatment: To date, only doxycycline 100 mg b.i.d. and frequent excisions by a plastic surgeon. I injected some active lesions with triamcinalone acetonide 10 mg/cc and am considering following the rifampicin and isotretinoin protocol reported in the reference below.

Reason Presented: For therapeutic suggestions

References:
1. Georgala S, et al. Dissecting cellulitis of the scalp treated with rifampicin and isotretinoin: case reports. Cutis. 2008 Sep;82(3):195-8.

Dissecting cellulitis of the scalp, or perifolliculitis capitis abscedens et suffodiens, is an uncommon chronic suppurative disease of the scalp manifested by follicular and perifollicular inflammatory nodules that suppurate and undermine, forming intercommunicating sinuses, and leading to scarring alopecia. Treatment generally fails to obtain a permanently successful result; thus, many therapeutic options have been proposed. We report 4 cases of dissecting cellulitis of the scalp successfully treated with oral rifampicin and oral isotretinoin. To our knowledge, this is the first report of oral rifampicin used concomitantly with oral isotretinoin in this disease entity. We also present a brief review of the literature on the topic.

2. Dissecting Cellulitis of the Scalp Emedicine.com chapter

Teledermatology Rules: Vasculitis

Abstract: 2o yo man with one week history of palpable purpura.
HPI: This 20 yo college student was started on isotretinoin for severe cystic acne a month before he developed a rash on his legs. He also had an upper respiratory infection two weeks before the eruption began. He is away at school (a two hour drive). His mother called the office and spoke to my secretary. Busy week. When I heard that he had a rash, I relayed the message that it was probably the common dermatitis we see with patients on isotretinoin and if worried to send me a photo. Two days later, this photo was sent:


The patient was then emailed and asked to come in the next day. Labs were ordered done before the visit.

O/E: Palpable purpura both L.E. Right ankle swollen and tender. Patient limping.

Lab: CBC normal, UA normal. Pending Labs: Throat culture, ANA, ASOT. (Hep C, Stool for OB, not ordered)

Path: Biopsy performed. Not back

Diagnosis: Leucocytoclastic vasculitis. Etiology: The URI, isotretinoin, idiopathic

Plan: Rest for a few days. No specific therapy at this time except stopping the isotretinoin. If he improves uneventfully without evidence of GI or renal involvement will offer a re-challenge with isotretinoin.

Discussion: A few cases of LCV have been reported with isotretinoin. This patient has severe cystic acne with scarring and it would be a shame to withhold drug if it were not putative for the LCV. I admit I did not pay proper attention to the first telephone call. This illustrates the power of teledermatology which can be almost standard in a few years as cell phone cameras become better and people know how to use them more adroitly.

Questions: What are your thoughts and suggestions?

Ear Keloids and Imiquimod

We presented this patient around a year ago (she is patient # 2). The woman, now 19 years old, presented in March of 2008 for a keloidal scar in the left triangular fossa. On 12/18/08 based on suggestions and a report in MEDLINE, the lesion was shave excised and a week after surgery, imiquimod was applied nightly for six weeks. She is now one month out after stopping imiquimod. At this point, she looks very good. We will have to see if this is a long term solution.

Reference:
1. Berman B, Kaufman J. Pilot study of the effect of postoperative imiquimod 5% cream on the recurrence rate of excised keloids. J Am Acad Dermatol. 2002 Oct;47(4 Suppl):S209-11.
New adjunctive treatments are needed to reduce the high recurrence rates (50%) of excised keloids. Interferon alfa injections have been shown to decrease the size of stable keloids. This study examined the effects of postoperative imiquimod 5% cream on the recurrence of 13 keloids excised surgically from 12 patients.Starting on the night of surgery, imiquimod 5% cream was applied for 8 weeks. Patients were examined at weeks 4, 8, 16, and 24 for local erythema, edema,
erosions, pigment alteration, and/or recurrence of keloids. Of the 11 keloids evaluated at 24 weeks, none (0%) recurred. Incidences of hyperpigmentation were 63.6%. Two cases of mild irritation and superficial erosion cleared withtemporary discontinuation of imiquimod. Both patients completed the 8 weeks of topical therapy and the final 24-week assessment. At 24 weeks, the recurrence rate of excised keloids treated with postoperative imiquimod 5% cream was lower than recurrence rates previously reported in the literature.

Nodules in Search of a Diagnosis

Presented by

J. Erin Reid, M.D. Dermatology Resident &
Stephen P. Stone, M.D. Professor of Dermatology
Southern Illinois School of Medicine

Abstract: 70 yo man with a five year history of exophytic nodules on the lower extremities.

HPI: A 70 year old white male presented with a five year history of exophytic nodules on the lower extremities. They were increasing in number. A few had been removed by shave excision, and the areas that were treated did not regrow.
Over the past few years he had numerous nodules measuring up to 4 cm in diameter. A few of them were excoriated and crusted. There was no lymphadenopathy. He also had extensive areas of erythema and scale on his forearms, upper arms, and thighs.
He had been in the Navy over 50 years ago and served in Japan. He also went to Bangkok and Hong Kong 20 years ago. No significant past medical history

O/E: On the pre-tibial area the patient has multiple nodular lesions, as well as some erythematous and hypopigmented scars where previous lesions have been removed by shave excision. The lesions range from 1 cm to 3-4 cm in diameter.

Photos:





Pathology: Many biopsies have been performed. In May, 2006, a biopsy showed “superficial perivascular dermatitis of the mixed type, with eosinophilic spongiosis and pustules consistent with an allergic etiology”.
In February, 2007, biopsies of the right anterior and lateral leg showed “marked epidermal hyperplasia, spongiosis, and mixed intraepidermal and superficial dermal inflammatory cell infiltrate”. There was no evidence of malignancy or infection at that time, but there was evidence of chronic venous stasis change.
In January, 2009, we excised another nodule. This was read as “marked epidermal hyperplasia with acute and chronic inflammation” and was negative for fungal, bacterial and acid fast bacilli stains. There is also no evidence of malignancy or carcinoma. Cultures for fungus, anaerobes and AFP were all negative. Flow cytometry was negative.

Diagnosis: What is your differential diagnosis?
Questions: What further information would you want? What additional studies? How would you treat this man?

References will be added when available.

Diseases Don't Read Textbooks

Abstact: 5 yo girl with enlarging plaque on back.

HPI: The patient is a 5 year old girl seen on February 27, 2009 with a 10 day history of an enlarging plaque on the left back. She had a similar, but less dramatic lesion in April 2008 which was treated with cefuroxime for two weeks. Her family lives in a wooded area and her mother had Lyme Disease last year. The patient feels well, may have had some mild arthralgias according to her mother. No neurological symptoms. She is allergic to penicillin, amocicillin and sulfonamides.

O/E: 17 x 12 cm plaque left back. 2 x 2 cm plaque right arm. These lesions are somewhat urticarial in appearance. The center of the larger lesion is paler than the periphery.

Photos:


Lab: Lyme titers pending

Diagnosis: Presumptive Lyme Disease. She was started on cefuroxime by her pediatrician.
Questions:
1) What else would you consider in the differential diagnosis
2) Can one have ECM more than once? This child had something similar 10 months ago.
3) Presuming this is Lyme -- how long shoud she be treated?

Reasons Presented: Lyme Disease is unusual in the winter. Can one have "primary lesions" with a reoccurence? In a young patient where tetracyclines are contraindicated with a proven allergy to penicillins, what is the best third line drug and how long to administer.

Interesting Follow-up: Paronychia in a Child

In October 2007, we presented the case of an eight year old girl with chronic paronychial inflammation located on the left index finger (Paronychia in a Child). She had no other dermatoses. The patient is adopted so we have no family history. We assumed this was some kind of localized psoriasis or acrodermatitis continua. Clobetasol ointment was prescribed which she has used since. (Photo above from 10/2007)

The patient was seen in follow-up recently. The paronycial inflammation had subsided but the finger tip was still abnormal, especially on the palmar surface and there is now hypopigmentation and atrophy distal to the area of inflammation. This latter is likely secondary to the clobetasol. Her topical therapy was switched to calcipotriene cream (the ointment is no longer available in the US.)

Photos:






Questions:
1) What do you think the diagnosis is?
2) Side-effects on the fingers from super-potent topical corticosteroids are rarely reported. One suspects that they are not that unusual. When does the treatment get worse than the disease? (I should have been more diligent in follow-up)
3) Who thinks that these preparations can cause bone changes?
Your comments will be appreciated.

References:
1. Deffer TA, Goette DK.. Distal phalangeal atrophy secondary to topical steroid therapy. Arch Dermatol. 1987 May;123(5):571-2.

2. Tosti A, Fanti PA, Morelli R, Bardazzi F. Psoriasiform acral dermatitis. Report of three cases. Acta Derm Venereol. 1992;72(3):206-7.
Department of Dermatology, University of Bologna, Italy.
The authors report 3 patients affected by psoriasiform acral dermatitis, a distinctive clinical entity characterized by a chronic dermatitis of the terminal phalanges, associated with marked shortening of the nail beds of the affected fingers. The skin biopsy showed in all cases the pathological features of a subacute spongiotic dermatitis. X-ray examination of affected fingers showed no bone or soft tissue changes. Differential diagnosis of psoriasiform acral dermatitis included psoriasis, atopic or contact dermatitis and corticosteroid-induced distal phalangeal atrophy.

3. Brill TJ, Elshorst-Schmidt T, Valesky EM, Kaufmann R, Thaçi D. Successful treatment of acrodermatitis continua of Hallopeau with sequential combination of calcipotriol and tacrolimus ointments. Dermatology. 2005;211(4):351-5.
Department of Dermatology, J.W. Goethe University, Frankfurt, Germany.
Acrodermatitis continua of Hallopeau (ACH) is a rare type of pustular psoriasis affecting the digits. We report on a 43-year-old female patient who had been suffering from ACH for more than 20 years. Despite the fact that the disease was localized on one finger during the whole period, several topical and systemic treatments resulted in only temporary or partial improvement of the lesion. Although the monotherapies with calcipotriol and tacrolimus ointments gave no satisfying results in the long-term management of the disease, the combination of both agents led to a continuous improvement of the patient's skin condition. Copyright 2005 S. Karger AG, Basel.

R/O Subungual Melanoma

70 yo man referred for suspected subungual melanoma.

HPI: The patient is a retired engineer with a one month history of subungual pigmentation. He suffers from Waldenstrom's macroglobulinemia and peripheral neuropathy. If he had injured his toe, he would not know.

O/E: The left middle toenail shows brown-blackish subungual pigmentation. It was difficult to appreciate if this was melanin or blood both clinically or dermoscopically. Hutshinson's sign is negative.


Dermoscopy before 3 mm punch biopsy

Diagnosis: Probably subungual hematoma. Need to r/o melanoma.

Procedure: Modification of Haneke Technique.

1. Patient soaks foot in warm water for 20 - 30 minutes
2. Carefully drive a 3 mm punch through the nail with care not to cut into the nail bed.
3. Lift off the cut disk of nail and observe the nail bed.


Dermoscopy after 3 mm punch biopsy and H2O2 to defect

In this case, what appeared to be dried blood was present. The area was cleaned with hydrogen peroxide and a normal appearing nail bed was see. There was no pigment noted. Dr. Hanecke's technique utilizes a Hemocult stick to test scraping from underside of nail, however, our strips were outdated and not reliable.

Note: Dr. Eckhart Haneke pioneered this technique but is not acknowledged in the literature. Here are his comments to this case: "Thank you very much for your email and the links, which I saw for the first time. Thank you also for giving me the credit.
You are completely right that we do not even need the hemoccult test strip for the correct diagnosis, but it is very convincing and impresses the patient. And of course, it is one more proof.
Also clinically, as this is no streaky lesion a melanoma is improbable - however, a very fast growing melanoma can appear like this.
When you apply hydrogen peroxide and the pigment disappears this is due to the hemodestructive action of H2O2 on erythrocytes: hemoglobin has a pseudocatalase action splitting H202 into H2O and O. That is why hydrogen peroxide is also a very good disinfective agent and I use it to cleanse my dermatosurgery field from blood."

Pseudocyst of the Auricle

The patient is a 20 yo college wrestler with a one week history of a painless swelling in the right ear. The area outlined is fluctuant but not inflamed.

This is an auricular pseudocyst. It is overly optimistic to think that simple drainage will ensure cure. A number of therapies have been proposed.

For an excellent (and reasonably succinct) review of this subject see eMedicine/Pseudocyst.

This patient was referred to a plastic surgeon -- I will put an addendum after I learn of the therapy. The problem is that most dermatologists do not have enough experience treating this entity. Inadequate treatment can result is a permanent deformity of the auricle.

Magic Cure?

Abstract: 45 yo man with two year history of painful fingers
Posted by DJ Elpern
HPI: The patient is a 45 yo electrician and professional pianist who developed hyperkeratotic patches on his hands two years ago. Nothing new in exposures. After much questioning, he remembered that his mother-in-law moved in with them around that time. (not kidding). The fissures are very painful, especially when playing keyboard. He can use gloves doing electrical work. Patch testing has not been done but is planned.
O/E: Hyperkeratotic areas around thumb and middle finger tips bilaterally. Fissures are deep but clean. He has had similar areas on thenar and hypothenar eminences in past. Remainder of cutaneous exam is unremarkable.
Photos:






Diagnosis: Hyperkeratotic Hand Eczema, Psoriasis variant? Fristional Contact Dermatitis
Treatment: He has tried potent topical steroids with occlusion and with the Soak and Smear technique. Crazy glue for fissures. Intralesional triamcinalone 10 mg/cc helped the palmar keratoses. He has had one month of methotrexate 10 mg per week. Only the intralesional TAC has helped but he does not want finger tips injected at this time.
Questions:
1. What do you think the diagnosis is? The role of trauma may be key as he works with his hands as an electrician and his fingers are "traumatized" on the keyboard.
2. Do you have any magical therapeutic suggestions?
3. I have heard that X-ray treatment was used in the past. Any rational for Grenz?
4. Further work-up
Reason Presented: This man is at his wit's end with pain. He can't play the piano since every time he hits a key he has exquisite pain. I have had one or two similar patients -- they just got better over a few years seemingly not related to treatment.
Reference:
E. McMullen, D.J. Gawkrodger, Physical friction is under-recognized as an irritant that can cause or contribute to contact dermatitis. Br J Dermatol. 2006:154;154-156
Department of Dermatology, Royal Hallamshire Hospital, Sheffield U.K.
Full Text of Article
Background The role of physical friction as an irritant in the causation of contact dermatitis is under-recognized. Frictional dermatitis is defined as an eczematous process in which physical frictional trauma contributes to the induction of a dermatitis process.
Objectives To examine the clinical background of patients in whom friction was contributing to dermatitis.
Methods Over a 30-month period during which 2700 new patients were seen, frictional irritancy was identified as playing a role in the dermatosis in 31 cases: in 27 of these, case notes were evaluated for a range of parameters.
Results Physical friction was identified as causing or contributing to the dermatitis in 18 men and nine women, mean age at onset 42 years. The hands, usually the fingers of the dominant hand, were affected in all but two cases. Occupational frictional activities were found in 25 cases: commonly handling small metal components, paper, cardboard or fabric, and driving. Potential frictional activities in hobbies were noted in 12 cases. Wet work irritancy contributed in four cases (15%). Patch testing showed relevant contact allergies as cofactors in seven of 25 subjects tested (26%). Psoriasis was a cofactor in four (15%), and atopic dermatitis in 11. The study was selective, being based in a teaching hospital clinic with a special interest in contact dermatitis. Frictional irritancy is often one of several factors contributing to dermatitis.
Conclusions The contribution of friction to contact dermatitis is under-recognized probably because dermatologists do not think about the potential for physical forces to induce eczematous changes in the skin.