Hi all, I should probably know this but I don't and much reading and searching have never revealed any clues So what is this commonly seen skin condition. It is usually seen on obese elderly women with oedematous legs.
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The pictures below are typical of an advanced case.
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Hi Dave,
About to hit the wooden stairs after a manic weekend, and in my tired state I can`t honestly provide a definitive diagnosis other than the broad term of stasis dermatitis/chronic venous insufficiency.
The lichenification (crusting) is a result of long term chronic oedema, which disrupts `normal` skin turnover. Sorry i cant deliver a more sciencey explanation right now.
Cheers,
Bel -
Yes thanks Bel, like you say stasis dermatitis and crusting but what is (how does it form) that vascularised filament pile that forms under the crusting i.e. like the top picture 2nd toe after removal of crusting?? Can it be treated and reversed to normal skin?? Is it a hypertrophic prickle cell layer exposed?
Dave -
Taken from Ivan`s `Text Atlas of Podiatric Dermatology`, page 46;
Lymphoedematous keratoderma – chronic lymphoedema on the lower limbs may cause prominent creasing and thickening of the skin on the dorsum of the foot. Chronic changes include fibrosis and papillomatous, wart-like projections.
As this is an endogenous (as opposed to exogenous) dermatitis, treatment is suppressive rather than curative, in the main. External factors may exacerbate the condition but are not causative. Topical emollients may improve skin hydration and quality, so hyperkeratotic return is slowed.
The following link does offer some short and long term treatment strategies;
stasis dermatitis
Hope that helps! -
Regards Dave -
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Cheers Bel, I'm going to read up and then ask you difficult questions:D
A treatment program that I am trying with one lady was to increase her visit frequency (domiciliary) to 4 weeks and soak the feet and ankles in warm water with a softener then apply potassium hydroxide to further soften, then debride the crusting with the blunt edge of a blade or the edge of a diamond deb file. Dry and apply urea cream, I have done this rigorously on the left foot and ankle and right foot but not the ankle so as to see the change. Over several months there has been a significant improvement in the skin condition mostly noticeable in that the fibrotic protrusions and much smaller and much less tender and less likely to bleed when the crust is abraded.
I'm wondering if even more regular treatment would result in improved outcomes, obviously there is a cost consideration but this particular lady is very pleased with the improvement and happy with the cost.
Dave -
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What are her finger nails like?
Yellow nail syndrome is associated with lymphoedema but affect all 20 nails.
Nina -
The most likely diagnosis is Pretibial Myxedema (PTM), a thyroid dermopathy usually associated with Graves Disease.
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Dave -
I agree that is a possible differential diagnosis. However, it is my understanding that myxoedema (UK version of PTM) is a fairly rare finding in patients with thyroid problems. Dave was asking about a common manifestation and posted the images as an example.
This also highlights the necessity of accurate history taking and including previous medical, surgical and drug history when presenting dermatological case studies on the Arena. Any thyroid condition would have been flagged up when the `history – examination – investigation` rule in dermatology was applied.
Cheers,
Bel -
Dave: Be careful. In my experience, patients -- especially the elderly -- are often unable to provide a sound review of their past medical history. Just because the patient denies thyroid illness doesn't mean she doesn't have it, or hasn't had it! I trust her primary care physician and/or internist has checked her TSH, T3, T4, and thyroid antibodies in the not too distant past? If so, I would certainly want to see the labs to confirm a negative diagnosis of Graves. Remember, she could be euthyroid following treatment and still show the cutaneous manifestations.
Bel: I may have misunderstood Dave's primary reason for posting the images. However, just out interest: Graves disease is the most common aetiology of hyperthyroidism, affecting 50 in 100,000 persons [1]. It affects 2% of women at sometime in their lives, and pretibial myxedema (PTM) is the most common cutaneous manifestation, affecting up to 4% of all patients and up to 15% of patients in patients with Graves-related opthalomopathy[2]. Okay, it's certainly nowhere near as common as the cutaneous manifestations of venous hypertension, but we do see it. In fact, I've seen 3 cases of PTM in the last 18-months in a population of 55,000.
The photographs show a classic presentation of PTM: Diffuse, elephantiasis-like, lymphodematous (non-pitting, I assume) edema with indurated plaques with a peau d'orange appearance, and polypoid lesions.
The precise pathogenesis of PTM remains a mystery. One theory suggests the edema is due to the accumulation of mucopolysaccharides (glycosaminoglycans) in the dermis that causes thickening of the skin. T cells sensitized to antigen or antigens that are shared by thyroid follicular cells and fibroblasts (e.g. a portion of the TSH receptor) infiltrate dermal tissue, release cytokines, and stimulate the synthesis of acid mucopolysaccharides [1].
Sincerely,
Ray
References:
1. Mclver B, et al. The pathogenesis of Graves' disease. Endocrinol Metab Clin North Am 1998; 27: 73.
2. Schwartz KM, et al. Extensive personal experience - dermopathy of Graves' disease (pretibial myxedema): long-term outcome. J Clin Endocrinol Metab 2002; 87: 438.
3. Georgala S, et al. Pretibial myxedema as the initial manifestation of Graves' disease. J Eur 2002; 16: 380. -
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Ray
I did send photo's and query letter to her GP for his further consideration and evaluation. But one of my main reasons for starting this thread was because a much younger woman of 49yrs old, she is extremely obese at about 125kg and 175cm tall. She has been a client for many years has presented at her last appointment with a milder version of this skin condition, that I would say is most likely related to the diagnosis stasis dermatitis (which appears to be a misnomer somewhat). She is one of those who has a brash disregards of advise and so I wanted to give her a more in depth evaluation that might be more convincing and encourage her to se her GP.
A query of hyperthyroidism might have been worth considering but she does not have any other outward signs of Graves disease. She did have thyroidectomy surgery for hyperthyroidism before 2002 and now takes thyroxine, so now she is more likely to be Hypothroid I would expect.
I've been studying the photo's of P.Myxedema and they are superficially similar but not really the same as the skin condition I have shown in the photos earlier, however, presumably do you think that they do resemble P. Myxedema?
Regards Dave Smith -
So, your 49-year old did have hyperthyroidism. Two points: 1) Infiltrative dermopathy may occur years after the treatment of Graves, with the patient euthyroid. 2) Opthalmopathy and other signs of Graves are not always clinically evident. A simple biopsy of the lesion may offer a definitive diagosis PTM in the euthyroid patient. See this interesting case history: http://bmhlibrary.info/15251711.pdf.
Regards
Ray -
"Pretibial myxedema develop in patients who are hyperthyroid, hypothyroid, or euthyroid. This condition may be seen with Graves` disease, after surgical or radioactive iodine treatment for thyrotoxicosis, or with Hashimotos thyroiditis. It may also develop in the abscence of hyperthyroidism..."
That`s why I said `thyroid problems` earlier. It isn`t just associated with Graves.
Interesting discussion guys!
Bel
Just realised I`m cross posting, sorry. But I think we`re singing from the same sheet.Last edited: Feb 22, 2012 -
A Comparison of the Efficacy of Pharmacological, Physical, and Compression Therapy in the Treatment of Stasis Dermatitis: A Literature Review
Marian Banh, B.A., Quang Pham, B.S.
Extremitas
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