Clinical Challenge: Fissuring Itchy Plaques

Asteatotic eczema (AE), or eczema craquelé, is a pruritic dermatitis caused by dry skin that can progress to fissuring and scaling.1 The superficial fissures occur in a curvilinear or polygonal pattern, which can resemble a dried riverbed and has been described...

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Asteatotic eczema (AE), or eczema craquelé, is a pruritic dermatitis caused by dry skin that can progress to fissuring and scaling.¹ The superficial fissures occur in a curvilinear or polygonal pattern, which can resemble a dried riverbed and has been described as “crazy-paving.”^1,2 The French word craquelé is used to refer to the “cracked” skin appearance of AE¹ and was first coined by Louis Brocq in 1907.³ The condition results from fewer free fatty acids in the stratum corneum, which results in significantly increased epidermal water loss. Cold weather and decreased humidity in the living environment, certain medications such as retinoids, and frequent handwashing contribute to epidermal water loss resulting in xerosis.¹

Although it may occur over the back, trunk, and arms, AE most commonly occurs in the elderly on the anterolateral lower legs.^1,4 The median age of patients who present with AE is 69 years old.¹ However, younger populations can also develop AE due to environmental factors. In this case, the patient described frequent hand scrubbing before surgery. The condition can also be caused by malnutrition, underlying malignancy, acute edema, or decreased sweat gland activity.^4-7

Although a skin biopsy is not necessary for the diagnosis of AE, a microscopic examination can be useful in differentiating AE from other skin conditions. Biopsy reveals a mild subacute spongiotic dermatitis with intracellular edema.¹ The results would also show a clear disruption of the stratum corneum, which corresponds to the gross appearance of erythematous borders and pavement pattern seen on patients with AE.⁴ Aside from an irregularly-shaped stratum corneum, the presence of lymphocytic infiltrates is another microscopic characteristic of AE.¹ Acanthosis and hyperkeratosis are additional histologic features that are consistent with AE.¹

The differential diagnosis for AE includes irritant and allergic contact, as well as nummular, stasis, and atopic dermatoses.¹ Asteatotic eczema is a clinical diagnosis, and a biopsy would reveal features common in other dermatoses—spongiotic dermatitis, intracellular edema, acanthosis, hyperkeratosis, and varying degrees of lymphocytic infiltrate.¹However, AE is unique for its cracked porcelain appearance and pruritus. Allergic contact dermatitis is typically acute, and the rash follows the distribution of allergen contact, although it can be chronic and generalized in cases of continued allergen exposure. Both nummular dermatitis and AE tend to occur in individuals over 55 years of age, although the nummular form is characterized by lichenified, coin-shaped lesions.²

The patient in the case also had a history of atopic dermatitis, which has a relapsing course, and is pruritic with scaly, excoriated plaques.² However, in this presentation, AE was diagnosed due to the characteristic appearance of the rash and concurrent use of isotretinoin.²

Other differential diagnoses can be considered in the appropriate clinical context. Stasis dermatitis can occur with a history of deep venous thrombosis, obesity, recent pregnancy, or prolonged immobilization.^1,8 Cellulitis patients usually present with warm, swollen areas of erythema on the extremities, sometimes accompanied by a fever.⁹ Acute edema/cutaneous distention syndrome has been reported to present with skin findings similar to those of AE in patients with circulation disturbance from underlying anorexia nervosa, heart failure, and liver disease.¹⁰

The basic management of these dermatitis includes patient education, avoidance of triggers or treatment of the underlying diagnosis, moisture replenishment, and barrier protection.^2,6,8,9 Topical corticosteroids are commonly used in all of the types of dermatitis, although some may be refractory to treatment.² Unresponsiveness to topical corticosteroids is commonly seen in patients with AE and concurrent internal malignancies, such as lymphomas.⁴

Patients should supplement topical steroids with emollients. Moisture replenishment can be achieved by using lotions with high oil content as opposed to those with high water content.¹ Corticosteroids, such as fluocinolone, triamcinolone, and betamethasone have been shown to improve moderate AE, whereas pimecrolimus cream 1% controls the pruritus associated with AE.¹ Additionally, patients should avoid overusing soaps and engaging in prolonged hot showers as these activities may further dry out the skin. 

Patient Outcome

The patient was treated with topical triamcinolone acetonide 0.1% cream applied twice daily to the affected areas in conjunction with over-the-counter moisturizing products, including petroleum jelly and oatmeal colloidal lotion. The patient was also advised to limit use of harsh soaps and hand sanitizers. Upon follow-up 2 weeks later, the AE had completely resolved (Figure 2). The patient continued her prescribed isotretinoin course while the AE was treated and the rash did not recur throughout the remaining 4 months of isotretinoin therapy.

Dina Zamil, BS, Sahifah Ansari, MS, and Nicole Nyamongo, BS are medical students at Baylor College of Medicine in Houston, Texas. Rajani Katta, MD is a dermatologist and patch testing specialist in Houston, Texas. 

References

1. Specht S, Persaud Y. Asteatotic eczema. In: StatPearls. StatPearls Publishing; 2022. Accessed December 25, 2022. http://www.ncbi.nlm.nih.gov/books/NBK549807/.

.2. Chan CX, Zug KA. Diagnosis and management of dermatitis, including atopic, contact, and hand eczemas. Med Clin North Am. 2021;105(4):611-626. doi:10.1016/j.mcna.2021.04.003

3. Brocq L. Traité élémentaire de dermatologie pratique, comprenant les syphilides cutanées: Généralités et entités morbides vraies. T. 1. O. Doin; 1907.

4. Sparsa A, Boulinguez S, Liozon E, et al. Predictive clinical features of eczema craquelé associated with internal malignancy. Dermatology. 2007;215(1):28-35. doi:10.1159/000102030

5. Ishiguro N, Hirohara D, Hotta M, Takano K, Kawashima M. Linear erythema craquele due to acute oedema in anorexia nervosa. Br J Dermatol. 2001;145(2):357-359. doi:10.1046/j.1365-2133.2001.04358.x

6. Cox NH. The acute edema/cutaneous distension syndrome. Arch Dermatol. 2003;139(2):224. doi:10.1001/archderm.139.2.224

7. Kitaba S, Matsui S, Iimuro E, et al. Four cases of atopic dermatitis complicated by Sjogren’s syndrome: link between dry skin and autoimmune anhidrosis. Allergology International. 2011;60(3):387-391. doi:10.2332/allergolint.10-CR-0265

8. Sundaresan S, Migden MR, Silapunt S. Stasis dermatitis: pathophysiology, evaluation, and management. Am J Clin Dermatol. 2017;18(3):383-390. doi:10.1007/s40257-016-0250-0

9. Raff AB, Kroshinsky D. Cellulitis: a review. JAMA. 2016;316(3):325-337. doi:10.1001/jama.2016.8825

10. Yamada S, Sawada Y, Ohmori S, et al. Acute edema/cutaneous distension syndrome representing as eczéma craquelé-like change: a case and published work review. J Dermatol. 2016;43(6):709-710. doi:10.1111/1346-8138.13267