As with many syndromes, the management scheme presented here emphasizes the diagnostic framework . The clinical approach to the SSS demands a thorough process of eliminating obvious as well as more subtle diagnoses. Once the diagnosis is made, deriving the appropriate treatment becomes a relatively simple task. Note that since much of the mechanisms of SSS are unknown, the clinician must be comfortable with a certain degree of ambiguity and uncertainty.
Underlying mechanisms of sensitive skin syndrome
It is reasonable to organize the differential diagnosis by dividing SSS into visible and invisible SSS. Some dermatoses that most clinicians find simple to diagnose may have atypical presentation and as a result lack the ‘expected’ morphology. Eczema, atopic dermatitis, and rosacea are likely the three most common causes of SSS related to barrier defect.[28
] Seborrheic dermatitis should probably be included in that category as well.[29
] Full discussion of these conditions is beyond the scope of this overview but we will highlight some common clinical features. Careful history, including family history and occupational history, combined with a detailed physical exam will often reveal the diagnosis. In the history particular consideration should be given to culprits such as the masking effect of other topical agents applied by the patient. The physical exam should include scrutiny of the face and scalp for subtle signs of minor inflammation, which are often masked in SSS with underlying endogenous dermatoses.[1
] In all of these conditions the patients are likely over-exfoliating their skin and thus exacerbating the barrier dysfunction. Therefore, following specific treatment to halt the acute pathological process, preventing recurrence with a proper skin care regimen is indicated. In eczema and atopic dermatitis, the careful clinician may resort to short-term (2-week) use of corticosteroids to stop the inflammatory process. Calcineurin inhibitors are alternatively indicated for delicate areas on the face.[30
] In an effort to control histamine release in atopic dermatitis, antihistamines can be added and a relatively allergen-free environment should be created. In rosacea, the mainstay of treatment is oral and topical antibiotics. In seborrhoeic dermatitis, azoles are the mainstay of treatment and low potency corticosteroids and emollients can be added acutely to treat the inflammatory process.[31
Contact dermatitis (CD) and photocontact dermatitis (PCD), as well as nonimmune contact urticaria (NICU) and immune contact urticaria (ICU), are all conditions that may elicit SSS symptomology, with transient objective findings on physical exam. Therefore, careful testing should be performed. CD and PCD can be visualized with skin patch and photopatch testing. Once the allergen has been identified, avoidance should lead to symptom resolution. Allergen-free products are now available and should be included as part of further skin care regimen in these patients. The main reason why NICU is often a missed diagnosis in patients presenting with the SSS is the transient nature of the reaction. Thus, after testing with small amounts of product on the skin, the patient should be carefully examined using minimal magnification: The lesions will be typically revealed within 20 minutes. Common trigger agents are fragrances (e.g. cinnamic aldehyde) and preservatives such as sorbic and benzoic acids.[1
] Once triggers are identified, simple avoidance defines the management. ICU can be demonstrated with open and occluded testing, followed by prick testing with appropriate positive and negative controls if no response is elicited.[33
] Various foods, latex, parabens, and other chemicals have been implicated in the causation of ICU.[34
However, there are cases in which no clinical clue is provided by the physical exam. In these cases, a 2-week trial of appropriate-strength corticosteroid may solve the mystery by pointing to an eczematous process in the case of symptoms resolution. Nonetheless, the careful clinician should consider avoiding prolonged use of topical corticosteroids since there is anecdotal clinical experience of topical corticosteroids inducing SSS[35
] and, at least in the case of barrier dysfunction, earlier and complete steroid tachyphylaxis has been demonstrated.[36
] If no symptomatic relief is observed, the patient's SSS is likely due to an invisible underlying cause.
The elusive category of invisible causes of SSS comprises subjective and objective irritation. In both of these cases defined by Maibach, no signs are present or can be elicited on the skin. In objective irritation the cause is presumed subclinical inflammation due to occult dermatopathology. In subjective irritation the mechanism is unknown and this diagnosis likely bundles more than one pathological process in it. Interestingly (and clinically frustratingly), Maibach considers subjective irritation to be the most common cause of CIS.[1
Finally, body dysmorphic disorder (BDD) should always be considered by the dermatologist when assessing skin complaints without objective findings. A recent cross-sectional study found a prevalence of 14% among patients in a cosmetic dermatology clinic.[35
] In the context of SSS, dermatologists should be aware that facial irritation complaints without any findings on exam are a common presentation in the dysmorphic patients and therefore extra caution is warranted. Referral to a mental health professional is indicated since these patients are at risk of suicidal behavior.[36
] Maibach notes that patients suspected of having BDD often require a detailed diagnostic process in order to build the trust needed to safely refer them to the mental health professional.[1
] summarizes the steps in the evaluation of a patient suspected to have SSS.
Systematic evaluation of sensitive skin syndrome