Facial Flushing: What It Is and How It Differs from Rosacea

What is Facial Flushing?

Your cheeks look hot and red in the mirror. Your face heats up the moment you start speaking in front of other people. A spicy meal or a single drink turns you red down to the neck. What people describe when they come in about flushing sits mostly inside that range.

In medical terms, flushing is what happens when the blood vessels close to the skin surface widen for a time, so more blood flows through them and the skin looks red. In a healthy person the reaction is usually temporary. Heat, heightened emotion, exercise, and a range of foods and drinks are common triggers, and the redness disappears once the vessels narrow again.

That is why flushing itself is a symptom, not a disease name. Menopausal hot flushes; medications such as niacin, calcium channel blockers, and PDE-5 inhibitors; thyroid dysfunction; and, less commonly, systemic conditions such as carcinoid syndrome, systemic mastocytosis, and pheochromocytoma all present as a face that turns red. Redness on its own does not narrow the cause.

Some repeated flushing is rosacea. The Korean Dermatological Association describes rosacea as a chronic skin disease of the central face — around the nose and across the cheeks, chin, and forehead — characterised by persistent erythema, papules and pustules, recurrent flushing, and telangiectasia. It is most common in people in their 30s to 50s and occurs more often in women, although severe disease appears mainly in men, and it does not resolve on its own; it relapses and remits.

The reason rosacea is not explained simply as "vessels that dilate easily" lies in its pathophysiology. Increased expression of channels such as TRPV-1 in sensory nerves and keratinocytes makes erythema and flushing easier to provoke, and overexpression of TLR-2 activates innate immunity, raising LL-37 (cathelicidin) and with it mast cell activity. An increase in Demodex folliculorum is also observed in affected skin, though the causal relationship is still not clear. In other words, chronic inflammation is layered on top of a vascular reaction.

The Other's Cause-Specific Treatment Design

Treatment for the redness divides into three lines — the vessels that have already dilated, the inflammation that dilates them, and the lifestyle factors that keep provoking both.

What the vascular laser handles is the first of these. The principle is selective photothermolysis. Oxyhaemoglobin in the blood preferentially absorbs light of particular wavelengths and converts it to heat; that heat is transferred to the vessel wall and causes coagulation and vessel closure. Short pulses at high power are central to this approach, so that heat does not spread into the surrounding tissue. The absorption peaks of oxyhaemoglobin are at 418, 542, and 577 nm, and in clinical practice the 532 nm and 595 nm ranges are the ones mainly used. Shorter wavelengths are absorbed well but do not penetrate deeply, which can be a disadvantage in thicker lesions; 595 nm emerged as a wavelength offering deeper penetration.

In the literature, the pulsed dye laser (PDL) and KTP are both used to treat persistent erythema and telangiectasia. In a prospective controlled study comparing 532 nm KTP with 595 nm PDL (n=45, mean age 51), the reduction in erythema was significant with both devices and the effect was comparable. Pain during treatment, however, was lower with KTP — 2.5 versus 4.1 for PDL on a 10-point scale — and meaningful purpura was observed only in the PDL group. That much is a comparison between devices in the literature. Vascular lasers are used in the treatment of flushing at The Other Dermatology; which device and wavelength are used, and how the detailed settings are chosen, depend on the lesion and are determined at the consultation.

What the laser cannot reach is handled by medication. The literature separates the drugs used for persistent erythema, those used for papules and pustules, and the oral drugs used when inflammatory lesions are numerous. What is used and in what order depends on the phenotype — whether vascular dilatation or papulopustular disease predominates — so it is settled at an in-person examination.

The third line is triggers. In a patient survey by the National Rosacea Society (n=1,066), the factors identified were sun exposure 81%, emotional stress 79%, hot weather 75%, wind 57%, exercise 56%, and alcohol 52%. Because the list differs from person to person, keeping a record of your own triggers for at least two weeks is treated as part of the treatment itself.

Aftercare

Ultraviolet light comes first. Sun exposure was the most frequently identified trigger in the patient survey (n=1,066), at 81%. The literature advises using an inorganic sunscreen containing zinc oxide or titanium dioxide at SPF 30 or above. After a vascular laser the same care is needed again, this time to reduce post-inflammatory hyperpigmentation.

Cleansing and moisturising stay simple, in the direction of less irritation. Use a gentle cleanser, moisturise often, and avoid exfoliants and products containing alcohol. Because damage to the skin barrier is itself counted among the aggravating factors in rosacea, layering on strong products to clear the redness faster works in the opposite direction.

Do not reach for a leftover steroid ointment and apply it to the face when the redness worsens. Topical corticosteroids can cause rebound flares and rosacea-like perioral dermatitis in rosacea, so rather than stopping or continuing them on your own, a tapering plan is set at an examination.

Other conditions that look similar

Not every red face is flushing or rosacea. The differential list in the literature includes acne, demodicosis, seborrhoeic dermatitis, eczema including contact dermatitis, perioral dermatitis, steroid-induced rosacea, dermatomyositis, systemic lupus erythematosus, and drug reactions. Two distinguishing points appear often in the literature — papulopustular rosacea has no comedones, which separates it from true acne, and seborrhoeic dermatitis is separated by whether scale sits on top of the erythema.

Sometimes the cause lies outside the skin. Menopausal hot flushes; medications such as niacin, calcium channel blockers, and PDE-5 inhibitors; thyroid dysfunction; and, less commonly, carcinoid syndrome, systemic mastocytosis, pheochromocytoma, and medullary thyroid carcinoma all present as flushing. If the redness comes with persistent watery diarrhoea, wheezing on breathing, severe headache accompanied by high blood pressure, or hives spreading beyond the face, those are signals that testing beyond the scope of dermatology is needed.

Frequently asked questions

This page is general information about a treatment and is not a diagnosis or a recommendation. The right choice differs by skin condition, so treatment is decided after an in-person examination. Individual results vary.

References

1. 주사(rosacea) Korean Dermatological Association
2. Rosacea DermNet NZ
3. ROSCO panel — phenotype-based diagnosis and treatment recommendations Br J Dermatol 2017;176:431
4. Rosacea StatPearls
5. Global epidemiology and clinical spectrum of rosacea, highlighting skin of color J Am Acad Dermatol 2018
6. Topical corticosteroid-induced rosacea-like dermatitis: a clinical study of 110 cases PubMed
7. Steroid rosacea DermNet NZ
8. Lasers for vascular lesions: standard guidelines of care IJDVL
9. Ocular injury in cosmetic laser treatments of the face J Clin Aesthet Dermatol
10. Underlying etiologies of cutaneous flushing Dermatology Advisor
11. New survey pinpoints leading factors that trigger symptoms National Rosacea Society