A bruise forms when a physical impact causes tiny blood vessels beneath the skin’s surface to break, allowing blood to leak into the surrounding tissue. This trapped blood causes the familiar reddish-purple mark. The body immediately begins a cleanup process to reabsorb this leaked blood, which creates the bruise’s changing colors. Exposure to ultraviolet (UV) light can significantly prolong and intensify the resulting discoloration, sometimes making it permanent.
The Biology of a Bruise
When capillaries rupture, red blood cells escape the circulatory system and pool in the tissue spaces. The oxygenated hemoglobin within these cells gives the fresh bruise its initial red or purple hue. Within a few minutes, the hemoglobin deoxygenates, which causes the bruise to deepen to a darker, bluish-black color.
Immune cells, specifically macrophages, are mobilized to the injury site to begin metabolizing the cellular debris. They initiate the breakdown of hemoglobin, converting the iron-containing protein into a sequence of pigments over one to two weeks. The first breakdown product is biliverdin, which gives the bruise a greenish tint.
Biliverdin is reduced to bilirubin, which is yellow and contributes to the final fading colors. The iron component of hemoglobin is eventually stored in a protein compound called hemosiderin, a golden-brown pigment. This hemosiderin is the final visible pigment before the bruise is cleared, but its presence creates a vulnerability that UV light exploits.
UV Exposure and Long-Term Discoloration
The main problem with sun exposure while bruising is the interaction between UV radiation and the iron-rich hemosiderin deposits. Hemosiderin staining, which presents as a persistent brownish-yellow patch, is the direct result of this iron pigment settling in the deeper layers of the skin. While hemosiderin is naturally cleared over time, UV light can exacerbate this staining process.
The UV radiation stimulates the skin’s pigment-producing cells, or melanocytes, to increase melanin production, resulting in a tan in the surrounding, uninjured skin. Crucially, the UV exposure intensifies the reaction with the iron-containing hemosiderin within the bruise site. This interaction causes the bruise site to darken significantly more than the surrounding tanned skin, a process known as post-inflammatory hyperpigmentation (PIH).
This darkening is not a normal tan but a phototoxic reaction that can “lock in” the hemosiderin pigment. The resulting hyperpigmented patch can persist for many months or even years after the initial trauma has healed. Sun exposure interferes with the body’s natural process of clearing the iron deposits, turning a temporary bruise into a long-term cosmetic concern.
Practical Steps for Bruise Protection
The most effective way to prevent a bruise from turning into a long-term discoloration is to shield the affected area from all UV radiation. This includes both natural sunlight and artificial sources like tanning beds, as both emit the UV rays that trigger hyperpigmentation. Protection is necessary until the bruise has completely resolved and the skin color has returned to its normal tone.
Physical barriers offer the most immediate and complete protection. Clothing made of tightly woven or dark fabric provides better UV blockage than light, loosely woven materials. For smaller or exposed areas, a simple bandage or a wide, non-transparent adhesive patch can serve as an opaque physical shield against the sun.
Chemical protection should be applied to any bruise that cannot be fully covered by clothing. A broad-spectrum sunscreen with an SPF of at least 30 is recommended, as it filters both UVA and UVB rays. Sunscreen must be applied generously and reapplied every two hours, especially if the area is exposed to water or sweat. Staying in the shade, particularly during peak sun hours, also significantly reduces the total UV dose the bruise receives.