Wash your clothing and then wash your hands after handling the dirty clothes.A second line of defense is to avoid sunlight, so as not to activate a phototoxic substance:

If you come in contact with a phototoxic substance, immediately wash the affected area with soap and cold water, and avoid any further exposure to sunlight for at least 48 hours. Heat and moisture can worsen the skin reaction, which is why it’s important to wash the affected area with soap and cold water. Stay indoors, if possible. Be sure to avoid light shining through windows. If staying indoors is not an option, cover the affected area with sun protective clothing. In lieu of sun-protective clothing, apply sunscreen to the affected areas after washing.Phytophotodermatitis is triggered by long wavelength ultraviolet light (called UVA) in the range of 320–380 nanometers, so the best sun-protective clothing and sunscreen products will block these wavelengths of UVA radiation. In 2011, the U.S. Food and Drug Administration (FDA) established a "broad spectrum" test for determining a sunscreen products UVA protection. Sunscreen products that pass the test are allowed to be labeled as "Broad Spectrum" sunscreens, which protect against both UVA and UVB rays. There is no equivalent test or FDA-approved labeling for sun-protective clothing. Some clothing is labeled with an Ultraviolet Protection Factor (UPF) but test results from Consumer Reports suggest that UPF is an unreliable indicator of UV protection. Treatment
Many different topical and oral medications may be used to treat the inflammatory reaction of phytophotodermatitis.
White blood cells may also bind to the endothelium of small capillaries, obstructing them and leading to more ischemia.Reperfusion injury plays a major part in the biochemistry of hypoxic brain injury in stroke. Similar failure processes are involved in brain failure following reversal of cardiac arrest; control of these processes is the subject of ongoing research. Repeated bouts of ischemia and reperfusion injury also are thought to be a factor leading to the formation and failure to heal of chronic wounds such as pressure sores and diabetic foot ulcer. Continuous pressure limits blood supply and causes ischemia, and the inflammation occurs during reperfusion. As this process is repeated, it eventually damages tissue enough to cause a wound.The main reason for the acute phase of ischemia-reperfusion injury  is oxygen deprivation and, therefore, arrest of generation of ATP (cellular energy currency) by mitochondria oxidative phosphorylation. Tissue damage due to the general energy deficit during ischemia is followed by reperfusion (increase of oxygen level) when the injury is enhanced. Mitochondrial complex I is thought to be the most vulnerable enzyme to tissue ischemia/reperfusion but the mechanism of damage is different in different tissues. For example brain ischemia/reperfusion injury is mediated via complex I redox-dependent inactivation. It was found that lack of oxygen leads to conditions in which mitochondrial complex I loses its natural cofactor, flavin mononucleotide (FMN) and become inactive. When oxygen is present the enzyme catalyzes a physiological reaction of NADH oxidation by ubiquinone, supplying electrons downstream of the respiratory chain (complexes III and IV).