Indocyanine green angiography or laser Doppler imaging can be used to reveal the underlying swollen choroidal vessels under the retinal pigment epithelium and assess the health of the retina in the affected area which can be useful in making a treatment decision. Treatment
Any ongoing corticosteroid treatment should be tapered and stopped, where possible. It is important to check current medication, including nasal sprays and creams, for ingredients of corticosteroids, if found seek advice from a medical practitioner for an alternative. Most eyes with CSR undergo spontaneous resorption of subretinal fluid within 3–4 months. Recovery of visual acuity usually follows. Treatment should be considered if resorption does not occur within 3–4 months, spontaneously or as the result of counselling. The available evidence suggests that half-dose (or half-fluence) photodynamic therapy is the treatment of choice for CSR with subretinalfluid for longer than 3–4 months.Due to the natural disease course of CSR - in which spontaneous resolution of subretinal fluid may occur - retrospective studies may erroneously report positive treatment outcomes and should, therefore, be evaluated with caution. Laser treatments
Full-dose photodynamic therapy (PDT) with verteporfin was first described in CSR in 2003. Later, reduced-settings PDT (half-dose, half-fluence, and half-time) was found to have the same efficacy and a lower chance of complications. Follow-up studies have confirmed the treatments long-term effectiveness including its effectiveness for the chronic variant of the disease. In the PLACE trial, half-dose photodynamic therapy was found to be superior compared to high-density subthreshold micropulse laser, both with regard to anatomical and functional outcomes.
Smokers melanosis is seen with the naked eye as a brown to black pigmentation of the oral tissue i.e. the gums, cheeks or palate  as well as in larynx. It is most often seen in the lower labial gingiva of tobacco users. Most easily it is found in Caucasians, due to their lack of a genetically caused melanin pigmentation.The brown to black colour is melanin. In skin, melanin prevents harmful UV-light from reaching deeper, sensible parts of the tissue. If UV-light penetrates deep, some of the toxic substances due to the UV-light damage to the cells, are bound to melanin in the epithelial cells and travel with the ageing cells to the skin surface, where they are expelled from the tissue surface. In this way the melanocytes and keratinocytes together protect the tissue, with melanin serving as a toxic defence and cleaning agent. In the oral mucosa, where the ageing epithelial cells move faster to the surface compared to skin, a similar defence-mechanism seems to be present, cleaning the mucosa from different toxic chemicals penetrating the epithelium. Besides chemicals in tobacco  also antimalaria-drugs cause an oral pigmentation. Smokers melanosis is like the genetic melanin pigmentations, a defence-system in action. The microscope shows smokers melanosis to be characterized by a melanin hyperpigmentation of the lower part of the oral epithelium, similar to sun-tanned skin. The hyperpigmentation consists of melanin granules which have the shape and colour of "coffea beans".