Superficial lymphatic malformation  is a congenital malformation of the superficial lymphatics, presenting as groups of deep-seated, vesicle-like papules resembling frog spawn, at birth or shortly thereafter. Lymphangioma circumscriptum is the most common congenital lymphatic malformation. It is a benign condition and treatment is not required if the person who has it does not have symptoms from it. Signs and symptoms
Lymphangioma circumscriptum is characterized by a rash on the skin featuring clear vesicles. The rash may be painful and is sometimes itchy. The vesicles often leak lymph and may bleed. The rash may appear similar to warts if the vesicles frequently break open. Diagnosis
A biopsy of the affected skin and histological examination under the microscope is necessary to diagnose lymphangioma circumscriptum. Differential diagnosis
Several other conditions may mimic lymphangioma circumscriptum. These conditions include infections such as an outbreak of herpes simplex, herpes simplex vegetans, molluscum contagiosum, verruca vulgaris, and condyloma acuminatum. Similarly, benign and cancerous non-infectious conditions may also present in a similar manner and include conditions such as angiokeratoma, dermatitis herpetiformis, hemangioma, epidermal nevus, lymphangiectasia, melanoma, angiosarcoma, and metastatic carcinomas. Treatment
The condition is benign and does not require treatment if the affected person does not have symptoms. Lymphangioma circumscriptum is often treated when it causes troubling symptoms to the affected person (itching, pain) or due to concerns about its cosmetic appearance. Surgical removal (excision) of the affected layers of skin is the most common and effective treatment.
The VMD2 gene provides instructions for making a protein called bestrophin. Although its exact function is uncertain, this protein likely acts as a channel that controls the movement of negatively charged chlorine atoms (chloride ions) into or out of cells in the retina. Mutations in the VMD2 gene probably lead to the production of an abnormally shaped channel that cannot regulate the flow of chloride. Researchers have not determined how these malfunctioning channels are related to the buildup of lipofuscin in the macula and progressive vision loss. The RDS gene provides instructions for making a protein called peripherin. This protein is essential for the normal function of light-sensing (photoreceptor) cells in the retina. Mutations in the RDS gene disrupt the structures in these cells that contain light-sensing pigments, leading to vision loss. It is unclear why RDS mutations affect only central vision in people with adult-onset vitelliform macular dystrophy. Diagnosis
Vitelliform macular dystrophy causes a fatty yellow pigment (lipofuscin) to build up in cells underlying the macula. The retinal pigment epithelium also degenerates. Over time, the abnormal accumulation of this substance can damage the cells that are critical for clear central vision. As a result, people with this disorder often lose their central vision and may experience blurry or distorted vision, and loss is rarely symmetric. Scotomata appear, first with red light and then for green; finally, relative (or in more serious cases, absolute) scotomata occur with white light. Vitelliform macular dystrophy does not affect side (peripheral) vision or the ability to see at night.