Vitiligo
Updated On: July 22, 2026
Anesthesia Implications
The skin needs no special handling - Vitiligo is a pigment defect, not a barrier defect. Tape, adhesive electrodes, NIBP cuffs, and routine positioning are all fine. Don't build a plan around the white patches.
Thyroid disease is the common companion - Thyroid abnormality is the most frequent autoimmune association. Check TSH and free T4; in a euthyroid patient with other autoimmune disease, anti-thyroglobulin and thyroid microsomal antibodies identify who is heading there.
Rule out adrenal insufficiency when other autoimmune disease is present - Vitiligo appears in 33% of polyglandular autoimmune syndrome type I and is a listed feature of type II alongside Addison disease, autoimmune thyroid disease, and type 1 diabetes. The diagnosis is a morning serum cortisol below 6.0 mcg/dL, or a cortisol below 18 mcg/dL 60 minutes after 250 mcg IV or IM cosyntropin.
Surgery is a documented trigger of adrenal crisis - If adrenal insufficiency is in the picture, expect hypotension, hyponatremia, hyperkalemia, and hypoglycemia under surgical stress. Treat with hydrocortisone 100 mg IV bolus followed by 50 to 100 mg IV every 6 hours over 24 hours; that dose carries enough mineralocorticoid activity that fludrocortisone is not needed acutely.
Check for pernicious anemia - Vitiligo occurs in 2% to 8% of pernicious anemia patients. Look at the CBC for macrocytosis — an MCV above 100 fL, with above 115 fL more specific for B12 deficiency — and hypersegmented neutrophils on smear before you attribute fatigue to anything else.
Ask what they are taking for it - Treatment runs from topical corticosteroids and calcineurin inhibitors through phototherapy to systemic corticosteroids in segmental disease, plus emerging JAK inhibitors including topical ruxolitinib. Prolonged topical steroid use causes skin atrophy; systemic steroid courses raise the question of perioperative coverage.
Trauma seeds new lesions - The Koebner phenomenon means new depigmented patches can appear at sites of cut, burn, or abrasion — including the surgical incision. It changes nothing about the anesthetic, but it is worth a word at consent for a patient who is already distressed by their appearance.
Pathophysiology
Vitiligo is an acquired depigmenting disorder — immune-mediated destruction of epidermal melanocytes producing well-demarcated milk-white macules and patches, most often on the hands, forearms, feet, and in a periocular or perioral distribution. Prevalence is about 0.1% to 2%, with peak onset in the second and third decades and no racial predilection. Biopsy shows complete loss of melanocytes with a perivascular and perifollicular CD4+ and CD8+ lymphocytic infiltrate at lesion margins.
The depigmentation itself does not change the anesthetic. What changes it is the company vitiligo keeps: it clusters with other autoimmune disease — thyroid disorder most commonly — and is a recognized feature of both polyglandular autoimmune syndromes, where primary adrenal insufficiency, type 1 diabetes, and pernicious anemia also live.