Case Presentation:

74–year–old man presents with blue–gray discoloration of the face, neck and upper thorax. The patient had a history of esophageal adenocarcinoma, completing definitive chemo radiation in 2006. His presenting complaint was of weight loss and early satiety for which endoscopic evaluation revealed numerous brown pigmented circumscribed lesions. He had noted tarry, brown stool and mentioned that he recently had 2 “moles” biopsied. On further questioning he also admitted to progressive shortness of breath, lightheadedness and intermittent “coffee–colored” urine. Vital signs were remarkable for a blood pressure of 85/47 mmHg with a pulse of 101 bpm and respiratory rate of 20 breaths per minute. He was afebrile with a pulse oximetry reading of 96% on room air. In general he was in mild distress due to shortness of breath with skin examination remarkable for a blue–gray discoloration of his face, neck and upper chest. He had no neck or facial swelling or venous engorgement. Cardiovascular examination revealed a click related to his mechanical mitral valve, otherwise no murmurs or extra sounds. His pulses were within normal limits. On lung examination there was wheezing throughout with decreased breath sounds on the left. He had no abdominal organomegaly or lower extremity edema. White blood cell count was 6.64 k/ul with a hemoglobin of 9.5 g/dl and platelet count of 59 k/ul with rare schistocytes. INR was 6.2 on warfarin therapy with a PTT of 109.7 seconds. Basic metabolic panel was normal with exception of a serum creatinine of 1.9 mg/dl which improved with hydration. Chest x–ray showed left lower lobe airspace disease and a left pleural effusion, consistent with prior findings on a recent CT of the thorax, abdomen, and pelvis which also revealed adenopathy in the chest and two liver lesions. A 2 D Echocardiogram showed a normal ejection fraction with the mechanical mitral valve in good position. Upper extremity dopplers were negative. Biopsies from the prior endoscopy as well as bone marrow examination (performed due to the thrombocytopenia as well as coagulopathy that did not resolve with withholding warfarin therapy) revealed metastatic melanoma. The bone marrow was greater than 40% infiltrated with melanocytes. Thus, it was deduced that the patient’s discoloration was due to melanosis arising from diffusely metastatic melanoma.


Melanosis due to widely metastatic melanoma is an uncommon phenomenon of unclear etiology. It is postulated that elevated serum levels of alpha–melanocyte stimulating hormone, hepatocyte growth factor, and endothelin–1 may cause activation of the pigment system as well as high proliferation of normal and malignant melanocytes. Melanosis in this setting is associated with a very poor prognosis.


The purpose of reporting this case is to have providers expand their differential for cyanosis to include melanosis, especially in suspicious clinical context.