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Background: Skin inflammation causes vasodilation and increased vascular permeability, which may result in decreased blood pressure and peripheral edema. Patients with erythroderma usually compensate for low blood pressure with fluid retention and increased cardiac output. However, if the heart cannot support increased cardiac output, blood pressure will stay low, resulting in severe compensatory fluid retention, which leads to decompensated congestive heart failure, and pulmonary edema. Treatment for high-output congestive heart failure focuses on the primary pathology, which is skin inflammation. However, aggressive treatment of the inflammation with glucocorticoids may result in rapid resorption of extravascular fluid into the intravascular space and occurrence or aggravation of pulmonary edema. Erythrodermic patients with no clinical heart failure are also at risk for developing pulmonary edema if they receive glucocorticoids and/or intravascular fluids. Most hospitalists and dermatologists are not familiar with fluid administration and ways to manage cardiovascular function and blood pressure in patients with skin inflammation. Objectives and methods: In this article, we discuss the pathophysiology of vascular and fluid changes in the context of diffuse skin inflammation and provide some basic guidelines that can be presented to hospitalists by dermatologists. Limitations: Most of the recommendations and guidelines in the article are based on basic science and on the personal experience of the authors and are not supported by controlled trials. Diffuse skin inflammation causes major changes in the cardiovascular system and in the perfusion of internal organs. We provide guidelines for management of fluid status and cardiovascular function in patients with diffuse skin inflammation. Dermatologists can provide hospitalists or primary care providers with these guidelines to help them with creating better treatment plans. [ABSTRACT FROM AUTHOR]