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Войти в исследования Journal of the American Academy of Dermatology · 2019
Acute inflammatory edema: A mimicker of cellulitis in critically ill patients.
СтатьяНазвание и аннотация: Перевод в очереди
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Marchionne Elizabeth M, McCalmont Timothy H, Pincus Laura B, LeBoit Philip E, Fox Lindy P
Аннотация
BACKGROUND: Inpatient dermatology consultations for treatment-refractory or atypical cellulitis are common. In critically ill patients, differentiating cellulitis from its mimickers can be challenging.
OBJECTIVE: We describe acute inflammatory edema, a likely underrecognized variant of pseudocellulitis.
METHODS: We reviewed the charts of 15 patients with this diagnosis, seen by the inpatient dermatology consultation service at the University of California at San Francisco between 2009 and 2017.
RESULTS: The cohort consisted of 9 women and 6 men with an age range of 52-73 years. Acute inflammatory edema presents as bilateral, erythematous, and edematous plaques, most commonly involving the thighs and lower abdomen, sparing areas of increased pressure on the skin. There is a predilection for patients with high body mass index and those with clinical or quantitative findings of fluid overload.
CONCLUSION: We propose a 3-part pathogenesis of acute inflammatory edema: 1) acute-onset volume overload 2) in patients with impaired lymphatic return 3) leads to dermal edema, microtears in connective tissue, and an influx of inflammation.
OBJECTIVE: We describe acute inflammatory edema, a likely underrecognized variant of pseudocellulitis.
METHODS: We reviewed the charts of 15 patients with this diagnosis, seen by the inpatient dermatology consultation service at the University of California at San Francisco between 2009 and 2017.
RESULTS: The cohort consisted of 9 women and 6 men with an age range of 52-73 years. Acute inflammatory edema presents as bilateral, erythematous, and edematous plaques, most commonly involving the thighs and lower abdomen, sparing areas of increased pressure on the skin. There is a predilection for patients with high body mass index and those with clinical or quantitative findings of fluid overload.
CONCLUSION: We propose a 3-part pathogenesis of acute inflammatory edema: 1) acute-onset volume overload 2) in patients with impaired lymphatic return 3) leads to dermal edema, microtears in connective tissue, and an influx of inflammation.