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Abnormal Vessel Architecture Persists in the Microvasculature of the Massive Weight- Loss Patient
Evan B Katzel, MD, Sameer Shakir, MD, Nataliya Kostereva, PhD, Bernd Lannau, MD, Michael L Gimbel, MD, Vu Nguyen, MD, Carolyn De La Cruz, MD, Kacey Marra, PhD, Jeffrey Gusenoff, MD
University of Pittsburgh Medical Center, Pittsburgh, PA
2015-03-14
Presenter: Evan B. Katzel
Affidavit:
Evan B. Katzel
Director Name: Joseph E Losee
Author Category: Resident Plastic Surgery
Presentation Category: Basic Science Research
Abstract Category: Breast (Aesthetic and Recon.)
Purpose
Studies have demonstrated a link between obesity and increased inflammatory cytokines, leading to changes in the microvasculature of these patients. Massive weight loss (MWL) patients often experience delayed wound healing following body contouring , however no studies exist exploring the inflammatory response of MWL on the microvasculature. This study hypothesizes MWL patients undergoing body contouring maintain persistently elevated inflammatory markers in the microvasculature that delay wound healing.
Methods
Descriptive data were queried from normal weight and MWL patient charts to assess baseline demographics. Superficial Inferior Epigastric Artery (SIEA) vessels were harvested during abdominally based free flap surgery and abdominal contouring surgery for normal weight and MWL patients, respectively. Vessels were histologically assessed using immunohistochemistry (IHC) to quantify anti-interleukin-1 (IL-1), IL-6, and TNFα expression. Trichrome staining was performed to assess vessel architecture between groups. Statistical analyses included independent samples two-tailed t-tests and Fisher's exact test.
Results
All patients (n=23) were female. There were no differences in patient demographics including pre-operative BMI. Quantitative analysis of IL-1, IL-6, and TNFα expression revealed no difference between normal weight and MWL patients. Trichrome staining demonstrated abnormal vessel architecture in the MWL group with decreased collagen composition of the tunica adventitia and disorganized smooth muscle in the tunica media.
Conclusions
These data suggest that previously obese MWL patients maintain abnormal vessel wall architecture despite normal inflammatory expression. These persisting changes may explain continued delayed wound healing after MWL. Further studies are warranted to determine the safety of the use of these vessels in microvascular reconstruction.
