Preoperative Risk Factors and Complication Rates of Thighplasty: Analysis of 1,493 Patients

The aim was to clarify how smoking and nicotine affects wound healing processes and to establish if smoking cessation and nicotine replacement therapy reverse the mechanisms involved. Smoking is a recognized risk factor for healing complications after surgery, but the pathophysiological mechanisms remain largely unknown. Pathophysiological studies addressing smoking and wound healing were identified through electronic databases (PubMed, EMBASE) and by hand-search of articles' bibliography. Of the 1460 citations identified, 325 articles were retained following title and abstract reviews. In total, 177 articles were included and systematically reviewed. Smoking decreases tissue oxygenation and aerobe metabolism temporarily. The inflammatory healing response is attenuated by a reduced inflammatory cell chemotactic responsiveness, migratory function, and oxidative bactericidal mechanisms. In addition, the release of proteolytic enzymes and inhibitors is imbalanced. The proliferative response is impaired by a reduced fibroblast migration and proliferation in addition to a downregulated collagen synthesis and deposition. Smoking cessation restores tissue oxygenation and metabolism rapidly. Inflammatory cell response is reversed in part within 4 weeks, whereas the proliferative response remains impaired. Nicotine does not affect tissue microenvironment, but appears to impair inflammation and stimulate proliferation. Smoking has a transient effect on the tissue microenvironment and a prolonged effect on inflammatory and reparative cell functions leading to delayed healing and complications. Smoking cessation restores the tissue microenvironment rapidly and the inflammatory cellular functions within 4 weeks, but the proliferative response remain impaired. Nicotine and nicotine replacement drugs seem to attenuate inflammation and enhance proliferation but the effect appears to be marginal.

The metabolic syndrome affects more than a third of the US population, predisposing to the development of type 2 diabetes and cardiovascular disease. The 2009 consensus statement from the International Diabetes Federation, American Heart Association, World Heart Federation, International Atherosclerosis Society, International Association for the Study of Obesity, and the National Heart, Lung, and Blood Institute defines the metabolic syndrome as 3 of the following elements: abdominal obesity, elevated blood pressure, elevated triglycerides, low high-density lipoprotein cholesterol, and hyperglycemia. Many factors contribute to this syndrome, including decreased physical activity, genetic predisposition, chronic inflammation, free fatty acids, and mitochondrial dysfunction. Insulin resistance appears to be the common link between these elements, obesity and the metabolic syndrome. In normal circumstances, insulin stimulates glucose uptake into skeletal muscle, inhibits hepatic gluconeogenesis, and decreases adipose-tissue lipolysis and hepatic production of very-low-density lipoproteins. Insulin signaling in the brain decreases appetite and prevents glucose production by the liver through neuronal signals from the hypothalamus. Insulin resistance, in contrast, leads to the release of free fatty acids from adipose tissue, increased hepatic production of very-low-density lipoproteins and decreased high-density lipoproteins. Increased production of free fatty acids, inflammatory cytokines, and adipokines and mitochondrial dysfunction contribute to impaired insulin signaling, decreased skeletal muscle glucose uptake, increased hepatic gluconeogenesis, and β cell dysfunction, leading to hyperglycemia. In addition, insulin resistance leads to the development of hypertension by impairing vasodilation induced by nitric oxide. In this review, we discuss normal insulin signaling and the mechanisms by which insulin resistance contributes to the development of the metabolic syndrome.

The authors evaluated the use of national databases to track surgical complications among abdominoplasty and breast augmentation patients. Their study population included all patients with abdominoplasty or breast augmentation in the Tracking Operations and Outcomes for Plastic Surgeons (TOPS) and CosmetAssure databases from 2003 to 2007. They evaluated the incidence of hematoma, infection, and/or deep venous thrombosis/pulmonary embolism. Chi-square and t tests were used for the analyses. The TOPS and CosmetAssure databases included 7310 and 3350 patients with abdominoplasty and 30,831 and 14,227 patients with breast augmentation, respectively. In the TOPS and CosmetAssure populations, the complication rates for abdominoplasty were 0.9 percent and 0.5 percent with hematoma (p = 0.29), 3.5 percent and 0.7 percent with infection (p < 0.001), and 0.3 percent and 0.1 percent with deep venous thrombosis/pulmonary embolism (p = 0.05), respectively. The complication rates for breast augmentation in TOPS and CosmetAssure were 0.6 percent and 0.7 percent with hematoma (p = 0.21), 0.3 percent and 0.1 percent with infection (p < 0.001), and 0.02 percent and less than 0.01 percent with deep venous thrombosis/pulmonary embolism (p = 0.31), respectively. Complication rates for abdominoplasty and breast augmentation were similar in TOPS and CosmetAssure, providing a measure of cross-validation. The low complication rates support the safety of these procedures when they are performed by plastic surgeons. These data should be used by individual practitioners for outcomes benchmarking.