Prospective Comparison of the Effect on Antiadhesive Barriers During Thyroid Surgery

The postsurgical adhesions remain a significant cause of morbidity for a large number of patients in thyroid and parathyroid surgeries, despite use of meticulous surgical techniques and regardless of surgical access via conventional open or endoscopy. Such adhesions represent not only adhesion reformation at sites of adhesiolysis, but also de novo adhesion formation at sites of surgical procedures. A number of products, in the form of film or fluid, are used to prevent postoperative adhesion formation. These products normally serve as barriers to separate the contact of the damaged tissue surfaces in many animal models and some clinical practices. However, there are few evidences for surgeons to use or no use, or choose the suitable products in their clinical practice in neck surgeries. Improved understanding of the pathophysiology of adhesion development and distinguishing variations in the molecular biologic mechanisms represent future opportunities to improve the reduction of postoperative adhesions.

After surgical tissue injury, there were local release of histamine, cytokines, and growth factors that lead to adhesion development . Local tissue inflammation processes initiate capillary leakage of serosanguineous fluid including clotting factors, and recruitment of macrophages and other cells, including fibroblasts. Cutting, fulguration, ligation of the macrovasculature and microvasculature leads to a state of tissue hypoxemia. Along with the accumulation of metabolic byproducts such as lactic acid, the lowering the pH of the injured tissue, and the conversion from aerobic to anaerobic metabolism within the injured tissues. Tissue hypoxia also results in creation of oxidative stress, with production of oxygen and nitrogen free radicals, which can result in DNA mutations, alterations of mitochondrial DNA, and generation of oxidized proteins.

Subsequently induce lipid peroxidation and protein nitration. The known factors involved in the inflammatory-like response that lead to adhesion development, are type 1 collagen, transforming growth factor b1 (TGF-b1), tumor necrosis factor a (TNF-a), interleukin 6 (IL-6), and vascular endothelial growth factor (VEGF). Of note, the scavenging of free radicals such as superoxide by superoxide dismutase can prevent the development of the adhesion phenotype . Other processes affected include plasminogen activator activity (PAA) (a function of tissue plasminogen activator and its inhibitor, plasminogen activator inhibitor-1), metalloproteinase activity, and extracellular matrix deposition (such as collagen 1, collagen 3, and fibronectin). There is also initiation of processes leading to angiogenesis, which can lead to new vessel formation that could resupply oxygen to these tissues as well as remove metabolic byproducts.