Comparative evaluation of the intensity of reparative processes in the lower extremity soft tissues of diabetic patients receiving local negative pressure wound treatment and standard wound care

Abstract

Aim. To study the intensity of soft tissue repair in patients with diabetic foot syndrome (DFS) during local negative pressure wound treatment versus standard wound care. Subjects and methods. The investigators estimated the clinical (wound sizes, local tissue oxygenation), histological (light microscopy), and immunohistochemical (CD31, CD68, MMP-9, and TIMP-1) markers for reparative processes in patients with DFS during vacuum therapy versus standard wound care. Forty-two patients with the neuropathic and neuroischemic (without critical ischemia) forms of DFS were examined after debridement. In the perioperative period, 21 patients received negative pressure wound therapy and 21 had standard wound care. Results. During vacuum therapy, the area and depth of wound defects decreased by 19.8±7.8 and 42.8±5.6%, respectively (p=0.002) (as compared to the baseline data). In the control group, these indicators were 17.0±19.4 and 16.6±21.6% (p=0.002). There was a significant intensification of local microhemodynamics according to transcutaneous oximetry readings in the negative pressure wound treatment group. After 9±2 days of treatment, histological examination of granulation tissue revealed a significant reduction in edema, cessation of inflammatory infiltration, and formation of mature granulation tissue in Group 1. Immunohistological examination indicated a more obvious increase in the count of macrophages (CD68 staining) and a significant increment in the number of newly formed vessels, as evidenced by anti-CD31 antibody staining. During the treatment, there was a decline of the expression of MMP-9 and an increase in that of TIMP-1, as compared to those in the control group. Conclusion. The findings are indicative of the enhanced intensity of reparative processes in patients with DFS during vacuum therapy versus standard wound care, resulting in more rapidly decreased wound sizes, increased local microhemodynamics, reduced inflammation, and accelerated wound transition from the inflammatory to the proliferative phase.

References

  1. Атлас диабета IDF. Седьмое издание, 2015.
  2. IWGDF Guidance on the diabetic foot 2015. International Working Group on the Diabetic Foot, Netherlands. 2015.
  3. Оболенский В.Н., Никитин В.Г., Семенистый А.Ю. Использование принципа локального отрицательного давления в лечении ран и раневой инфекции. Новые технологии и стандартизация в лечении осложненных ран. М.; 2011.
  4. MuhammedY. Hasan, Rachel Teo, Aziz Nather. Negative pressure wound therapy for management of diabetic foot wounds: A review if the mechanism of action, clinical applications, and recent developments. Diabetic Foot & Ankle. 2015;6:27618. doi: 10.3402/dfa.v6.27618
  5. Morykwas MJ, Argenda LC. Vacuum-assisted closure: a new method for wound control and treatment: clinical experience. Ann Plast Surg. 1997;38(6):563-576. doi: 10.1097/00000637-199706000-00001
  6. Алгоритмы специализированной медицинской помощи больным сахарным диабетом 7-й выпуск под редакцией И.И. Дедова, М.В. Шестаковой. М.: ФГБУ Эндокринологический научный центр; 2015.
  7. Stansby G, Wealleans V, Wilson L, Morrow D. Clinical experience of a new NWPT system in diabetic foot ulcers and post-amputation wound. J Wound Care. 2010;19(11):499-503. doi: 10.12968/jowc.2010.19.11.79706
  8. Lavery L, Murdoch D, Kim P, Fontaine J, Thakral G, Davis K. Negative Pressure Wound Therapy With Low Pressure and Gauze Dressings to Treat Diabetic Foot Wounds. J Diabet Sciе Technol. 2014;8(2):346-349. doi: 10.1177/1932296813519012
  9. Blakytny R, Jude EB, Gibson JM, Boulton AJM, Ferguson MWJ. Lack of insulin-like growth factor I (IGF I) in the basal keratinocyte layer of diabetic skin and diabetic foot ulcers. J Pathol. 2000;190:589-594. doi: 10.1002/(sici)1096-9896(200004)190:5<589::aid-path553>3.0.co;2-t
  10. Blakytny R, Jude E. The molecular biology of chronic wounds and delayed healing in diabetes. Diabet Med. 2006;23:594-608. doi: 10.1111/j.1464-5491.2006.01773.x
  11. Basseto F, Lancerotto L, Salmaso R, Pandis L, Pajardi G, Schiavond M, Tiengo C, Vindigni V. Histological evolution of chronic wounds under negative pressure. J Plastic, Reconstructive, Aesthetic Surg. 2012;65:91-99. doi: 10.1016/j.bjps.2011.08.016
  12. Liu Y, Min D, et al. Increased matrix metalloproteinase-9 predicts poor wound healing in diabetic foot ulcers. Diabetes Care. 2009;32(1):117-119. doi: 10.2337/dc09-0770
  13. Muller M, Trocme C et al. Matrix metalloproteinases and diabetic foot ulcers: The ratio of MMP-1 to TIMP-1 is a predictor of wound healing. DiabetMed. 2008;25(4):419-426. doi: 10.1111/j.1464-5491.2008.02414.x

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