Yoshida Shuhei, Koshima Isao, Hamada Yuichi, Sasaki Ayano, Fujioka Yumio, Nagamatsu Shogo, Yokota Kazunori, Harima Mitsunobu, Yamashita Shuji
The International Center for Lymphedema, Hiroshima University Hospital, Hiroshima, Japan.
Plastic and Reconstructive Surgery, Japanese Red Cross Fukuoka Hospital, Fukuoka, Japan.
Adv Wound Care (New Rochelle). 2019 Jun 1;8(6):263-269. doi: 10.1089/wound.2018.0871. Epub 2019 Jun 6.
Delayed wound healing in lymphedema is assumed to be caused by two reasons, pathophysiological and immunological effects of lymphedema. The aim of this review is to establish how impaired lymphatics alter wound healing pathophysiologically and immunologically, and to propose treatment modalities that can promote wound healing in lymphedema. Lymphaticovenular anastomoses (lymphovenous anastomoses [LVAs]) were performed on patients who had recurrent cellulitis several times with lymphorrhea and developed severe ulcers that were refractory to skin grafts, flaps, and conservative therapy. The lymphorrhea and the ulcer had healed by 4 weeks. Moreover, the lymphedema improved without compression therapy. Lymphedema is characterized pathophysiologically by localized peripheral edema that compresses the microvasculature and lymphatic vasculature and impairs tissue remodeling. Another suspected mechanism is an imbalance in the differentiation of participating immune cells. Profound suppression of T helper (Th)1 cells is likely to increase the risk of infection, and excessive differentiation of Th2 cells, including M2 macrophage polarization, may promote fibrosis, which disrupts the carefully orchestrated wound healing process. Although negative-pressure wound therapy is useful for the treatment of delayed wound healing in lymphedema, LVAs may be necessary to treat the fundamental problem of lymphedema. LVAs are considered to create a bypass to the lymph nodes through which dendritic cells (DCs) can transmit antigen information to T cells. LVAs are considered to neutralize chronic inflammation by allowing more DCs to return into the circulation, thereby improving wound healing.
淋巴水肿中伤口愈合延迟被认为是由两个原因导致的，即淋巴水肿的病理生理效应和免疫效应。本综述的目的是确定受损的淋巴管如何在病理生理和免疫方面改变伤口愈合，并提出能够促进淋巴水肿中伤口愈合的治疗方式。对多次复发性蜂窝织炎伴淋巴漏且出现严重溃疡（对皮肤移植、皮瓣移植和保守治疗均无效）的患者进行了淋巴管静脉吻合术（淋巴静脉吻合术[LVAs]）。淋巴漏和溃疡在4周内愈合。此外，淋巴水肿在未进行压迫治疗的情况下有所改善。淋巴水肿在病理生理上的特征是局部外周水肿，它会压迫微血管和淋巴管并损害组织重塑。另一种可疑机制是参与免疫的细胞分化失衡。辅助性T（Th）1细胞的深度抑制可能会增加感染风险，而Th2细胞的过度分化，包括M2巨噬细胞极化，可能会促进纤维化，从而破坏精心编排的伤口愈合过程。尽管负压伤口疗法对治疗淋巴水肿中的伤口愈合延迟有用，但LVAs可能是治疗淋巴水肿根本问题所必需的。LVAs被认为可建立一条通向淋巴结的旁路，通过该旁路树突状细胞（DCs）可以将抗原信息传递给T细胞。LVAs被认为可通过使更多DCs返回循环来中和慢性炎症，从而改善伤口愈合。
