Introduction to the ANTI∙DF principle for diabetic foot prevention and treatment

doi:10.12307/2023.483

Abstract

Abstract: BACKGROUND: Diabetic foot has serious mortality and disability rate. Therefore, it is necessary to summarize and understand how to prevent and treat diabetic foot, thereby providing some ideas and directions for the prevention and treatment of diabetic foot.
OBJECTIVE: To summarize the etiology, prevention measures, and treatments of diabetic foot, thus proposing the academic viewpoints of the ANTI∙DF principle to guide the prevention and treatment of diabetic foot.
METHODS: As per the ANTI∙DF principle, we summarized several aspects such as deformity caused by diabetes, foot ulcer caused by deformity, treatment and prevention of diabetic foot. With reference to relevant international and Chinese guidelines and literature, 73 articles were selected from the Chinese and English databases according to the inclusion criteria and were used to summarize the principles of diabetic foot prevention and treatment.
RESULTS AND CONCLUSION: There are 10 factors related to the formation of diabetic foot wounds and refractory wounds: artery, nerve, tissue nonviable, infection or inflammation, muscle, osteoarticular lesion, subcutaneous tissue, tendon, deformity, and foot ulcer. The 10 factors hereinafter will be represented by their initials, which can be summarized as the ANTI∙MOST∙DF principle. Deformity (D) includes the morphological changes of the four anatomical structures – MOST. Therefore, these four factors, MOST, can be simplified and the principle is referred to as the ANTI∙DF principles. Etiologically, among the six factors of the ANTI∙DF principle, deformity (D, including the morphological changes of the four anatomical structures of MOST) is the “real culprit,” and neurological (N) lesions are the “crime culprit.” Arterial (A) ischemia often acts as the “accomplice.” Tissue (T) necrosis, infection (I), and foot ulcers (F) are only “external manifestations.” From the perspective of diabetic foot prevention and treatment, relieving the pressure caused by deformity (D), improving neuroprotection (N) function, and restoring arterial (A) blood supply are the premises for the prevention and treatment of necrotic tissue, infection or inflammation, and foot ulcers (TIF). Debridement of necrotic tissue (T) is the prerequisite for infection (I) control; debridement of necrotic tissue (T) and infection (I) control are the prerequisite for closure of foot ulcers (F). The ANTI∙DF principle is expected to provide clinical practitioners with a basis for the clinical prevention and treatment of diabetic foot, to achieve rapid wound healing and prevent recurrence in patients with diabetic foot.

Key words: diabetic foot, diabetic peripheral neuropathy, diabetic peripheral vascular disease, foot deformities, plantar high pressure, foot ulcer, infection, treatment

CLC Number:

Li Rui, Ou Xiaolan, Liu Jun, Tian Heng, Qu Wenrui, Zhu Zhe, Zhang Zhenyu, Liu Qianqian, Guo Wenlai. Introduction to the ANTI∙DF principle for diabetic foot prevention and treatment[J]. Chinese Journal of Tissue Engineering Research, 2023, 27(14): 2291-2296.

Figures/Tables 4

2 糖尿病引发的相关畸形(D) Diabetes mellitus-related deformities (D) 2.1 MOST形态改变就是畸形(D) 畸形(D)是MOST这4个解剖结构的形态发生改变。糖尿病足的MOST这4个解剖结构本身的形态发生改变，产生畸形(D)。肌肉(M)萎缩、缺损等变化影响肌力平衡，导致局部应力集中；骨关节(O)变化，例如骨折畸形愈合、关节脱位和关节僵硬等，导致局部应力集中；肌腱(T)粘连、挛缩也会导致局部应力集中，皮下组织(S)萎缩或变薄导致应力集中部位易破溃。 2.2 神经(N)病变导致MOST形态改变神经(N)病变导致MOST这4个解剖结构的形态发生改变，产生畸形(D)。神经病变(N)可使足内、外在肌肉(M)萎缩、瘫痪，屈肌和伸肌平衡失调，步态改变[17]；可造成夏科氏(Charcot)骨关节(O)病变[18]；还可造成肌腱(T)、韧带退化；可造成皮肤及皮下组织(S)失神经营养病变变薄、萎缩等。因此导致足形态变化[畸形 (D)][19]，例如爪形趾、锤状趾、跖骨头突出、拇外翻、马蹄内翻足等畸形，导致局部压力增加[5，19-22]。如马蹄足(跟腱挛缩)可造成前足底压力增加，内翻足造成足外侧压力增加，跖骨头突出可造成跖骨头下压力增加。在感觉神经病变的情况下(失去保护性感觉)，在行走的过程中缺乏必要的反馈，导致行走过程中足底压力进一步增加且不被察觉，病变进一步加重[23-25]。植物(自主舒缩性)神经病变可导致皮肤出汗减少，干燥易破裂和形成裂隙[26]。因此，神经病变和机械应力升高共同作用下导致畸形、组织损伤和足部溃疡[27-28]。 2.3 动脉(A)缺血间接导致MOST形态改变动脉(A)缺血也可影响MOST这4个解剖结构的形态，间接导致畸形(D)。例如缺血性肌肉(M)挛缩、骨关节(O)僵硬、皮下组织(S)萎缩及肌腱(T)退化等，导致形态改变，发生畸形(D)[17，29-30]。 2.4 畸形(D)导致足部溃疡(F) 2.4.1 畸形(D)导致局部应力集中足底可分为10个基于解剖学的分区，包括足后跟的内侧、外侧，足中部，第1-5个跖骨，足拇趾，及剩余4个足趾。畸形(D)可导致足底某一分区局部压力压强峰值及累积冲量增加，持续反复的高压导致胼胝体的形成、局部组织(T)破溃坏死，继发感染(I)，产生足部溃疡(F)。 2.4.2 失神经(N)保护感觉神经病变可导致痛觉、温度觉、触觉、振动觉和位置觉的减退或丧失[1]。因此当脚受到过度压力、机械或创伤(刺伤、烫伤和擦伤)等原因导致组织(T)损伤时，在丧失保护性感觉的情况下不易被察觉[3]，导致局部组织(T)进一步破溃坏死、感染(I)，形成足部溃疡(F)[25]，同时自主神经病变后局部血液供应减少[26]，病变进一步加重，发生严重的难治性溃疡。 2.4.3 动脉(A)缺血动脉(A)缺血导致畸形(D)局部应力集中部位更容易发生组织(T)坏死，增加感染(I)机会，产生足部溃疡(F)。而且动脉(A)缺血时，感染(I)更难控制，足部溃疡(F)更难愈合。 2.5 足部溃疡(F)治疗及预防该课题组认为，足部溃疡(F)的预防和治疗顺序为先缓解畸形(D)造成的局部压力，改善神经(N)保护功能，改善动脉(A)供血，然后彻底清创坏死组织(T)、控制感染(I)，最后闭合足部溃疡(F)。缓解畸形(D)造成的压力、改善神经(N)保护性感觉、恢复动脉(A)供血是预防及治疗的前提；清创坏死组织(T)是控制感染(I)的前提；清创坏死组织(T)和控制感染(I)是闭合足部溃疡(F)的前提。控制血糖、降压、降脂、改变生活方式(戒烟、节食、运动)等基础治疗应伴随糖尿病患者的治疗的始终。 2.5.1 缓解畸形(D)造成的局部减压(Off-loading) 外在保护性减压(Off-loading)：起到暂时缓解畸形(D)造成的局部压力的作用，改善神经和血管的功能。主要方式为保守治疗：不行走(拐杖、轮椅或卧床)、减压鞋及鞋垫、毛毡减压垫、减压敷料、石膏、支具等[24，31-36]。适用于轻症，或感染尚未控制，可能造成畸形矫正手术部位感染的患者。减压应始终是预防和治疗计划的一部分[23]。内在结构性减压(Off-loading)：尽管保守治疗可取得一定的减压效果，但畸形依然存在，溃疡会反复复发。然而手术治疗既可有效减压、纠正畸形，还能防止复发，故而有效解压的主要方式为手术治疗。按部位分为足趾、跖骨、中足、后足及踝关节等的畸形矫正术；按组织器官分为MOST这4个解剖结构的畸形矫正术。肌肉(M)可行松解术、延长术及短缩术等；骨关节(O)可行截骨术、关节融合术、植骨术及关节囊及韧带松解或短缩术等[36-38]；皮下组织(S)萎缩或缺损可行皮瓣转移术；肌腱(T)可行延长、短缩、移位或固定术[39]。根据关节柔软型或半僵硬型可采取： (1)足趾畸形矫正：爪形趾、锤状趾及槌状趾等畸形可采用微创趾短屈肌腱切断术及微创趾长短屈肌腱切断术等[40-41]；拇外翻可采取经皮微创Akin术及经皮微创Lapidus术等。 (2)跖骨头突出畸形矫正：可采用经皮微创跖骨远端漂浮截骨术[36]。中后足畸形矫正：包括各跗骨截骨术、融合术、关节囊及韧带松解术、肌腱移位术及肌腱固定术等[36，38]。跟腱挛缩可行腓肠肌松解术或经皮微创跟腱延长术。僵硬型可采取相应关节的融合术。 2.5.2 改善神经(N)保护功能外在保护性减压(Off-loading)：外在保护性减压同样起到暂时弥补失神经保护功能的作用。主要方式为保守治疗：不行走(拐杖、轮椅或卧床)、减压鞋及鞋垫、毛毡减压垫、减压敷料、石膏、支具等。适用于轻症，或感染尚未控制，可能造成神经手术部位感染的患者。神经松解术：药物对糖尿病足的神经病变收效甚微。Dellon神经松解术包括腓总神经、腓深神经和胫神经松解术[42-43]，常会使患者部分恢复神经保护性感觉。 2.5.3 改善动脉(A)供血足背动脉，胫后动脉应该分别评判踝肱指数，并按照缺血程度分为4级。正常：0.8-1.3；轻度0.79-0.6；中度：0.59-0.4；重度：≤0.39[7，44]。以作者经验来看，ABI为中度时创面难以愈合，踝肱指数为重度时截肢可能性大。感染等原因不适合手术时，可暂时使用扩血管药物，前列地尔常有一定效果。手术治疗包括腔内治疗(经皮腔内血管成形术、腔内球囊成形术)、支架植入术、血管旁路重建术、横向骨搬移和骨膜牵张等[45-51]。腔内治疗对于糖尿病足患者而言有一些局限，因为动脉常是长节段钙化、堵塞[52]。横向骨搬移或骨膜牵张术对不愿意接受或不适合其他手术的患者，有一定效果[53]。股动脉或腘动脉旁路(搭桥)手术引血到足部是目前效果最确切最持久的治疗手段。动脉旁路(搭桥)手术不但能够重建足部血供，还能同时为足部游离皮瓣供血[54]。 2.5.4 彻底清创坏死组织(T) 锐性清创：是迅速、彻底清创坏死组织的首选，可采用手术刀剪锐性清创[36，55]。此外，水刀(水动力系统)对去除生物膜很有效[56-57]。其他降解：主要包括物理化学降解(酶)或生物讲解(蛆)，适用于不愿意接受手术或全身状况不适合手术的患者、手术难以达到的深部创面或难以一次达到理想清创的创面等[55，58-59]。 2.5.5 控制感染(I) 全身应用抗生素：早期根据经验用药(可结合当地细菌谱)，药敏试验结果出来后，根据药敏选用敏感药。抗生素骨水泥：局部应用抗生素骨水泥，可迅速控制严重、顽固的深部组织感染[60]。负压创面治疗(Negative pressure wound therapy，NPWT)：常规NPWT或一次性NPWT，可有效控制感染[61-62]。抗生素骨水泥表面覆盖NPWT效果更佳。敷料：浅表组织的较轻感染，且不愿意接受手术或全身状况不适合手术的患者，也可采用具有抗菌成分的敷料[63]。 2.5.6 闭合足部溃疡(F) 自愈：适用于基床良好的浅小创面，可采用敷料、常规NPWT或一次性NPWT等换药方法。其缺点需要良好的基床，愈合缓慢且愈合的皮肤不耐磨、不耐压(常瘢痕愈合)。如果需要4周以上的大创面，就得不偿失了。缝合：适用于可直接缝合或拉拢延展缝合的创面。植皮：适用于基床良好的任意大小的浅创面，愈合迅速(2周内)，NPWT可提高成活率[64-66]。缺点是皮下组织薄时，不耐磨、不耐压[67]。皮瓣：与自愈或植皮等方式相比，皮瓣治疗不需要有肉芽组织覆盖骨和肌腱的良好基床[68-69]，整体基床好坏无所谓，适用范围更广。愈合时间短，2周内可愈合，愈合后耐磨、耐压，且费用低。皮瓣分为带血管蒂皮瓣和游离皮瓣，游离皮瓣的适用性更广。然而糖尿病足患者血管条件通常较差，严重影响皮瓣的存活率。有研究汇总了18篇文献，共528例患者，总结出了糖尿病足采用皮瓣的适应证[70]。 "

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