【压疮感染的特征】。

Q4 Medicine Acta Medica Croatica Pub Date : 2016-01-01
N Kučišec-Tepeš
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An open lesion without\nprotective barrier becomes contaminated immediately, and, shortly afterwards, colonized by physiological microflora of the\nhost and microbes from the environment. In the absence of preventive measures, the wound becomes critically colonized\nand infected. The characteristic of chronic wound/pressure ulcer is that it is colonized, and the infection develops depending\non various factors in 5% to 80% of cases. The ability of microbes to cause infection depends on a number of factors,\nwhich include the pathogen and the host. The number and quantity of virulent factors, microbes, determines the virulence\ncoefficient, which is responsible for overcoming the host’s immune system and development of infection. In the development\nof pressure ulcer infection, two essential microbial factors predominate, i.e. the presence of adhesin and association with\nbiofilm. 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引用次数: 0

摘要

压疮是皮肤和/或邻近组织的局部损伤,通常在骨突出部位以上。它是压力与剪应力、摩擦和湿度共同作用的结果。至于长寿和延迟愈合,这是一个慢性伤口。压疮是微栓塞、缺血和肌坏死共同作用的结果。这些病理生理过程为微生物(主要是细菌)的增殖和感染的发生提供了理想的培养基。压疮的发展是一个动态的过程,表现为不同阶段,每个阶段都有其自身的生理解剖特点和微生物状态。没有保护屏障的开放性病变立即被污染,并在不久之后被宿主的生理微生物群和环境中的微生物定植。在没有预防措施的情况下,伤口就会严重定植和感染。慢性伤口/压疮的特点是具有定植性,5% ~ 80%的病例感染的发展取决于各种因素。微生物引起感染的能力取决于许多因素,其中包括病原体和宿主。毒力因子和微生物的数量和数量决定了毒力系数,它负责克服宿主的免疫系统和感染的发展。在压疮感染的发展过程中,两个重要的微生物因素占主导地位,即黏附素的存在和与生物膜的关联。因此,压疮感染作为一种慢性伤口,其特点是微生物的多菌性和异质性,90%的病例中生物膜表型是主要致病因素,物种表型高变异性,病原体对所有类型的杀菌剂具有耐药性或耐受性。最重要的毒力因素是生物膜。它是一个由群体感应分子管理的结构清晰的微生物群落。正是通过它们,物种之间的交流得以发生,表型和毒力发生变化,并在基因组水平上产生耐药性。生物膜的形成分几个阶段进行,其速度以小时为单位。生物膜中的微生物受到保护,不受宿主免疫系统的作用,同样,它们对抗生素、防腐剂和压力具有耐受性或耐药性。引起压疮感染的细菌具有机会性,但也主要是致病性的。种类的优势和组合取决于压疮的持续时间、部位和分期。主要病原为金黄色葡萄球菌、化脓性链球菌、铜绿假单胞菌和胃链球菌,目前以多重耐药菌株为主,如MRSA、不动杆菌等。慢性伤口,如压疮,是理想的感染发展,特别是如果没有采取有针对性的预防措施。感染的诊断是复杂的,它基于原发性和继发性临床症状、伤口组织、伤口环境状况、炎症标志物和目标样本的微生物学检查结果——活检,这是金标准。在诊断感染时,区分严重定植和深部组织感染是至关重要的,这是基于nerds - stones的临床标准。压疮感染的发生率为5% ~ 80%,90%的病例存在生物膜。掌握压疮的流行病学及感染等并发症的随访是了解慢性创面、努力改进必要护理、预防、制定和应用联合治疗策略的基础。
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[CHARACTERISTIC FEATURES OF PRESSURE ULCER INFECTION].

Pressure ulcer is a localized injury of the skin and/or adjacent tissue, usually above bone protrusions. It is a result of pressure or pressure combined with shear stress, friction and humidity. With regard to long life and delayed healing, it is a chronic wound. Pressure ulcer appears as a consequence of a combination of micro-embolism, ischemia and myonecrosis. These pathophysiological processes provide an ideal medium for proliferation of microorganisms, predominantly bacteria, and development of infection. Progression in the development of pressure ulcer is a dynamic process manifesting in phases, each of which is characterized by its own physiological-anatomical peculiarities and microbiological status. An open lesion without protective barrier becomes contaminated immediately, and, shortly afterwards, colonized by physiological microflora of the host and microbes from the environment. In the absence of preventive measures, the wound becomes critically colonized and infected. The characteristic of chronic wound/pressure ulcer is that it is colonized, and the infection develops depending on various factors in 5% to 80% of cases. The ability of microbes to cause infection depends on a number of factors, which include the pathogen and the host. The number and quantity of virulent factors, microbes, determines the virulence coefficient, which is responsible for overcoming the host’s immune system and development of infection. In the development of pressure ulcer infection, two essential microbial factors predominate, i.e. the presence of adhesin and association with biofilm. Thus, pressure ulcer infection as a chronic wound is characterized by a polymicrobial and heterogeneous population of microbes, domination of biofilm phenotype as a primary factor of virulence present in 90% of cases, phenotype hypervariability of species, and resistance or tolerance of the etiological agents to all types of biocides. The most significant virulence factor is biofilm. It is a corporative community of microbes with a clear architecture managed by quorum sensing molecules. It is through them that the communication between species takes place, the phenotype and virulence change, and resistance develops at the level of genome. The formation of biofilm takes place in several stages, and the speed is measured in hours. Microorganisms in the biofilm are protected from the action of the host’s immune system and, likewise, they are tolerant or resistant to antibiotics, antiseptics, and stress. Bacteria causing pressure ulcer infection are characterized as opportunistic, but also primarily pathogenic. The dominance and combination of species depend on the duration, localization and stage of pressure ulcer. The predominant etiological agents are Staphylococcus aureus, Streptococcus pyogenes, Pseudomonas aeruginosa and Peptostreptococcus spp. Nowadays, multiple-resistant strains predominate, such as MRSA, Acinetobacter spp. and Pseudomonas spp. A chronic wound such as pressure ulcer is ideal for the development of infection, especially if targeted preventive measures are not applied. The diagnosis of infection is complex and is based on the combination of primary and secondary clinical symptoms, tissue in the wound, status of the wound environment, inflammation markers, and results of microbiological examination of targeted samples – biopsies, which are the gold standard. In reaching the diagnosis of infection, it is crucial to differentiate critical colonization from deep tissue infection, which is based on clinical criteria called NERDS-STONEES. The frequency of pressure ulcer infection is 5% to 80%, and biofilm is present in 90% of cases. Due knowledge of the epidemiology of pressure ulcer and follow up of complications such as infection make the basis for the understanding of chronic wound, efforts to improve necessary care, prevention of development and application of a combination of treatment strategies.

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Acta Medica Croatica
Acta Medica Croatica Medicine-Medicine (all)
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期刊介绍: ACTA MEDICA CROATICA publishes original contributions to medical sciences, that have not been previously published. All manuscripts should be written in English.
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