Wound chronic

Author: Prof. Dr. med. Peter Altmeyer

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Last updated on: 02.03.2024

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Chronic ulcer; chronic wound

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Polyätiological, chronic substance defect of the skin, which despite causal and appropriate local treatment shows no tendency to heal within 3 months or does not heal spontaneously after 12 months (see skin ulcer below).

General information
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Wound healing itself is highly dependent on the orderly sequence of interactions between the individual biological, biochemical and immunological processes. In chronic wounds, this process is disturbed. Various influences such as pressure, ischaemia or hyperglycaemia lead to permanent irritation of and damage to vascular walls. Adhesion molecules mark these sites and thus enable the attachment of inflammation sites (e.g. neutrophil granulocytes and monocytes). These induce a continuous inflammatory reaction by means of proinflammatory cytokines (e.g. interleukin 1ß (see below interleukins) or TNF alpha). This leads to an overexpression of tissue-degrading proteases (e.g. matrix metalloproteinases) and a simultaneous reduction of protease inhibitors (TIMPs) and growth factors. This leads to wound chronification.

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Various essential indirect or direct triggers are possible for the development of chronic wounds (> 3 months) (see skin ulcer).

Regardless of their genesis, chronic wounds show a largely uniform pathophysiological pattern in their healing process. Tissue hypoxia, neurological disorders (reduced or absent sensory function), infections, malnutrition, disturbed moisture balance, excess of proteases and deficiency of growth factors as well as a dysbalance of macrophage and leukocyte function play a decisive role.

A special etiopathogenetic role is played by neuropathic ulcers, which develop in skin areas where schema sensation and sympathetic skin innervation are disturbed.

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Wound infections are common, especially in immunocompromised patients or in diabetic foot. In addition to Gram-positive staphylococci (see also MRSA) and streptococci, Gram-negative bacteria such as Pseudomonas aeruginosa, Proteus vulgaris, Enterobacter cloacae and anaerobes of the Bacteroides group play an increasing role.

Contact sensitization (type IV sensitization). In a group of patients with chronic venous leg ulcer the following contact sensitizations were observed (status 2015):

External therapy
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  • The aim of phase-oriented local therapy is to return a chronic wound to an active wound with a physiological healing process. The principle of moist wound treatment with the aid of hydroactive wound dressings has proved to be helpful here.
  • The acronym "TIME" was coined for wound treatment, which is a schematic guideline for better understanding of the healing of a chronic wound.
    • T (tissue management): stands for the debridement of necrotic tissue (see wound debridement below)
    • I (inflammation and infection): inflammation and infection control
    • M (moisture balance): balancing and regulating the moisture balance
    • E (epithelial advancement): Promotion of epithelialization.

Notice! In general, it is recommended to treat the wound itself and the wound environment as indifferently as possible to prevent complicated sensitisation (see wound treatment below).

Internal therapy
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Here, the genesis and the findings of the wound, its duration and condition, questionable sensitisations as well as the physical condition of the patient himself must be taken into account (see below wound treatment).

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In naturopathy, bee honey plays an important role in the treatment of wounds. see also under wound treatment. see also cod liver oil.


Last updated on: 02.03.2024