A Anke Stekelenburg

Deep tissue injury: how deep is our understanding?

Deep pressure ulcers, necessarily involving deep tissue injury (DTI), arise in the muscle layers adjacent to bony prominences because of sustained loading. They represent a serious type of pressure ulcer because they start in underlying tissues and are often not visible until they reach an advanced stage, at which time treatment becomes problematic. Underlying mechanisms of DTI require further investigation if appropriate preventive measures are to be determined. The present commentary illustrates a hierarchic research approach selected to study these mechanisms. To differentiate between the individual roles of deformation and ischemia in the onset of skeletal muscle damage, 2 complementary approaches have been selected. In an in vivo animal model, the effects of ischemia combined with deformation and ischemia per se were studied. An in vitro muscle model was used to study the separate effects of deformation and several aspects of ischemia, including hypoxia, glucose depletion, and tissue acidification, in more detail. Based on the results of both models a sequence of events leading to cell necrosis is proposed. Deformation levels exceeding a threshold value can result in rapid tissue damage that may persist, whereas ischemia has a more gradual effect as a result of glucose depletion and tissue acidification.

Compression-induced damage and internal tissue strains are related.

Prolonged mechanical loading of soft tissues adjacent to bony prominences can lead to degeneration of muscle tissue, resulting in a condition termed pressure-related deep tissue injury. This type of deep pressure ulcers can develop into a severe wound, associated with problematic healing and a variable prognosis. Limited knowledge of the underlying damage pathways impedes effective preventive strategies and early detection. Traditionally, pressure-induced ischaemia has been thought to be the main aetiological factor for initiating damage. Recent research, however, proposes tissue deformation per se as another candidate for initiating pressure-induced deep tissue injury. In this study, different strain parameters were evaluated on their suitability as a generic predictive indicator for deep tissue injury. With a combined animal-experimental numerical approach, we show that there is a reproducible monotonic increase in damage with increasing maximum shear strain once a strain threshold has been exceeded. This relationship between maximum shear strain and damage seems to reflect an intrinsic muscle property, as it applied across a considerable number of the experiments. This finding confirms that tissue deformation per se is important in the aetiology of deep tissue injury. Using dedicated finite element modeling, a considerable reduction in the inherent biological variation was obtained, leading to the proposal that muscle deformation can prove a generic predictive indicator of damage.

Effect of Continuous and Intermittent Mechanical Loading on the Development of Skeletal Muscle Damage - A Combined Experimental/Numerical Approach

Prolonged mechanical loading of soft tissues, as present when individuals are bedridden or wheelchair-bound, can lead to degeneration of skeletal muscle tissue. This can result in a condition termed pressure-related deep tissue injury (DTI), a severe kind of pressure ulcer that initiates in deep tissue layers, e.g. skeletal muscle, near bony prominences and progresses towards the skin. Complications associated with DTI include sepsis, renal failure, and myocardial infarction. Damage pathways leading to DTI involve ischemia, ischemia-reperfusion injury, impaired lymphatic drainage, and sustained tissue deformation. Recently, the role of tissue deformation in the onset of skeletal muscle damage was established by combining animal experiments with finite element (FE) modeling [1]. After 2 hours of continuous loading, a clear correlation between maximum shear strain and damage was found.Copyright

Oorzaken van decubitus

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