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Deep tissue injury: how deep is our understanding?
Anke Stekelenburg1, Debby Gawlitta, Dan L Bader
1Department of Biomedical Engineering, Eindhoven University of Technology, Eindhoven, The Netherlands. A.Stekelenburg@tue.nl
Deep tissue injury (DTI) mechanisms were explored using animal and cell models. Deformation causes rapid damage, while ischemia, including hypoxia and acidification, leads to gradual cell necrosis, informing prevention strategies.
Area of Science:
- Biomedical Engineering
- Tissue Mechanics
- Cellular Physiology
Background:
- Deep pressure ulcers involve deep tissue injury (DTI) originating in muscle layers near bony prominences due to sustained loading.
- DTI is serious as it starts internally, often undetected until advanced, complicating treatment.
- Understanding DTI mechanisms is crucial for developing effective preventive measures.
Purpose of the Study:
- To investigate the underlying mechanisms of deep tissue injury (DTI) in skeletal muscle.
- To differentiate the roles of mechanical deformation and ischemia in DTI.
- To propose a sequence of events leading to cell necrosis in DTI.
Main Methods:
- Utilized a hierarchical research approach combining in vivo animal models and in vitro muscle models.
- In vivo: Studied effects of combined ischemia and deformation, and ischemia alone.
- In vitro: Examined isolated effects of deformation, hypoxia, glucose depletion, and acidification.
Main Results:
- Deformation exceeding a threshold can cause rapid, persistent tissue damage.
- Ischemia, driven by glucose depletion and acidification, induces damage more gradually.
- A sequence of events leading to skeletal muscle cell necrosis was proposed based on experimental findings.
Conclusions:
- Mechanical deformation and ischemic factors contribute distinctly to DTI.
- The proposed sequence of events provides insight into DTI pathogenesis.
- Findings support the development of targeted preventive strategies for deep pressure ulcers.
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