Advances in Skin & Wound Care:
Richard “Sal” Salcido, MD, EdD, is the Editor-in-Chief of Advances in Skin & Wound Care and the Course Director for the Annual Clinical Symposium on Advances in Skin & Wound Care. He is the William Erdman Professor, Department of Physical Medicine and Rehabilitation; Senior Fellow, Institute on Aging; and Associate, Institute of Medicine and Bioengineering, at the University of Pennsylvania Health System, Philadelphia, Pennsylvania.
This month’s continuing education article (page 133) focuses on an exploratory study of suspected deep tissue injury (DTI). Viewpoints continue to vary on the topic of DTI, and I’d like to offer a brief overview of the DTI concept. The identification of DTI as an entity and its pathophysiologic etiology remain elusive and are more complex than is typically explained or referenced in a given manuscript. The collective parameters that together attempt to explain the phenomenon of DTI or “suspected” DTI are fragments of a complex puzzle, which has missing and inadequate pieces that preclude a full explanation of the evolving definition of the elusive DTI. Some of the etiopathological concepts linked to DTI have been passed on uncritically through less than comprehensive literature reviews, annotated bibliographies, and faulty hypotheses and conclusions.
To be sure, the issue is more complicated than researchers and clinicians appreciate in their presentations and manuscripts. The knowledge gaps in the literature span etiology, pathophysiology, epidemiology, prevention, and recommendations for further research or practice. Although I am sure that DTI exists, I remain inquisitive about the conclusions we draw about this entity from the literature frequently cited or, on the other hand, literature ignored or overlooked.
Unification Needed for Causation Hypothesis
A recent review of the basis for DTI, for example, points to a position paper on the subject from the National Pressure Ulcer Advisory Panel (NPUAP),1 which invokes a hypothesis based on “oxygen-free radicals.” “The reasons for the rapid deterioration seen with DTI may be a combination of direct ischemic and reperfusion injury (IRI) from oxygen-free radicals, cytokines, and neutrophilic adhesion to microvascular endothelium.”1 The NPUAP paper extrapolates the IRI hypothesis from a 1988 paper on free-radical damage mechanisms in other critical organs, such as the liver.2 Research directly related to oxygen–free-radical production in pressure ulcers is not cited or reviewed in the position paper.3–6
A more recent research paper cites apoptosis (accelerated preprogrammed cell death) as a mechanism or co-contributor to DTI in an animal model, confirming previous findings in an animal model research.7 Finally, Smart8 suggests an elimination of the DTI construct in favor of “hypoxic reperfusion ulcer” rather than a DTI. Smart states that the term “DTI lacks specificity and opens the door for potential unfounded litigation”; again, this hypothesis is based on an article extrapolating concepts from “compartment syndrome and peripheral ischemia.”9
From a research perspective, Bader et al10 masterfully cover the biomechanical, clinical, and research gaps in the DTI dilemma. We must challenge each other not to quit, but find ways to collaborate in our enthusiastic quest for unraveling the complexities and the treatment of the DTI concept.
“Years wrinkle the skin, but to give up enthusiasm wrinkles the soul.”—General Douglas MacArthur
Richard “Sal” Salcido, MD, EdD
2. Parks DA, Granger DN. Ischemia-reperfusion injury: a radical view. Hepatology 1988; 8: 680–2.
3. Salcido R, Popescu A, Ahn C. Animal models in pressure ulcer research. J Spinal Cord Med 2007; 30: 107–16.
4. Patel S, Knapp CF, Donofrio JC, Salcido R. Temperature effects on surface pressure-induced changes in rat skin perfusion: implications in pressure ulcer development. J Rehabil Res Dev 1999; 36: 189–201.
5. Herrman EC, Knapp CF, Donofrio JC, Salcido R. Skin perfusion responses to surface pressure-induced ischemia: implication for the developing pressure ulcer. J Rehabil Res Dev 1999; 36: 109–20.
6. Linder-Ganz E, Engelberg S, Scheinowitz M, Gefen A. Pressure-time cell death threshold for albino rat skeletal muscles as related to pressure sore biomechanics. J Biomech 2006; 39: 2725–32.
7. Siu PM, Tam EW, Teng BT, et al. Muscle apoptosis is induced in pressure-induced deep tissue injury. J Appl Physiol 2009; 107: 1266–75.
8. Smart H. Deep tissue injury: what is it really? Adv Skin Wound Care 2013; 26: 56–8.
9. Strauss M. Crush injury, compartment syndrome and other acute peripheral ischemias. In: Kindwall EP, Whelan HT, eds. Hyperbaric Medicine Practice. Flagstaff, AZ: Best Publishing Company; 1999: 753–78.
10. Bader D, Bouton C, Colion D, Oomens C, eds. Pressure Ulcer Research: Current and Future Perspectives. Berlin, Germany: Springer; 2005.
© 2014 Wolters Kluwer Health | Lippincott Williams & Wilkins. All world rights reserved.