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Guest Editorial: Deep Tissue Injury: An Evolving Science
Deep tissue injury (DTI) was first described by the National Pressure Ulcer Advisory Panel1 in 2002 as a unique form of pressure ulcers. Little was known about DTI at that time, but its seriousness was evident in case after case. Over the years, the interest in DTI has grown and the science is evolving.
Since I published the first case study2 on DTI, two additional cases series have been completed here in the US — one by me3 and one by Mona Baharestani.4 We both have discovered a wide range of ages and outcomes in patients with DTI ranging from recovery of injured tissue to horrendous ulcers. My case series included patients who died of DTI-induced sepsis and other patients who underwent amputation or colostomy. Dr. Baharestani noted that 36% of her reported cases resolved; interestingly, 90% of these patients had anemia. I found that the first acknowledgment of purple intact skin occurred 48 hours after the time of injury or “confinement event” as I called it. This confinement event included lying unconscious on the floor at home or on the operating table or supine in hospital beds. I also discovered that a thin epidermal blister developed approximately 72 hours from the time of injury.
I was fortunate to have a colleague (Dr. Janet Cuddigan) who was willing to work with me to develop a conceptual model of the DTI phenomenon. Together, we attempted to explain all the possible threads of pathogenesis of this unique pressure ulcer. Theories under discussion today include pressure and tissue deformation,5 ischemia, reperfusion injury,6 and shearing injury. Drs. Berlowitz and Brienza’s7 recent thinking regarding the role of DTI as the cause of all Stage III and Stage IV pressure ulcers is again pushing the envelope of our understanding of pressure ulcer pathogenesis. We will need to re-examine the pressure-time curve to comprehend DTIs. I have a conceptual model on display outside my office; I promise to get it published so others can make use of it.
Several groups in Europe and Western Asia have embraced the concept of DTI and completed some stunning research. Dr. Anke Stekelenburg8 created DTI in a lab setting and reported that pressure alone is the cause of the injury. When she created ischemia by tying off an artery, the same pressure-induced changes occurred. This is an interesting finding. We have struggled to understand the significance of ischemia as a risk factor for pressure ulcers. Dr. Stekelenburg’s work continues to challenge all of us to better understand pressure ulcer risk and pathogenesis. Dr. Amit Geffen and his colleagues5 in Israel developed an algorithm to predict DTI onset in patients confined to wheelchairs. Prediction is a complex science; this work on tissue deformation will be crucial to our understanding of biomechanical risk.
Last year, the US government payor system, the Centers for Medicare and Medicaid, added an ICD-9 code to classify DTI. This action will provide data on the burden to society from these ulcers. We also may be able to examine regional and seasonal trends in the data.
The science of DTI is evolving through the work of many scientists and clinicians but much has yet to be discovered. For example, what is the natural history of DTI? What happens if we do nothing to treat DTI? What happens if we fully offload? How long does it take a DTI to develop? What are the comorbidities that make DTI unavoidable? Meanwhile, we continue to seek a diagnostic instrument to help us distinguish DTI from all the other purple wounds. Random controlled trials to guide practice are challenging to design and conduct.
I have been fortunate to have been present at the ground-breaking of DTI science and privileged to have talked with many of you about these complex and confusing pressure ulcers. Although DTI might be rare, we have an obligation to discover all we can to prevent and treat it. The journey is just beginning!
1. Black J, the National Pressure Ulcer Advisory Panel. Moving toward consensus on deep tissue injury and pressure ulcer staging. Advances Skin Wound Care. 2005;8(8):415–421.
2. Black J, Black S. Deep tissue injury. WOUNDS. 2003;15(11):380.
3. Black J. Case series of deep tissue injury. Presented at the European Pressure Ulcer Advisory Meeting, Berlin, Germany. August 28, 2007.
4. Baharestani M. Case series of deep tissue injury. Presented at the Symposium on Advanced Wound Care, San Diego, CA. April 24–27, 2008.
5. Linder-Ganz E, Gefen A. Stress analyses coupled with damage laws to determine biomechanical risk factors for deep tissue injury during sitting. J Biomech Engineer. 2009;131(1):011003.
6. Parks DA, Granger DN. Ischemia-reperfusion injury: a radical view. Hepatology. 1988;8(3):680–682.
7. Berlowitz D, Brienza D. Are all pressure ulcers the result of deep tissue injury? Ostomy Wound Manage. 2007;53(10):34–38.
8. Stekelenburg A. Gawlitta D, Bader DL, Oomens CW. Deep tissue injury: how deep is our understanding. Arch Phys Med Rehabil. 2008;89(7):1410–1413.
